BACKGROUND Superior mesenteric artery(SMA)injuries rarely occur during blunt abdominal injuries,with an incidence of<1%.The clinical manifestations mainly include abdominal hemorrhage and peritoneal irritation,whic...BACKGROUND Superior mesenteric artery(SMA)injuries rarely occur during blunt abdominal injuries,with an incidence of<1%.The clinical manifestations mainly include abdominal hemorrhage and peritoneal irritation,which progress rapidly and are easily misdiagnosed.Quick and accurate diagnosis and timely effective treatment are greatly significant in managing emergent cases.This report describes emergency rescue by a multidisciplinary team of a patient with hemorrhagic shock caused by SMA rupture.CASE SUMMARY A 55-year-old man with hemorrhagic shock presented with SMA rupture.On admission,he showed extremely unstable vital signs and was unconscious with a laceration on his head,heart rate of 143 beats/min,shallow and fast breathing(frequency>35 beats/min),and blood pressure as low as 20/10 mmHg(1 mmHg=0.133 kPa).Computed tomography revealed abdominal and pelvic hematocele effusion,suggesting active bleeding.The patient was suspected of partial rupture of the distal SMA branch.The patient underwent emergency mesenteric artery ligation,scalp suture,and liver laceration closure.In view of conditions with acute onset,rapid progression,and high bleeding volume,key points of nursing were conducted,including activating emergency protocol,opening of the green channel,and arranging relevant examinations with various medical staff for quick diagnosis.The seamless collaboration of the multidisciplinary team helped shorten the preoperative preparation time.Emergency laparotomy exploration and mesenteric artery ligation were performed to mitigate hemorrhagic shock while establishing efficient venous accesses and closely monitoring the patient’s condition to ensure hemodynamic stability.Strict measures were taken to avoid intraoperative hypothermia and infection.CONCLUSION After 3.5 h of emergency rescue and medical care,bleeding was successfully controlled,and the patient’s condition was stabilized.Subsequently,the patient was transferred to the intensive care unit for continuous monitoring and treatment.On the sixth day,the patient was weaned off the ventilator,extubated,and relocated to a specialized ward.Through diligent medical intervention and attentive nursing,the patient made a full recovery and was discharged on day 22.The follow-up visit confirmed the patient’s successful recovery.展开更多
Objective: To evaluate the immunoprotective effects of HSH resuscitation on rats with hemorrhagic shock. Methods: Controlled hemorrhagic shock was induced by blood withdrawal. The animals were divided into 3 groups: s...Objective: To evaluate the immunoprotective effects of HSH resuscitation on rats with hemorrhagic shock. Methods: Controlled hemorrhagic shock was induced by blood withdrawal. The animals were divided into 3 groups: sham group (n=16), RL group (n=18), and HSH group (n=18). Then RL group and HSH group were divided into 3 subgroups. The rats were killed 1, 2 and 4 h after resuscitation. HE staining, transmission electron microscope and TUNEL staining were used to detect apoptosis of lymphocytes in the spleen. Apoptosis index (AI) of each group was calculated. Realtime quantitative RT-PCR was performed to record TNF-α mRNA copies in the spleen. Results: There was no difference in AI among HSH group and 1 h subgroup of RL and sham group(P>0.05); AI of the 2 and 4 h subgroups of RL group was higher than that of other groups (P<0.05); there was no significant difference in AI among HSH subgroups(P>0.05). The expression of TNF-α mRNA was higher in RL 1 h subgroup than the others (P<0.05),and there was no difference between HSH 4 h subgroup and sham group. Conclusion: HSH can down-regulate the expression of TNF-α mRNA in the spleen, reduce excessive apoptosis of lymphocytes in the spleen, and protect the immunofunction following hemorrhagic shock.展开更多
AIM:To investigate whether electroacupuncture(EA)at Zusanli(ST36)prevents intestinal barrier and remote organ dysfunction following prolonged hemorrhagic shock through a vagus anti-inflammatory mechanism.METHODS:Sprag...AIM:To investigate whether electroacupuncture(EA)at Zusanli(ST36)prevents intestinal barrier and remote organ dysfunction following prolonged hemorrhagic shock through a vagus anti-inflammatory mechanism.METHODS:Sprague-Dawley rats were subjected to about 45%of total blood volume loss followed by delayed fluid replacement(DFR)with Ringer lactate 3h after hemorrhage.In a first study,rats were randomly divided into six groups:(1)EAN:EA at non-channel acupoints followed by DFR;(2)EA:EA at ST36 after hemorrhage followed by DFR;(3)VGX/EA:vagotomy(VGX)before EA at ST36 and DFR;(4)VGX/EAN:VGX before EAN and DFR;(5)α-bungarotoxin(α-BGT)/EA:intraperitoneal injection ofα-BGT before hemorrhage,followed by EA at ST36 and DFR;and(6)α-BGT/EAN group:α-BGT injection before hemorrhage followed by EAN and DFR.Survival and mean arterial pressure(MAP)were monitored over the next 12 h.In a second study,with the same grouping and treatment,cytokine levels in plasma and intestine,organ parameters,gut injury score,gut permeability to 4 kDa FITC-dextran,and expression and distribution of tight junction protein ZO-1 were evaluated.RESULTS:MAP was significantly lowered after blood loss;EA at ST36 improved the blood pressure at corresponding time points 3 and 12 h after hemorrhage.EA at ST36 reduced tumor necrosis factor-αand interleukin(IL)-6 levels in both plasma and intestine homogenates after blood loss and DFR,while vagotomy or intraperitoneal injection ofα-BGT before EA at ST36reversed its anti-inflammatory effects,and EA at ST36did not influence IL-10 levels in plasma and intestine.EA at ST36 alleviated the injury of intestinal villus,the gut injury score being significantly lower than that of EAN group(1.85±0.33 vs 3.78±0.59,P<0.05).EA at ST36 decreased intestinal permeability to FITCdextran compared with EAN group(856.95 ng/mL±90.65 ng/mL vs 2305.62 ng/mL±278.32 ng/mL,P<0.05).EA at ST36 significantly preserved ZO-1 protein expression and localization at 12 h after hemorrhage.However,EA at non-channel acupoints had no such effect,and abdominal vagotomy andα-BGT treatment could weaken or eliminate the effects of EA at ST36.Besides,EA at ST36 decreased blood aminotransferase,MB isoenzyme of creatine kinase and creatinine vs EAN group at corresponding time points.At the end of 12-h experiment,the survival rate of the EA group was significantly higher than that of the other groups.CONCLUSION:EA at ST36 attenuates the systemic inflammatory response,protects intestinal barrier integrity,improves organ function and survival rate after hemorrhagic shock via activating the cholinergic antiinflammatory mechanism.展开更多
AIM To compare the effects of extract F of red-rooted Salvia (EFRRS) on mucosal lesions of gastric corpus and antrum induced by hemorrhagic shock and reperfusion in rats.``METHODS The rats were subject to hemorrhagic ...AIM To compare the effects of extract F of red-rooted Salvia (EFRRS) on mucosal lesions of gastric corpus and antrum induced by hemorrhagic shock and reperfusion in rats.``METHODS The rats were subject to hemorrhagic shock and followed by reperfusion, and were divided randomly into two groups. Group 1 received saline, and group 2received EFRRS intravenously. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesional area in the corpus or antrum. The degree of gastric mucosal lesions (DGML) was catalogued grade 0,1. 2 and 3. The concentrations of prostaglandins (lags)were measured by radioimmunoassay. The concentration of MDA was measured according to the procedures of Asakawa. The activity of SOD was measured by the biochemical way. The growth rates or inhibitory rates of above-mentioned parametes were calculated.``RESULTS As compared with IGML (%), grade 3 damage (%) and MDA content (nmol/g tissue) of gastric antrum which were respectively 7.96 ± 0.59, 34.86± 4.96 and 156.98± 16.12. those of gastric corpus which were respectively 23.18 ± 6.82, 58.44 ± 9.07 and 230.56 ± 19.37increased markedly (P<0.01), whereas the grade 0damage, grade 1 damage, the concentrations of PGE2 and PGI2(pg/ mg tissue), the ratio of PGI2/ TXA2 and the activity of SOD (U/ g tissue) of corpus which were respectively 3.01 _- 1.01, 8.35 + 1.95, 540.48 _+ 182.78,714.38 ± 123.74, 17.38 ± 5.93 and 134.29 ± 13.35 were markedly lower than those of antrum which were respectively 13.92 ± 2.25, 26.78 ± 6.06, 2218.56 ± 433.12,2531.76 ± 492.35, 43.46 ± 8.51 and 187.45 ± 17.67( P<0.01 ) after hemorrhagic shock and reperfusion. After intravenous EFRRS, the growth rates (%) of grade 0damage, grade 1 damage, the concentrations of PGE2 and PGI2, the ratio of PGI2/TXA2 and the activity of SOD of corpus which were respectively 632.56, 308.62, 40.75,74.75, 92.29 and 122.25 were higher than those in antrum which were respectively 104,89, 58.40, 11.12, 56.58,30.65 and 82.64, whereas the inhibitory rates (%) ofIGML, grade 3 damage and MDA content of gastric corpus were 82.93, 65.32 and 59.09, being higher than those of gastric antrum which were 76.64, 53.18 and 42.37.``CONCLUSION After hemorrhagic shock-reperfusion, the gastric mucosal lesions in the corpus were more severe than those in the antrum, which were related not only to the different distribution of endogenous PGs in the mucosa, but also to the different ability of anti-oxidation of the mucosa. The protective effect of EFRRS on the gastric mucosa in the corpus was more evident than that in the antrum, which was related to higher growth degree of PGs contents and anti-oxitative ability in gastric corpus after administration of EFRRS.展开更多
Objective: To explore the protection and molecular mechanism of histone deacetylase inhibitors(HDACIs) on the spleen of rats with hemorrhagic shock. Methods: A total of 60 SPF male SD rats were selected for the modeli...Objective: To explore the protection and molecular mechanism of histone deacetylase inhibitors(HDACIs) on the spleen of rats with hemorrhagic shock. Methods: A total of 60 SPF male SD rats were selected for the modeling of severe hemorrhagic shock using the method of arterial and venous cannulation with the time-divided bleeding. The measurement of mean arterial blood pressure and blood lactic acid was used to verify the modeling. The modeled rats were randomly divided into shock group, shock+suberoylanilide hydroxamic acid(SAHA) group, shock+autogenous transfusion group, and shock+SAHA+autogenous transfusion group. Three hours after the treatment, the spleen of rats was collected and TUNEL method was employed to detect the apoptosis of spleen cells in each group. Afterwards, real-time PCR and western blot were employed to detect the expression of BCL-2, BAX, and caspass3 in the spleen of rats in each group. Results: A total of 55 rats had successful modeling of severe hemorrhagic shock, with success rate of 92%. Cell apoptosis in the severe hemorrhagic model group was the most serious. After the intervention of HDACIs and the autogenous transfusion, the tissue injury was a bit recovered. Cell apoptosis was least in the shock+SAHA+autogenous transfusion group(P<0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BCL-2 was significantly increased(P<0.05), with highest relative expression of BCL-2 in shock+SAHA+autogenous transfusion group(P<0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BAX was significantly decreased(P<0.05), with lowest relative expression of BAX in the intervention group of single HDACIs. The change in the expression of caspass3 was similar to BAX, namely the relative expression of caspass3 was significantly decreased after the intervention of HDACIs and the autogenous transfusion(P<0.05). Conclusions: HDACIs and autogenous transfusion can all protect the spleen injury because of the severe hemorrhagic shock. Its molecular mechanism may be related to the regulation on the expression of BCL-2/BAX and caspass3, which may affect the apoptosis process of cells.展开更多
BACKGROUND:Hypothermia is associated with poor outcome in trauma patients;however,hemorrhagic shock(HS)model with anesthetized swine was different from that of clinical reality.To identify the effects of environmental...BACKGROUND:Hypothermia is associated with poor outcome in trauma patients;however,hemorrhagic shock(HS)model with anesthetized swine was different from that of clinical reality.To identify the effects of environmental hypothermia on HS,we investigated hemodynamics and oxygen dynamics in an unanesthetized swine model of HS under simulating hypothermia environment.METHODS:Totally 16 Bama pigs were randomly divided into ambient temperature group(group A)and low temperature group(group B),8 pigs in each group.Venous blood(30 mL/kg)was continuously withdrawn for more than 15 minutes in conscious swine to establish a hemorrhagic shock model.Pulmonary arterial temperature(Tp),heart rate(HR),mean arterial pressure(MAP),pulmonary arterial pressure(PAP),pulmonary arterial wedge pressure(PAWP),central venous pressure(CVP),cardiac output(CO),hemoglobin(Hb),saturation of mixed venous blood(SvO_2)and blood gas analysis were recorded at the baseline and different hemorrhagic shock time(HST).The whole body oxygen delivery indices,DO_2l and VO_2l,and the O_2 extraction ratio(O_2ER)were calculated.RESULTS:Core body temperature in group A decreased slightly after the hemorrhagic shock model was established,and environmental hypothermia decreased in core body temperature.The mortality rate was significantly higher in group B(50%)than in group A(0%).DO_2l and VO_2l decreased significantly after hemorrhage.No difference was found in hemodynamics,DO_2l and VO_2l between group A and group B,but the difference in pH,lactic acid and O_2ER was significant between the two groups.CONCLUSION:Environmental hypothermia aggravated the disorder of oxygen metabolism after hemorrhagic shock,which was associated with poor prognosis.展开更多
AIM: To characterize differences of arterial(ABG) and venous(VBG) blood gas analysis in a rabbit model of hemorrhagic shock. METHODS: Following baseline arterial and venous blood gas analysis, fifty anesthetized, vent...AIM: To characterize differences of arterial(ABG) and venous(VBG) blood gas analysis in a rabbit model of hemorrhagic shock. METHODS: Following baseline arterial and venous blood gas analysis, fifty anesthetized, ventilated New Zealand white rabbits were hemorrhaged to and maintained at a mean arterial pressure of 40 mm Hg until a state of shock was obtained, as defined by arterial p H ≤ 7.2 and base deficit ≤-15 mmol/L. Simultaneous ABG and VBG were obtained at 3 minute intervals. Comparisons of p H, base deficit, p CO2, and arteriovenous(a-v) differences were then made between ABG and VBG at baseline and shock states. Statistical analysis was applied where appropriate with a significance of P < 0.05. RESULTS: All 50 animals were hemorrhaged to shockstatus and euthanized; no unexpected loss occurred. Significant differences were noted between baseline and shock states in blood gases for the following parameters: p H was significantly decreased in both arterial(7.39 ± 0.12 to 7.14 ± 0.18) and venous blood gases(7.35 ± 0.15 to 6.98 ± 0.26, P < 0.05), base deficit was significantly increased for arterial(-0.9 ± 3.9 m Eq/L vs-17.8 ± 2.2 m Eq/L) and venous blood gasses(-0.8 ± 3.8 m Eq/L vs-15.3 ± 4.1 m Eq/L, P < 0.05). p CO2 trends(baseline to shock) demonstrated a decrease in arterial blood(40.0 ± 9.1 mm Hg vs 28.9 ± 7.1 mm Hg) but an increase in venous blood(46.0 ± 10.1 mm Hg vs 62.8 ± 15.3 mm Hg), although these trends were non-significant. For calculated arteriovenous differences between baseline and shock states, only the p CO2 difference was shown to be significant during shock.CONCLUSION: In this rabbit model, significant differences exist in blood gas measurements for arterial and venous blood after hemorrhagic shock. A widened p CO2 a-v difference during hemorrhage, reflective of poor tissue oxygenation, may be a better indicator of impending shock.展开更多
AIM: To investigate the functional, morphological changes of the gut barrier during the restitution process after hemorrhagic shock, and the regional differences of the large intestine and small intestine in response ...AIM: To investigate the functional, morphological changes of the gut barrier during the restitution process after hemorrhagic shock, and the regional differences of the large intestine and small intestine in response to ischemia/reperfusion injury.METHODS: Forty-seven Sprague-Dawley rats with body weight of 250-300 g were divided into two groups: control group (sham shock n = 5) and experimental group (n = 42).Experimental group was further divided into six groups (n = 7 each) according to different time points after the hemorrhagic shock, including 0th h group, 1st h group, 3rd h group, 6th h group, 12th h group and 24th h group. All the rats were gavaged with 2 mL of suspension of lactulose (L) (100 mg/2 mL) and mannitol (M) (50 mg/each) at the beginning and then an experimental rat model of hemorrhagic shock was set up. The specimens from jejunum, ileum and colon tissues and the blood samples from the portal vein were taken at 0, 1, 3, 6, 12 and 24 h after shock resuscitation, respectively. The morphological changes of the intestinal mucosa, including the histology of intestinal mucosa, the thickness of mucosa, the height of villi, the index of mucosal damage and the numbers of goblet cells, were determined by light microscope and/or electron microscope. The concentrations of the bacterial endotoxin lipopolysaccharides (LPS) from the portal vein blood, which reflected the gut barrier function, were examined by using Limulus test. At the same time point,to evaluate intestinal permeability, all urine was collected and the concentrations of the metabolically inactive markers such as L and M in urine were measured by using GC-9A gas chromatographic instrument.RESULTS: After the hemorrhagic shock, the mucosal epithelial injury was obvious in small intestine even at the 0th h, and it became more serious at the 1st and the 3rd h. The tissue restitution was also found after 3 h,though the injury was still serious. Most of the injured mucosal restitution was established after 6 h and completed in 24 h. Two distinct models of cell deathapoptosis and necrosis-were involved in the destruction of rat intestinal epithelial cells. The number of goblet cells on intestinal mucosa was reduced significantly from 0 to 24 h (the number from 243±13 to 157±9 for ileum, 310±19 to 248±18 for colon; r = -0.910 and -0.437 respectively,all P<0.001), which was the same with the large intestine, but the grade of injury was lighter with the values of mucosal damage index in 3 h for jejunum,ileum, and colon being 2.8, 2.6, 1.2, respectively. The mucosal thickness and the height of villi in jejunum and ileum diminished in 1 h (the average height decreased from 309±24 to 204±23 μm and 271±31 to 231±28 μm,r = -0.758 and -0.659, all P<0.001; the thickness from 547±23 to 418±28 μm and 483±45 to 364±35 μm, r= -0.898 and -0.829, all P<0.001), but there was no statistical difference in the colon (F= 0.296, P = 0.934). Compared with control group, the urine L/M ratio and the blood LPS concentration in the experimental groups raised significantly,reaching the peak in 3-6 h (L/M: control vs 3 h vs 6 h was 0.029±0.09 vs 0.063±0.012 vs 0.078±0.021, r=-0.786,P<0.001; LPS: control vs 3 h vs6 h was 0.09±0.021 vs 0.063±0.012 vs 0.25±0.023, r= -0.623, P<0.001), and it kept increasing in 24 h.CONCLUSION: The gut barrier of the rats was seriously damaged at the early phase of ischemic reperfusion injury after hemorrhagic shock, which included the injury and atrophy in intestinal mucosa and the increasing of intestinal permeability. Simultaneously, the intestinal mucosa also showed its great repairing potentiality, such as the improvement of the intestinal permeability and the recovery of the morphology at different phases after ischemic repeffusion injury. The restitution of gut barrier function was obviously slower than that of the morphology and there was no direct correlation between them.Compared with the small intestine, the large intestine had stronger potentiality against injury. The reduction of the amount of intestinal goblet cells by injury did not influence the ability of intestinal mucosal restitution at a certain extent and it appeared to be intimately involved in the restitution of the epithelium.展开更多
AIM: To investigate the effects of biliary tract external drainage(BTED) on intestinal barrier injury in rats with hemorrhagic shock(HS). METHODS: BTED was performed via cannula insertion into the bile duct of rats. H...AIM: To investigate the effects of biliary tract external drainage(BTED) on intestinal barrier injury in rats with hemorrhagic shock(HS). METHODS: BTED was performed via cannula insertion into the bile duct of rats. HS was induced by drawing blood from the femoral artery at a rate of 1 m L/min until a mean arterial pressure(MAP) of 40 ± 5 mm Hg was achieved. That MAP was maintained for 60 min. A total of 99 Sprague-Dawley rats were randomized into a sham group, an HS group and an HS + BTED group. Nine rats in the sham group were sacrificed 0.5 h after surgery. Nine rats in each of the HS and HS + BTED groups were sacrificed 0.5 h, 1 h, 2 h, 4 h and 6 h after resuscitation. Plasma tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), and lipopolysaccharide(LPS) levels were analyzed using enzyme-linked immunosorbent assay. Plasma D-lactate levels were analyzed using colorimetry. The expression levels of occludin and claudin-1 in the ileum were analyzed using Western blot and immunohistochemistry. Histology of the ileumwas evaluated by hematoxylin and eosin staining. RESULTS: Plasma TNF-α levels in the HS + BTED group decreased significantly compared with the HS group at 1 h and 6 h after resuscitation(P < 0.05). Plasma IL-6 levels in the HS + BTED group decreased significantly compared with the HS group at 0.5 h, 1 h and 2 h after resuscitation(P < 0.05). Plasma D-lactate and LPS levels in the HS + BTED group decreased significantly compared with the HS group at 6 h after resuscitation(P < 0.05). The expression levels of occludin in the HS + BTED group increased significantly compared with the HS group at 4 h and 6 h after resuscitation(P < 0.05). The expression levels of claudin-1 in the HS + BTED group increased significantly compared with the HS group at 6 h after resuscitation(P < 0.05). Phenomena of putrescence and desquamation of epithelial cells in the ileal mucosa were attenuated in the HS + BTED group. Ileal histopathologic scores in the HS + BTED group decreased significantly compared with the HS group at 2 h, 4 h and 6 h after resuscitation(P < 0.05). CONCLUSION: BTED protects against intestinal barrier injury in HS rats.展开更多
BACKGROUND Esophageal submucosal hematoma is a rare condition.Although the exact etiology remains uncertain,vessel fragility with external factors is believed to have led to submucosal bleeding and hematoma formation;...BACKGROUND Esophageal submucosal hematoma is a rare condition.Although the exact etiology remains uncertain,vessel fragility with external factors is believed to have led to submucosal bleeding and hematoma formation;the vessel was ruptured by a sudden increase in pressure due to nausea,and the hematoma was enlarged by antiplatelet or anticoagulant therapy.Serious conditions are rare,with a better prognosis.We present the first known case of submucosal esophageal hematoma-subsequent hemorrhagic shock due to Mallory-Weiss syndrome.CASE SUMMARY A 73-year-old female underwent endovascular treatment for an unruptured cerebral aneurysm.The patient received aspirin and clopidogrel before surgery and heparin during surgery,and was well during the surgery.Several hours after returning to the ICU,she complained of chest discomfort,vomited 500 m L of fresh blood,and entered hemorrhagic shock.Esophageal submucosal hematoma with Mallory-Weiss syndrome was diagnosed through an endoscopic examination and computed tomography.In addition to a massive fluid and erythrocyte transfusion,we performed a temporary compression for hemostasis with a Sengstaken-Blakemore(S-B)tube.Afterwards,she became hemodynamically stable.On postoperative day 1,we performed an upper gastrointestinal endoscopy and confirmed no expansion of the hematoma nor any recurring bleeding;therefore,we removed the S-B tube and clipped the gastric mucosal laceration at the esophagogastric junction.We started oral intake on postoperative day 10.The patient made steady progress,and was discharged on postoperative day 33.CONCLUSION We present the first known case of submucosal esophageal hematoma subsequent hemorrhagic shock due to Mallory-Weiss syndrome.展开更多
AIM: To study the protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats.METHODS: A total of 32 SD rats were randomly divided into four g...AIM: To study the protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats.METHODS: A total of 32 SD rats were randomly divided into four groups (n = 8, each group): normal group,model group, low dosage group (treated with 10 g/kg Astragalus membranaceus) and high dosage group (treated with 20 g/kg Astragalus membranaceus). The model of hemorrhagic shock for 60 min and reperfusion for 90 min was established. Therapeutic solution (3 mL)was administrated before reperfusion. At the end of the study, the observed intestinal pathology was analyzed. The blood concentrations of lactic acid (LD), nitric oxide (NO),endothelin-1 (ET-1), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) in intestinal mucosa were determined.RESULTS: The intestinal mucosa pathology showed severe damage in model group and low dosage group,slight damage in high dosage group and no obvious damage in normal group. The Chiu's score in low dose group and high dose group was significantly lower than that in model group. The content of MDA in model group was higher than that in low and high dose groups, while that in high dose group was almost the same as in normal group. The activity of SOD and GSH-PX was the lowest in model group and significantly higher in high dose group than in normal and low dose groups. The concentrations of LD and ET-1 in model group were the highest. The concentrations of NO in model group and low dose group were significantly lower than those in high dose group and normal group.CONCLUSION: High dose Astragalus membranaeus has much better protective effect on hemorrhagic shockreperfusion injury of intestinal mucosa than low dose Astragalus membranaceus. The mechanism may be that Astragalus membranaceus can improve antioxidative effect and regulate NO/ET level during hemorrhagic reperfusion.展开更多
To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 (HO-1) expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscit...To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 (HO-1) expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscitation (HTS), normal saline resuscitation (NS) and sham groups. HO-1 mRNA, protein expression and apoptosis were evaluated in organs. In the HTS group, significant difference was noted in HO-1 protein in small intestinal mucosa and liver compared with the NS and sham groups, and in HO-1 mRNA in liver and kidney compared with the sham group. The apoptosis of small intestinal mucosa, liver, heart, and lung was significantly lower in the HTS group than that in the NS group. In this study, small volume resuscitation with HTS can efficiently up-regulate the expression level of HO-1 in small intestinal mucosa and liver, which may be one of the mechanisms alleviating organ damage.展开更多
AIM: To determine the time course of intestinal permeability changes to proteolytically-derived bowel peptides in experimental hemorrhagic shock. METHODS: We injected fluorescently-conjugated casein protein into the s...AIM: To determine the time course of intestinal permeability changes to proteolytically-derived bowel peptides in experimental hemorrhagic shock. METHODS: We injected fluorescently-conjugated casein protein into the small bowel of anesthetized Wistar rats prior to induction of experimental hemorrhagic shock. These molecules, which fluoresce when proteolytically cleaved, were used as markers for the ability of proteolytically cleaved intestinal products to access the central circulation. Blood was serially sampled to quantify the relative change in concentration of proteolytically-cleaved particles in the systemic circulation. To provide spatial resolution of their location, particles in the mesenteric microvasculature were imaged using in vivo intravital fluorescent microscopy. The experiments were then repeated using an alternate measurement technique, fluorescein isothiocyanate(FITC)-labeled dextrans 20, to semi-quantitatively verify the ability of bowel-derived low-molecular weight molecules(< 20 k D) to access the central circulation.RESULTS: Results demonstrate a significant increase in systemic permeability to gut-derived peptides within 20 min after induction of hemorrhage(1.11 ± 0.19 vs 0.86 ± 0.07, P < 0.05) compared to control animals. Reperfusion resulted in a second, sustained increase in systemic permeability to gut-derived peptides in hemorrhaged animals compared to controls(1.2 ± 0.18 vs 0.97 ± 0.1, P < 0.05). Intravital microscopy of the mesentery also showed marked accumulation of fluorescent particles in the microcirculation of hemorrhaged animals compared to controls. These results were replicated using FITC dextrans 20 [10.85 ± 6.52 vs 3.38 ± 1.11 fluorescent intensity units(× 105, P < 0.05, hemorrhagic shock vs controls)], confirming that small bowel ischemia in response to experimental hemorrhagic shock results in marked and early increases in gut membrane permeability. CONCLUSION: Increased small bowel permeability in hemorrhagic shock may allow for systemic absorption of otherwise retained proteolytically-generated peptides, with consequent hemodynamic instability and remote organ failure.展开更多
AIM To evaluate the effects of mineralocorticoid receptor(MR) antagonists on mortality and inflammatory responses after hemorrhagic shock(HS) in rats.METHODS One hundred and two male Sprague–Dawley rats were randomly...AIM To evaluate the effects of mineralocorticoid receptor(MR) antagonists on mortality and inflammatory responses after hemorrhagic shock(HS) in rats.METHODS One hundred and two male Sprague–Dawley rats were randomly assigned to one of the following three groups: Control, spironolactone (SPL), and eplerenone(EP) groups. HS was induced by the removal of blood. One half of rats were evaluated to determine mortality, hemodynamics, plasma tumor necrosis factor-alpha(TNF-α) concentrations, and arterial blood gas at 8 h afterHS recovery. In the remainder of rats, the expression levels of genes encoding cytokines were evaluated in liver tissue samples at 1 h after HS recovery. RESULTS The survival rates 8 h after HS recovery were 71%, 94%, and 82% in the control, SPL, and EP groups, respectively. There were no significant differences in survival rates among the three groups (P = 0.219). Furthermore, there were no significant differences in gene expression levels in the liver or plasma TNF-α concentrations among the three groups(P = 0.888).CONCLUSION Pretreatment with MR antagonists did not improve mortality or cytokine responses in the liver after HS recovery in rats.展开更多
Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was esta...Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was established in 32 SD (Sprague-Dawley) rats. The rats were randomly divided into control group, no fluid resuscitation group (NF group), controlled fluid resuscitation group (NS40 group) and rapid large scale fluid resuscitation group (NS80 group). Each group contained 8 rats. The curative effects were compared. At the same time, the apoptosis in liver, kidney, lung and small intestinal mucosa of survivors after hemorrhage and resuscitation was detected by light microscopy in HE (hematoxylin and eosin) stained tissue sections, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Results: The survival rate of early fluid resuscitation (14/16) was markedly higher than that of NF group (3/8). There was some apoptosis in liver, kidney, lung and small intestinal mucosa of all survivors. Compared with NF and NS40 groups, the apoptosis of liver, kidney and small intestinal mucosa of NS80 group was obviously increased. Conclusions: Among three fluid resuscitation methods, controlled fluid resuscitation can obviously improve the early survival rate and the apoptosis of liver, kidney and small intestinal mucosa in rats with severe and uncontrolled hemorrhagic shock, and may benefit improvement of prognosis.展开更多
Objective: To investigate the potential and early effect of hypertonic saline resuscitation on T-lymphocyte sub- populations in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was es...Objective: To investigate the potential and early effect of hypertonic saline resuscitation on T-lymphocyte sub- populations in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 18 Sprague-Dawley (SD) rats. The rats were randomly divided into Sham group, HTS group (hypertonic saline resuscitation group) and NS group (normal saline resuscitation group). Each group contained 6 rats. The CD4+ and CD8+ subpopulations of T-lymphocytes in peripheral blood were detected respectively before shock and after resuscitation by double antibody labelling and flow cytometry. Results: In the early stage after hemorrhagic shock, fluid resuscitation and emergency treatment, the CD4+ lymphocytes of peripheral blood in HTS and NS groups markedly increased. Small volume resuscitation with HTS also induced peripheral CD8+ lymphocytes to a certain extent, whereas NS resuscitation showed no effect in this respect. Consequently, compared with Sham and HTS groups, CD4+/CD8+ ratio of peripheral blood in NS group was obviously increased, and showed statistically differences. Conclusion: In this model of rat with severe hemorrhagic shock, small volume resuscitation with HTS is more effective than NS in reducing immunologic disorders and promoting a more balanced profile of T-lymphocyte subpopula- tions regulating network.展开更多
Objective. To investigate clinically useful markers for determining the seventy of hemorrhagic shock and adequacy of resuscitation Methods. Prospective study was undertaken in 12 dogs, using an established model for h...Objective. To investigate clinically useful markers for determining the seventy of hemorrhagic shock and adequacy of resuscitation Methods. Prospective study was undertaken in 12 dogs, using an established model for hemorrhagic shock. The anesthetized dogs were bled to a mean arterial pressure of 40 mmHg which was maintained for 3 hours. Then each animal was resuscitated with heperinized whole blood followed by intravenous infusion of dobutamine at a rate of 5 ug. kg-1. min-1 for 10 minutes. Arterial and mixed venous blood gases, arterial lactate concentrations and hemodynamic Parameters were measured throughout the study. Results. A difference in the PCO2 and pH values between arterial and mixed venous blood was observed. Arterial-venous PCO2 and pH difference increased significantly after sustained shock. The arteriovenous carbon dioxide and pH gradients recovered more rapidly than arterial lactate levels after successful resuscitation with blood and dobutamine. Conclusion. Arterial blood gases fail to reflect the acid-base status of tissues during hemorrhagic shock. The differences in PCO2 and pH values between arterial and mixed venous blood could be used as clinical in- dicators for assessing the seventy of shock and efficacy of resuscitation.展开更多
Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rat...Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer's lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuated injury of the lung and decreased the concentration of lactic acid and the number of in situ TdT-mediated dUTP nick-end labelling (TUNEL)-positive cells. Moreover, immunohistochemistry performed 24 h after reperfusion revealed increases in the level of nuclear factor κB (NF-κB), and phosphorylated p38 mitogen-activated protein kinase (MAPK) in the albumin-untreated group was down-regulated by albumin treatment when compared with the sham rats. Conclusion: Resuscitation with albumin attenuates tissue injury and inhibits T/HS-induced apoptosis in the lung via the p38 MAPK signal transduction pathway that functions to stimulate the activation of NF-κB.展开更多
基金Supported by The Health Science and Technology Program of Zhejiang Province,No.2022KY836.
文摘BACKGROUND Superior mesenteric artery(SMA)injuries rarely occur during blunt abdominal injuries,with an incidence of<1%.The clinical manifestations mainly include abdominal hemorrhage and peritoneal irritation,which progress rapidly and are easily misdiagnosed.Quick and accurate diagnosis and timely effective treatment are greatly significant in managing emergent cases.This report describes emergency rescue by a multidisciplinary team of a patient with hemorrhagic shock caused by SMA rupture.CASE SUMMARY A 55-year-old man with hemorrhagic shock presented with SMA rupture.On admission,he showed extremely unstable vital signs and was unconscious with a laceration on his head,heart rate of 143 beats/min,shallow and fast breathing(frequency>35 beats/min),and blood pressure as low as 20/10 mmHg(1 mmHg=0.133 kPa).Computed tomography revealed abdominal and pelvic hematocele effusion,suggesting active bleeding.The patient was suspected of partial rupture of the distal SMA branch.The patient underwent emergency mesenteric artery ligation,scalp suture,and liver laceration closure.In view of conditions with acute onset,rapid progression,and high bleeding volume,key points of nursing were conducted,including activating emergency protocol,opening of the green channel,and arranging relevant examinations with various medical staff for quick diagnosis.The seamless collaboration of the multidisciplinary team helped shorten the preoperative preparation time.Emergency laparotomy exploration and mesenteric artery ligation were performed to mitigate hemorrhagic shock while establishing efficient venous accesses and closely monitoring the patient’s condition to ensure hemodynamic stability.Strict measures were taken to avoid intraoperative hypothermia and infection.CONCLUSION After 3.5 h of emergency rescue and medical care,bleeding was successfully controlled,and the patient’s condition was stabilized.Subsequently,the patient was transferred to the intensive care unit for continuous monitoring and treatment.On the sixth day,the patient was weaned off the ventilator,extubated,and relocated to a specialized ward.Through diligent medical intervention and attentive nursing,the patient made a full recovery and was discharged on day 22.The follow-up visit confirmed the patient’s successful recovery.
文摘Objective: To evaluate the immunoprotective effects of HSH resuscitation on rats with hemorrhagic shock. Methods: Controlled hemorrhagic shock was induced by blood withdrawal. The animals were divided into 3 groups: sham group (n=16), RL group (n=18), and HSH group (n=18). Then RL group and HSH group were divided into 3 subgroups. The rats were killed 1, 2 and 4 h after resuscitation. HE staining, transmission electron microscope and TUNEL staining were used to detect apoptosis of lymphocytes in the spleen. Apoptosis index (AI) of each group was calculated. Realtime quantitative RT-PCR was performed to record TNF-α mRNA copies in the spleen. Results: There was no difference in AI among HSH group and 1 h subgroup of RL and sham group(P>0.05); AI of the 2 and 4 h subgroups of RL group was higher than that of other groups (P<0.05); there was no significant difference in AI among HSH subgroups(P>0.05). The expression of TNF-α mRNA was higher in RL 1 h subgroup than the others (P<0.05),and there was no difference between HSH 4 h subgroup and sham group. Conclusion: HSH can down-regulate the expression of TNF-α mRNA in the spleen, reduce excessive apoptosis of lymphocytes in the spleen, and protect the immunofunction following hemorrhagic shock.
基金Supported by The National Basic Research Program of China,973 Program,Grant No.2012CB518101
文摘AIM:To investigate whether electroacupuncture(EA)at Zusanli(ST36)prevents intestinal barrier and remote organ dysfunction following prolonged hemorrhagic shock through a vagus anti-inflammatory mechanism.METHODS:Sprague-Dawley rats were subjected to about 45%of total blood volume loss followed by delayed fluid replacement(DFR)with Ringer lactate 3h after hemorrhage.In a first study,rats were randomly divided into six groups:(1)EAN:EA at non-channel acupoints followed by DFR;(2)EA:EA at ST36 after hemorrhage followed by DFR;(3)VGX/EA:vagotomy(VGX)before EA at ST36 and DFR;(4)VGX/EAN:VGX before EAN and DFR;(5)α-bungarotoxin(α-BGT)/EA:intraperitoneal injection ofα-BGT before hemorrhage,followed by EA at ST36 and DFR;and(6)α-BGT/EAN group:α-BGT injection before hemorrhage followed by EAN and DFR.Survival and mean arterial pressure(MAP)were monitored over the next 12 h.In a second study,with the same grouping and treatment,cytokine levels in plasma and intestine,organ parameters,gut injury score,gut permeability to 4 kDa FITC-dextran,and expression and distribution of tight junction protein ZO-1 were evaluated.RESULTS:MAP was significantly lowered after blood loss;EA at ST36 improved the blood pressure at corresponding time points 3 and 12 h after hemorrhage.EA at ST36 reduced tumor necrosis factor-αand interleukin(IL)-6 levels in both plasma and intestine homogenates after blood loss and DFR,while vagotomy or intraperitoneal injection ofα-BGT before EA at ST36reversed its anti-inflammatory effects,and EA at ST36did not influence IL-10 levels in plasma and intestine.EA at ST36 alleviated the injury of intestinal villus,the gut injury score being significantly lower than that of EAN group(1.85±0.33 vs 3.78±0.59,P<0.05).EA at ST36 decreased intestinal permeability to FITCdextran compared with EAN group(856.95 ng/mL±90.65 ng/mL vs 2305.62 ng/mL±278.32 ng/mL,P<0.05).EA at ST36 significantly preserved ZO-1 protein expression and localization at 12 h after hemorrhage.However,EA at non-channel acupoints had no such effect,and abdominal vagotomy andα-BGT treatment could weaken or eliminate the effects of EA at ST36.Besides,EA at ST36 decreased blood aminotransferase,MB isoenzyme of creatine kinase and creatinine vs EAN group at corresponding time points.At the end of 12-h experiment,the survival rate of the EA group was significantly higher than that of the other groups.CONCLUSION:EA at ST36 attenuates the systemic inflammatory response,protects intestinal barrier integrity,improves organ function and survival rate after hemorrhagic shock via activating the cholinergic antiinflammatory mechanism.
基金Supported by the National Natural Science Foundation of China.No.3870890
文摘AIM To compare the effects of extract F of red-rooted Salvia (EFRRS) on mucosal lesions of gastric corpus and antrum induced by hemorrhagic shock and reperfusion in rats.``METHODS The rats were subject to hemorrhagic shock and followed by reperfusion, and were divided randomly into two groups. Group 1 received saline, and group 2received EFRRS intravenously. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesional area in the corpus or antrum. The degree of gastric mucosal lesions (DGML) was catalogued grade 0,1. 2 and 3. The concentrations of prostaglandins (lags)were measured by radioimmunoassay. The concentration of MDA was measured according to the procedures of Asakawa. The activity of SOD was measured by the biochemical way. The growth rates or inhibitory rates of above-mentioned parametes were calculated.``RESULTS As compared with IGML (%), grade 3 damage (%) and MDA content (nmol/g tissue) of gastric antrum which were respectively 7.96 ± 0.59, 34.86± 4.96 and 156.98± 16.12. those of gastric corpus which were respectively 23.18 ± 6.82, 58.44 ± 9.07 and 230.56 ± 19.37increased markedly (P<0.01), whereas the grade 0damage, grade 1 damage, the concentrations of PGE2 and PGI2(pg/ mg tissue), the ratio of PGI2/ TXA2 and the activity of SOD (U/ g tissue) of corpus which were respectively 3.01 _- 1.01, 8.35 + 1.95, 540.48 _+ 182.78,714.38 ± 123.74, 17.38 ± 5.93 and 134.29 ± 13.35 were markedly lower than those of antrum which were respectively 13.92 ± 2.25, 26.78 ± 6.06, 2218.56 ± 433.12,2531.76 ± 492.35, 43.46 ± 8.51 and 187.45 ± 17.67( P<0.01 ) after hemorrhagic shock and reperfusion. After intravenous EFRRS, the growth rates (%) of grade 0damage, grade 1 damage, the concentrations of PGE2 and PGI2, the ratio of PGI2/TXA2 and the activity of SOD of corpus which were respectively 632.56, 308.62, 40.75,74.75, 92.29 and 122.25 were higher than those in antrum which were respectively 104,89, 58.40, 11.12, 56.58,30.65 and 82.64, whereas the inhibitory rates (%) ofIGML, grade 3 damage and MDA content of gastric corpus were 82.93, 65.32 and 59.09, being higher than those of gastric antrum which were 76.64, 53.18 and 42.37.``CONCLUSION After hemorrhagic shock-reperfusion, the gastric mucosal lesions in the corpus were more severe than those in the antrum, which were related not only to the different distribution of endogenous PGs in the mucosa, but also to the different ability of anti-oxidation of the mucosa. The protective effect of EFRRS on the gastric mucosa in the corpus was more evident than that in the antrum, which was related to higher growth degree of PGs contents and anti-oxitative ability in gastric corpus after administration of EFRRS.
基金supported by the National Natural Science Foundation of China(No.81160230)the Natural Science Foundation of Jiangxi Province of China(No.20114BAB205003)
文摘Objective: To explore the protection and molecular mechanism of histone deacetylase inhibitors(HDACIs) on the spleen of rats with hemorrhagic shock. Methods: A total of 60 SPF male SD rats were selected for the modeling of severe hemorrhagic shock using the method of arterial and venous cannulation with the time-divided bleeding. The measurement of mean arterial blood pressure and blood lactic acid was used to verify the modeling. The modeled rats were randomly divided into shock group, shock+suberoylanilide hydroxamic acid(SAHA) group, shock+autogenous transfusion group, and shock+SAHA+autogenous transfusion group. Three hours after the treatment, the spleen of rats was collected and TUNEL method was employed to detect the apoptosis of spleen cells in each group. Afterwards, real-time PCR and western blot were employed to detect the expression of BCL-2, BAX, and caspass3 in the spleen of rats in each group. Results: A total of 55 rats had successful modeling of severe hemorrhagic shock, with success rate of 92%. Cell apoptosis in the severe hemorrhagic model group was the most serious. After the intervention of HDACIs and the autogenous transfusion, the tissue injury was a bit recovered. Cell apoptosis was least in the shock+SAHA+autogenous transfusion group(P<0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BCL-2 was significantly increased(P<0.05), with highest relative expression of BCL-2 in shock+SAHA+autogenous transfusion group(P<0.05). After the intervention of HDACIs and the autogenous transfusion, the relative expression of BAX was significantly decreased(P<0.05), with lowest relative expression of BAX in the intervention group of single HDACIs. The change in the expression of caspass3 was similar to BAX, namely the relative expression of caspass3 was significantly decreased after the intervention of HDACIs and the autogenous transfusion(P<0.05). Conclusions: HDACIs and autogenous transfusion can all protect the spleen injury because of the severe hemorrhagic shock. Its molecular mechanism may be related to the regulation on the expression of BCL-2/BAX and caspass3, which may affect the apoptosis process of cells.
基金supported by a grant from 11th Five-Year Plan Medical Science Scientific Research Fund of the Chinese People's Liberation Army(08G002)
文摘BACKGROUND:Hypothermia is associated with poor outcome in trauma patients;however,hemorrhagic shock(HS)model with anesthetized swine was different from that of clinical reality.To identify the effects of environmental hypothermia on HS,we investigated hemodynamics and oxygen dynamics in an unanesthetized swine model of HS under simulating hypothermia environment.METHODS:Totally 16 Bama pigs were randomly divided into ambient temperature group(group A)and low temperature group(group B),8 pigs in each group.Venous blood(30 mL/kg)was continuously withdrawn for more than 15 minutes in conscious swine to establish a hemorrhagic shock model.Pulmonary arterial temperature(Tp),heart rate(HR),mean arterial pressure(MAP),pulmonary arterial pressure(PAP),pulmonary arterial wedge pressure(PAWP),central venous pressure(CVP),cardiac output(CO),hemoglobin(Hb),saturation of mixed venous blood(SvO_2)and blood gas analysis were recorded at the baseline and different hemorrhagic shock time(HST).The whole body oxygen delivery indices,DO_2l and VO_2l,and the O_2 extraction ratio(O_2ER)were calculated.RESULTS:Core body temperature in group A decreased slightly after the hemorrhagic shock model was established,and environmental hypothermia decreased in core body temperature.The mortality rate was significantly higher in group B(50%)than in group A(0%).DO_2l and VO_2l decreased significantly after hemorrhage.No difference was found in hemodynamics,DO_2l and VO_2l between group A and group B,but the difference in pH,lactic acid and O_2ER was significant between the two groups.CONCLUSION:Environmental hypothermia aggravated the disorder of oxygen metabolism after hemorrhagic shock,which was associated with poor prognosis.
基金Carolinas Health Care System,Department of Surgery,Charlotte,North Carolina,United States
文摘AIM: To characterize differences of arterial(ABG) and venous(VBG) blood gas analysis in a rabbit model of hemorrhagic shock. METHODS: Following baseline arterial and venous blood gas analysis, fifty anesthetized, ventilated New Zealand white rabbits were hemorrhaged to and maintained at a mean arterial pressure of 40 mm Hg until a state of shock was obtained, as defined by arterial p H ≤ 7.2 and base deficit ≤-15 mmol/L. Simultaneous ABG and VBG were obtained at 3 minute intervals. Comparisons of p H, base deficit, p CO2, and arteriovenous(a-v) differences were then made between ABG and VBG at baseline and shock states. Statistical analysis was applied where appropriate with a significance of P < 0.05. RESULTS: All 50 animals were hemorrhaged to shockstatus and euthanized; no unexpected loss occurred. Significant differences were noted between baseline and shock states in blood gases for the following parameters: p H was significantly decreased in both arterial(7.39 ± 0.12 to 7.14 ± 0.18) and venous blood gases(7.35 ± 0.15 to 6.98 ± 0.26, P < 0.05), base deficit was significantly increased for arterial(-0.9 ± 3.9 m Eq/L vs-17.8 ± 2.2 m Eq/L) and venous blood gasses(-0.8 ± 3.8 m Eq/L vs-15.3 ± 4.1 m Eq/L, P < 0.05). p CO2 trends(baseline to shock) demonstrated a decrease in arterial blood(40.0 ± 9.1 mm Hg vs 28.9 ± 7.1 mm Hg) but an increase in venous blood(46.0 ± 10.1 mm Hg vs 62.8 ± 15.3 mm Hg), although these trends were non-significant. For calculated arteriovenous differences between baseline and shock states, only the p CO2 difference was shown to be significant during shock.CONCLUSION: In this rabbit model, significant differences exist in blood gas measurements for arterial and venous blood after hemorrhagic shock. A widened p CO2 a-v difference during hemorrhage, reflective of poor tissue oxygenation, may be a better indicator of impending shock.
基金Supported by the Grants from the Health Research Foundation (A2003189) and the Science Research Project (2004B30601001) of Guangdong Province, China
文摘AIM: To investigate the functional, morphological changes of the gut barrier during the restitution process after hemorrhagic shock, and the regional differences of the large intestine and small intestine in response to ischemia/reperfusion injury.METHODS: Forty-seven Sprague-Dawley rats with body weight of 250-300 g were divided into two groups: control group (sham shock n = 5) and experimental group (n = 42).Experimental group was further divided into six groups (n = 7 each) according to different time points after the hemorrhagic shock, including 0th h group, 1st h group, 3rd h group, 6th h group, 12th h group and 24th h group. All the rats were gavaged with 2 mL of suspension of lactulose (L) (100 mg/2 mL) and mannitol (M) (50 mg/each) at the beginning and then an experimental rat model of hemorrhagic shock was set up. The specimens from jejunum, ileum and colon tissues and the blood samples from the portal vein were taken at 0, 1, 3, 6, 12 and 24 h after shock resuscitation, respectively. The morphological changes of the intestinal mucosa, including the histology of intestinal mucosa, the thickness of mucosa, the height of villi, the index of mucosal damage and the numbers of goblet cells, were determined by light microscope and/or electron microscope. The concentrations of the bacterial endotoxin lipopolysaccharides (LPS) from the portal vein blood, which reflected the gut barrier function, were examined by using Limulus test. At the same time point,to evaluate intestinal permeability, all urine was collected and the concentrations of the metabolically inactive markers such as L and M in urine were measured by using GC-9A gas chromatographic instrument.RESULTS: After the hemorrhagic shock, the mucosal epithelial injury was obvious in small intestine even at the 0th h, and it became more serious at the 1st and the 3rd h. The tissue restitution was also found after 3 h,though the injury was still serious. Most of the injured mucosal restitution was established after 6 h and completed in 24 h. Two distinct models of cell deathapoptosis and necrosis-were involved in the destruction of rat intestinal epithelial cells. The number of goblet cells on intestinal mucosa was reduced significantly from 0 to 24 h (the number from 243±13 to 157±9 for ileum, 310±19 to 248±18 for colon; r = -0.910 and -0.437 respectively,all P<0.001), which was the same with the large intestine, but the grade of injury was lighter with the values of mucosal damage index in 3 h for jejunum,ileum, and colon being 2.8, 2.6, 1.2, respectively. The mucosal thickness and the height of villi in jejunum and ileum diminished in 1 h (the average height decreased from 309±24 to 204±23 μm and 271±31 to 231±28 μm,r = -0.758 and -0.659, all P<0.001; the thickness from 547±23 to 418±28 μm and 483±45 to 364±35 μm, r= -0.898 and -0.829, all P<0.001), but there was no statistical difference in the colon (F= 0.296, P = 0.934). Compared with control group, the urine L/M ratio and the blood LPS concentration in the experimental groups raised significantly,reaching the peak in 3-6 h (L/M: control vs 3 h vs 6 h was 0.029±0.09 vs 0.063±0.012 vs 0.078±0.021, r=-0.786,P<0.001; LPS: control vs 3 h vs6 h was 0.09±0.021 vs 0.063±0.012 vs 0.25±0.023, r= -0.623, P<0.001), and it kept increasing in 24 h.CONCLUSION: The gut barrier of the rats was seriously damaged at the early phase of ischemic reperfusion injury after hemorrhagic shock, which included the injury and atrophy in intestinal mucosa and the increasing of intestinal permeability. Simultaneously, the intestinal mucosa also showed its great repairing potentiality, such as the improvement of the intestinal permeability and the recovery of the morphology at different phases after ischemic repeffusion injury. The restitution of gut barrier function was obviously slower than that of the morphology and there was no direct correlation between them.Compared with the small intestine, the large intestine had stronger potentiality against injury. The reduction of the amount of intestinal goblet cells by injury did not influence the ability of intestinal mucosal restitution at a certain extent and it appeared to be intimately involved in the restitution of the epithelium.
基金Supported by National Natural Science Foundation of ChinaNo.81171789
文摘AIM: To investigate the effects of biliary tract external drainage(BTED) on intestinal barrier injury in rats with hemorrhagic shock(HS). METHODS: BTED was performed via cannula insertion into the bile duct of rats. HS was induced by drawing blood from the femoral artery at a rate of 1 m L/min until a mean arterial pressure(MAP) of 40 ± 5 mm Hg was achieved. That MAP was maintained for 60 min. A total of 99 Sprague-Dawley rats were randomized into a sham group, an HS group and an HS + BTED group. Nine rats in the sham group were sacrificed 0.5 h after surgery. Nine rats in each of the HS and HS + BTED groups were sacrificed 0.5 h, 1 h, 2 h, 4 h and 6 h after resuscitation. Plasma tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), and lipopolysaccharide(LPS) levels were analyzed using enzyme-linked immunosorbent assay. Plasma D-lactate levels were analyzed using colorimetry. The expression levels of occludin and claudin-1 in the ileum were analyzed using Western blot and immunohistochemistry. Histology of the ileumwas evaluated by hematoxylin and eosin staining. RESULTS: Plasma TNF-α levels in the HS + BTED group decreased significantly compared with the HS group at 1 h and 6 h after resuscitation(P < 0.05). Plasma IL-6 levels in the HS + BTED group decreased significantly compared with the HS group at 0.5 h, 1 h and 2 h after resuscitation(P < 0.05). Plasma D-lactate and LPS levels in the HS + BTED group decreased significantly compared with the HS group at 6 h after resuscitation(P < 0.05). The expression levels of occludin in the HS + BTED group increased significantly compared with the HS group at 4 h and 6 h after resuscitation(P < 0.05). The expression levels of claudin-1 in the HS + BTED group increased significantly compared with the HS group at 6 h after resuscitation(P < 0.05). Phenomena of putrescence and desquamation of epithelial cells in the ileal mucosa were attenuated in the HS + BTED group. Ileal histopathologic scores in the HS + BTED group decreased significantly compared with the HS group at 2 h, 4 h and 6 h after resuscitation(P < 0.05). CONCLUSION: BTED protects against intestinal barrier injury in HS rats.
文摘BACKGROUND Esophageal submucosal hematoma is a rare condition.Although the exact etiology remains uncertain,vessel fragility with external factors is believed to have led to submucosal bleeding and hematoma formation;the vessel was ruptured by a sudden increase in pressure due to nausea,and the hematoma was enlarged by antiplatelet or anticoagulant therapy.Serious conditions are rare,with a better prognosis.We present the first known case of submucosal esophageal hematoma-subsequent hemorrhagic shock due to Mallory-Weiss syndrome.CASE SUMMARY A 73-year-old female underwent endovascular treatment for an unruptured cerebral aneurysm.The patient received aspirin and clopidogrel before surgery and heparin during surgery,and was well during the surgery.Several hours after returning to the ICU,she complained of chest discomfort,vomited 500 m L of fresh blood,and entered hemorrhagic shock.Esophageal submucosal hematoma with Mallory-Weiss syndrome was diagnosed through an endoscopic examination and computed tomography.In addition to a massive fluid and erythrocyte transfusion,we performed a temporary compression for hemostasis with a Sengstaken-Blakemore(S-B)tube.Afterwards,she became hemodynamically stable.On postoperative day 1,we performed an upper gastrointestinal endoscopy and confirmed no expansion of the hematoma nor any recurring bleeding;therefore,we removed the S-B tube and clipped the gastric mucosal laceration at the esophagogastric junction.We started oral intake on postoperative day 10.The patient made steady progress,and was discharged on postoperative day 33.CONCLUSION We present the first known case of submucosal esophageal hematoma subsequent hemorrhagic shock due to Mallory-Weiss syndrome.
基金Supported by the Chinese Traditional Medicine Foundation of Guangdong Province, China, No. 102061
文摘AIM: To study the protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury and its mechanism after hemorrhagic shock in rats.METHODS: A total of 32 SD rats were randomly divided into four groups (n = 8, each group): normal group,model group, low dosage group (treated with 10 g/kg Astragalus membranaceus) and high dosage group (treated with 20 g/kg Astragalus membranaceus). The model of hemorrhagic shock for 60 min and reperfusion for 90 min was established. Therapeutic solution (3 mL)was administrated before reperfusion. At the end of the study, the observed intestinal pathology was analyzed. The blood concentrations of lactic acid (LD), nitric oxide (NO),endothelin-1 (ET-1), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) in intestinal mucosa were determined.RESULTS: The intestinal mucosa pathology showed severe damage in model group and low dosage group,slight damage in high dosage group and no obvious damage in normal group. The Chiu's score in low dose group and high dose group was significantly lower than that in model group. The content of MDA in model group was higher than that in low and high dose groups, while that in high dose group was almost the same as in normal group. The activity of SOD and GSH-PX was the lowest in model group and significantly higher in high dose group than in normal and low dose groups. The concentrations of LD and ET-1 in model group were the highest. The concentrations of NO in model group and low dose group were significantly lower than those in high dose group and normal group.CONCLUSION: High dose Astragalus membranaeus has much better protective effect on hemorrhagic shockreperfusion injury of intestinal mucosa than low dose Astragalus membranaceus. The mechanism may be that Astragalus membranaceus can improve antioxidative effect and regulate NO/ET level during hemorrhagic reperfusion.
基金supported by the Zhejiang Provincial Natural Science Foundation of China (No.Y2100430)the Zhejiang Provincial Education and Research Foundation of China (No. Y201019154)
文摘To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 (HO-1) expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscitation (HTS), normal saline resuscitation (NS) and sham groups. HO-1 mRNA, protein expression and apoptosis were evaluated in organs. In the HTS group, significant difference was noted in HO-1 protein in small intestinal mucosa and liver compared with the NS and sham groups, and in HO-1 mRNA in liver and kidney compared with the sham group. The apoptosis of small intestinal mucosa, liver, heart, and lung was significantly lower in the HTS group than that in the NS group. In this study, small volume resuscitation with HTS can efficiently up-regulate the expression level of HO-1 in small intestinal mucosa and liver, which may be one of the mechanisms alleviating organ damage.
基金Supported by Career Development Award(CDA2)1IK2BX-001277-01A1 from the Department of Veterans Affairs,Veterans Health Administration,Office of Research and Developmentthe Foundation for Anesthesia Education and Research and the American Society of Critical Care Anesthesiologists and NIH GM085072-06
文摘AIM: To determine the time course of intestinal permeability changes to proteolytically-derived bowel peptides in experimental hemorrhagic shock. METHODS: We injected fluorescently-conjugated casein protein into the small bowel of anesthetized Wistar rats prior to induction of experimental hemorrhagic shock. These molecules, which fluoresce when proteolytically cleaved, were used as markers for the ability of proteolytically cleaved intestinal products to access the central circulation. Blood was serially sampled to quantify the relative change in concentration of proteolytically-cleaved particles in the systemic circulation. To provide spatial resolution of their location, particles in the mesenteric microvasculature were imaged using in vivo intravital fluorescent microscopy. The experiments were then repeated using an alternate measurement technique, fluorescein isothiocyanate(FITC)-labeled dextrans 20, to semi-quantitatively verify the ability of bowel-derived low-molecular weight molecules(< 20 k D) to access the central circulation.RESULTS: Results demonstrate a significant increase in systemic permeability to gut-derived peptides within 20 min after induction of hemorrhage(1.11 ± 0.19 vs 0.86 ± 0.07, P < 0.05) compared to control animals. Reperfusion resulted in a second, sustained increase in systemic permeability to gut-derived peptides in hemorrhaged animals compared to controls(1.2 ± 0.18 vs 0.97 ± 0.1, P < 0.05). Intravital microscopy of the mesentery also showed marked accumulation of fluorescent particles in the microcirculation of hemorrhaged animals compared to controls. These results were replicated using FITC dextrans 20 [10.85 ± 6.52 vs 3.38 ± 1.11 fluorescent intensity units(× 105, P < 0.05, hemorrhagic shock vs controls)], confirming that small bowel ischemia in response to experimental hemorrhagic shock results in marked and early increases in gut membrane permeability. CONCLUSION: Increased small bowel permeability in hemorrhagic shock may allow for systemic absorption of otherwise retained proteolytically-generated peptides, with consequent hemodynamic instability and remote organ failure.
文摘AIM To evaluate the effects of mineralocorticoid receptor(MR) antagonists on mortality and inflammatory responses after hemorrhagic shock(HS) in rats.METHODS One hundred and two male Sprague–Dawley rats were randomly assigned to one of the following three groups: Control, spironolactone (SPL), and eplerenone(EP) groups. HS was induced by the removal of blood. One half of rats were evaluated to determine mortality, hemodynamics, plasma tumor necrosis factor-alpha(TNF-α) concentrations, and arterial blood gas at 8 h afterHS recovery. In the remainder of rats, the expression levels of genes encoding cytokines were evaluated in liver tissue samples at 1 h after HS recovery. RESULTS The survival rates 8 h after HS recovery were 71%, 94%, and 82% in the control, SPL, and EP groups, respectively. There were no significant differences in survival rates among the three groups (P = 0.219). Furthermore, there were no significant differences in gene expression levels in the liver or plasma TNF-α concentrations among the three groups(P = 0.888).CONCLUSION Pretreatment with MR antagonists did not improve mortality or cytokine responses in the liver after HS recovery in rats.
文摘Objective: To observe the effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock and active bleeding was established in 32 SD (Sprague-Dawley) rats. The rats were randomly divided into control group, no fluid resuscitation group (NF group), controlled fluid resuscitation group (NS40 group) and rapid large scale fluid resuscitation group (NS80 group). Each group contained 8 rats. The curative effects were compared. At the same time, the apoptosis in liver, kidney, lung and small intestinal mucosa of survivors after hemorrhage and resuscitation was detected by light microscopy in HE (hematoxylin and eosin) stained tissue sections, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Results: The survival rate of early fluid resuscitation (14/16) was markedly higher than that of NF group (3/8). There was some apoptosis in liver, kidney, lung and small intestinal mucosa of all survivors. Compared with NF and NS40 groups, the apoptosis of liver, kidney and small intestinal mucosa of NS80 group was obviously increased. Conclusions: Among three fluid resuscitation methods, controlled fluid resuscitation can obviously improve the early survival rate and the apoptosis of liver, kidney and small intestinal mucosa in rats with severe and uncontrolled hemorrhagic shock, and may benefit improvement of prognosis.
文摘Objective: To investigate the potential and early effect of hypertonic saline resuscitation on T-lymphocyte sub- populations in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 18 Sprague-Dawley (SD) rats. The rats were randomly divided into Sham group, HTS group (hypertonic saline resuscitation group) and NS group (normal saline resuscitation group). Each group contained 6 rats. The CD4+ and CD8+ subpopulations of T-lymphocytes in peripheral blood were detected respectively before shock and after resuscitation by double antibody labelling and flow cytometry. Results: In the early stage after hemorrhagic shock, fluid resuscitation and emergency treatment, the CD4+ lymphocytes of peripheral blood in HTS and NS groups markedly increased. Small volume resuscitation with HTS also induced peripheral CD8+ lymphocytes to a certain extent, whereas NS resuscitation showed no effect in this respect. Consequently, compared with Sham and HTS groups, CD4+/CD8+ ratio of peripheral blood in NS group was obviously increased, and showed statistically differences. Conclusion: In this model of rat with severe hemorrhagic shock, small volume resuscitation with HTS is more effective than NS in reducing immunologic disorders and promoting a more balanced profile of T-lymphocyte subpopula- tions regulating network.
文摘Objective. To investigate clinically useful markers for determining the seventy of hemorrhagic shock and adequacy of resuscitation Methods. Prospective study was undertaken in 12 dogs, using an established model for hemorrhagic shock. The anesthetized dogs were bled to a mean arterial pressure of 40 mmHg which was maintained for 3 hours. Then each animal was resuscitated with heperinized whole blood followed by intravenous infusion of dobutamine at a rate of 5 ug. kg-1. min-1 for 10 minutes. Arterial and mixed venous blood gases, arterial lactate concentrations and hemodynamic Parameters were measured throughout the study. Results. A difference in the PCO2 and pH values between arterial and mixed venous blood was observed. Arterial-venous PCO2 and pH difference increased significantly after sustained shock. The arteriovenous carbon dioxide and pH gradients recovered more rapidly than arterial lactate levels after successful resuscitation with blood and dobutamine. Conclusion. Arterial blood gases fail to reflect the acid-base status of tissues during hemorrhagic shock. The differences in PCO2 and pH values between arterial and mixed venous blood could be used as clinical in- dicators for assessing the seventy of shock and efficacy of resuscitation.
基金Project supported by the National Natural Science Foundation of China (No. 30672071) the Traditional Chinese Medicine Foun- dation of Zhejiang Province, China (No. 2004C071)
文摘Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer's lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuated injury of the lung and decreased the concentration of lactic acid and the number of in situ TdT-mediated dUTP nick-end labelling (TUNEL)-positive cells. Moreover, immunohistochemistry performed 24 h after reperfusion revealed increases in the level of nuclear factor κB (NF-κB), and phosphorylated p38 mitogen-activated protein kinase (MAPK) in the albumin-untreated group was down-regulated by albumin treatment when compared with the sham rats. Conclusion: Resuscitation with albumin attenuates tissue injury and inhibits T/HS-induced apoptosis in the lung via the p38 MAPK signal transduction pathway that functions to stimulate the activation of NF-κB.