Emergency rescue of a patient with hemorrhagic shock caused by superior mesenteric artery rupture:A case report

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.

Analysis of the Emergency Rescue Nursing Intervention Effect and Rescue Success Rate for Patients with Traumatic Hemorrhagic Shock

Objective:To analyze the value of emergency rescue nursing intervention in the care of patients with traumatic hemorrhagic shock and its impact on the success rate of rescue efforts.Methods:A total of 80 patients with traumatic hemorrhagic shock were selected as samples,with the timeframe from July 2022 to July 2023.The patients were randomly divided into two groups using a random number table method.Group A received emergency rescue nursing,while Group B received routine nursing care.The success rate of rescue,rescue indicators,complication rates,and family satisfaction with nursing care were compared between the two groups.Results:The rescue success rate in Group A was higher than in Group B(P<0.05);the total blood loss in Group A was less,and the rescue time,full transportation time,and hospitalization time were shorter than in Group B(P<0.05);the complication rate of patients with traumatic hemorrhagic shock in Group A was lower than in Group B(P<0.05);the family satisfaction with emergency nursing care in Group A was higher than in Group B(P<0.05).Conclusion:Emergency rescue interventions for patients with traumatic hemorrhagic shock can reduce blood loss,shorten rescue times,and improve the success rate of shock rescue,providing a safe and effective approach.

Effects of extract F of red-rooted Salvia on mucosal lesions of gastric corpus and antrum induced by hemorrhagic shock-reperfusion in rats

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 2 received 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 (PGs) 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 parameters 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 +/- 19.37 increased markedly (P 【0.01), whereas the grade 0 damage, grade 1 damage, the concentrations of PGE(2) and PGI(2)(pg/mg tissue), the ratio of PGI(2)/TXA(2) 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 0 damage, grade 1 damage, the concentrations of PGE(2) and PGI(2), the ratio of PGI(2)/TXA(2) 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 (%) of IGML, 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.

Protective effect of Astragalus membranaceus on intestinal mucosa reperfusion injury after hemorrhagic shock in rats

AIM： To study the protective effect of Astragalus rnernbranaceus 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 Astraga/us 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.

Gastric mucosal injury due to hemorrhagic reperfusion and efficacy of Salvia miltiorrhizae extract F and cimetidine

AIM: To observe the gastric mucosal injury caused by hemorrhagic shock and reperfusion and to compare the effect between Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) on it. METHODS: A model of hemorrhage/reperfusion injury was produced by Itoh method. Wistar rats were randomly divided into three groups: 0.9% sodium chloride treatment group (NS group), SEF treatment group (SEF group), and CI treatment group (CI group). Saline, SEF and CI were injected respectively. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesion area in the gastric mucosa. The degree of gastric mucosal lesions was categorized into grades 0, 1, 2, 3. Atom absorption method was used to measure the intracellular calcium content. Radioimmunoassay was used to measure the concentrations of prostaglandins. RESULTS: IGML (%) and grade 3 (%) were 23.18±6.82, 58.44±9.07 in NS group, 4.42±1.39, 20.32±6.95 in SEF group and 3.74±1.56, 23.12±5.09 in CI group, and the above parameters in SEF group and CI group decreased significantly (IGML: SEF vs NS, t=6.712, P=0.000<0.01; CI vs NS, t=6.943, P=0.000<0.01; grade 3: SEF vs HS, t=8.386, P=0.000; CI vs HS, t=8.411, P= 0.000), but the grade 0 and grade 1 damage in SEF group (22.05±5.96, 34.12±8.12) and CI group (18.54±4.82, 30.15±7.12) were markedly higher than those in NS group (3.01±1.01, 8.35±1.95; grade 0: SEF vs HS, t=8.434, P=0.000<0.01; CI vs NS, t=7.950, P=0.000<0.01; grade 1: SEF vs NS, t =8.422, P=0.000<0.01; CI vs NS, t=8.448, P=0.000<0.01). The intracellular calcium content (μg/mg) in SEF group (0.104±0.015) and CI group (0.102±0.010) was markedly lower than that in NS group (0.131±0.019, SEF vs NS, t=2.463, P=0.038<0.05; CI vs HS, t=3.056, P=0.017<0.05). The levels (pg/mg) of PGE_2, 6-keto-PGF_(1α) and 6-keto-PGF_(1α)/TXB_2 were 540±183, 714±124,17.38±5.93 in NS group and 581±168, 737±102, 19.04±8.03 in CI group, 760±192,1 248±158, 33.42±9.24 in SEF group, and the above parameters in SEF group markedly raised (PGE_2: SEF vs NS, t=2.282, P=0.046<0.05; SEF vs CI, t=2.265, P=0.047<0.05; 6-keto-PGF_(1α): SEF vs NS, t=6.583, P=0.000<0.000; SEF vs CI, t=6.708, P=0.000<0.01; 6-keto-PGF_(1α)/TXB_2: SEF vs NS, t=3.963, P=0.003<0.001; SEF vs Cl, t=3.243, P=0.009<0.01), whereas TXB_2 level in SEF group (45.37±7.54) was obviously lower than that in NS group (58.28±6.74, t=3.086, P=0.014<0.05) and CI group (54.32±6.89, t=2.265, P=0.047<0.05). No significant difference was shown between NS group and CI group (PGE_2: t=0.414, P=0.688>0.05; 6-keto-PGF_(1α): t=0.310, P=0.763>0.05; TXB_2: t=1.099, P=0.298>0.05; 6-keto-PGF_(1α)/TXB_2: t=0.372, P=0.718>0.05). CONCLUSION: Both SEF and CI could inhibit reperfusioninduced injury in gastric mucosa, but with different mechanisms. SEF could not only enhance the protective effect of gastric mucosa, but also abate the injury factors, while CI can only abate the injury factors.

Electroacupuncture improves gut barrier dysfunction in prolonged hemorrhagic shock rats through vagus anti-inflammatory mechanism

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.

Functional and morphological changes of the gut barrier during the restitution process after hemorrhagic shock

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 0^th group, 1^st group, 3^rd group, 6th h group, 12^th group and 24^th 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 1^stand the 3^rd 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 pm and 271±31 to 231±28 pm, r = -0.758 and -0.659, all P〈0.001, the thickness from 547±23 to 418±28μm and 483±45 to 364±35μm, 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 vs6 h was 0.029±0.09 vs 0.063±0.012 vs 0.078±0.021, r = -0.786, P〈0.001; LPS： control vs3 h vs6 h was 0.09±0.021 vs 0.063±0.012 vs0.25±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 reperfusion 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.

Mesenteric lymph reperfusion may exacerbate brain injury in a rat model of superior mesenteric artery occlusion shock

BACKGROUND：The intestinal lymphatic pathway and intestinal ischemia/reperfusion are mainly involved in mesenteric lymph duct ligation or drainage; moreover,intervention by reducing the lymph liquid reflux might relieve lung and other organ dysfunction induced by intestinal ischemia/reperfusion; however,research addressing mesenteric lymph reperfusion （MLR） and brain injury has not yet to be reported.OBJECTIVE：To observe the effect of MLR on brain tissue in a rat model of superior mesenteric artery occlusion （SMAO） shock,and to explore the molecular mechanism of MLR.DESIGN,TIME AND SETTING：A randomized,controlled,animal experiment at a neuro-pathophysiology level was performed at the Institute of Microcirculation,Hebei North University; Department of Pathophysiology,Basic Medical College; Department of Pathology,the First Hospital of Hebei North University between December 2007 and March 2009.MATERIALS：Adenosine triphosphate （ATP） standard was provided by the National Institute for the Control of Pharmaceutical and Biological Products; lactic acid （LA）,superoxide dismutase （SOD）,malonaldehyde （MDA）,nitrogen monoxidum （NO）,nitric oxide synthase （NOS）,myeloperoxidase （MPO） and ATPase assay kits were provided by Nanjing Jiancheng Bioengineering Institute,China.METHODS：A total of 24 male Wistar rats were randomly divided into four groups.In the sham-surgery group （n = 6）,both the mesenteric lymph duct and the superior mesenteric artery were not blocked; in the MLR group （n = 6）,the mesenteric lymph duct was occluded for 1 hour followed by 2-hour reperfusion; in the SMAO group （n = 6）,the superior mesenteric artery was occluded for 1 hour followed by 2-hour reperfusion; in the MLR ＋ SMAO group （n = 6）,both the mesenteric lymph duct and superior mesenteric artery were occluded for 1 hour followed by 2-hour reperfusion.MAIN OUTCOME MEASURES：Mean arterial blood pressure prior to and following ischemia/reperfusion; brain tissue morphology levels of LA,MDA,SOD,NO,NOS,MPO,ATPase and ATP following reperfusion.RESULTS：MLR did not cause changes in mean arterial blood pressure,brain tissue morphology,LA,MDA,NO,ATP,SOD,NOS,MPO and ATPase.However,SMAO caused a rapid decrease and gradual increase of mean arterial blood pressure.Neuronal necrosis,degeneration and swelling were observed in brain tissue.Contents of MDA,NO,LA and ATP as well as activities of NOS and MPO were significantly increased （P〈 0.05）,but activities of SOD and Na＋-K＋-ATPase were significantly decreased （P 〈 0.05）.MLR aggravated neuronal damage in a rat model of SMAO shock.Following MLR,mean arterial blood pressure was significantly decreased （P 〈 0.05）,contents of MDA and NO as well as activities of NOS and MPO were significantly increased （P 〈0.05）,but activities of Ca2＋-ATPase,Mg2＋-ATPase and Ca2＋-Mg2＋-ATPase as well as ATP content were significantly decreased （P〈 0.05）.CONCLUSION：MLR aggravates brain injury in a rat model of SMAO shock,which correlates with oxygen-derived free radical injury,NO synthesis and release,sequestration of neutrophilic granulocytes,decreasing activity of cell membrane pumps and energy metabolism dysfunction.Pathogenesis of the intestinal lymphatic pathway should be thoroughly investigated to prevent ischemia/reperfusion injury.

Influence of Tanshinone lla on heat shock protein 70,Bcl-2 and Bax expression in rats with spinal ischemia/reperfusion injury

Tanshinone lla is an effective monomer component of Danshen, which is a traditional Chinese medicine for activating blood circulation to dissipate blood stasis. Tanshinone Ila can effectively improve brain tissue ischemia/hypoxia injury. The present study established a rat model of spinal cord ischemia/reperfusion injury and intraperitoneally injected Tanshinone lla, 0.5 hour prior to model establishment. Results showed that Tanshinone Ila promoted heat shock protein 70 and Bcl-2 protein expression, but inhibited Bax protein expression in the injured spinal cord after ischemia/reperfusion injury. Furthermore, Nissl staining indicated a reduction in nerve cell apoptosis and fewer pathological lesions in the presence of Tanshinone Ila, compared with positive control Danshen injection.

Hypertonic saline resuscitation maintains a more balanced profile of T-lymphocyte subpopulations in a rat model of hemorrhagic shock

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.

Hypertonic saline resuscitation reduces apoptosis of intestinal mucosa in a rat model of hemorrhagic shock

Objective: To investigate the early effects of hypertonic and isotonic saline solutions on apoptosis of intestinal mucosa in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 21 Sprague-Dawley (SD) rats. The rats were randomly divided into the sham group, normal saline resuscitation (NS) group, and hypertonic saline resuscitation (HTS) group, with 7 in each group. We detected and compared the apoptosis in small intestinal mucosa of rats after hemorrhagic shock and resuscitation by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), FITC (fluo- rescein-iso-thiocyanate)-Annexin V/PI (propidium iodide) double staining method, and flow cytometry. Results: In the early stage of hemorrhagic shock and resuscitation, marked apoptosis of small intestinal mucosa in the rats of both NS and HTS groups was observed. The numbers of apoptotic cells in these two groups were significantly greater than that in the sham group (P<0.01). In the HTS group, the apoptic cells significantly decreased, compared with the NS group (P<0.01). Conclusion: In this rat model of severe hemorrhagic shock, the HTS resuscitation of small volume is more effective than the NS resuscitation in reducing apoptosis of intestinal mucosa in rats, which may improve the prognosis of trauma.

Protection mechanism of deacetylase inhibitor on spleen of rats with severe hemorrhagic shock

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.

Effects of environmental hypothermia on hemodynamics and oxygen dynamics in a conscious swine model of hemorrhagic shock

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.

Influence of mesenteric lymph reperfusion on neurotransmitter expression in brain tissue of a superior mesenteric artery occlusion shock rat model

BACKGROUND： Previous studies have shown that mesenteric lymph reperfusion （MLR） exacerbates brain injury in a rat model of superior mesenteric artery occlusion （SMAO） shock. However, little is known about the influence of MLR on neurotransmitter expression in brain tissue. OBJECTIVE： To observe the effect of MLR on brain tissue injury by measuring monoamine and cholinergic neurotransmitter levels. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Microcirculation, Hebei North University, China; Research Room of Microcirculation and Laboratory of Biochemistry, Department of Pathophysiology, Basic Medical College, Hebei North University between December 2007 and March 2009. MATERIALS： Choline acetyltransferase （CHAT） and acetylcholine esterase （ACHE） kits were provided by Nanjing Jiancheng Bioengineering Institute, China; dopamine （DA） and noradrenalin （NE） standards were provided by the National Institute for the Control of Pharmaceutical and Biological Products; HP1100 chromatograph of liquid was provided by Agllent, USA. METHODS： A total of 24 male, Wistar rats were randomly assigned to 4 groups： sham-surgery, MLR SMAO, and MLR ＋ SMAO groups, with 6 rats in each group. In the MLR or SMAO groups, the mesenteric lymph duct or superior mesenteric artery was blocked for 1 hour. In the MLR ＋ SMAO group, the mesenteric lymph duct and superior mesenteric artery were occluded for 1 hour, followed by 2-hour repeffusion. ChAT and AChE levels were measured using the synthesized and hydrolyzed acetylcholine method, respectively. Liquid chromatography was employed to quantitatively analyze DA and NE levels, using relative retention time and the external standard method. MAIN OUTCOME MEASURES： CHAT, ACHE, DA, and NE levels. RESULTS： AChE levels were significantly increased, but ChAT levels were significantly decreased in the MLR and MLR ＋ SMAO groups following 2-hour repeffusion （P〈 0.01）. However, AChE activity in the MLR ＋ SMAO group was greater than in the MLR group （P 〈 0.05）. DA and NE levels were significantly decreased in the SMAO and MLR ＋ SMAO groups （P〈 0.01）, while DA levels in the MLR ＋ SMAO group were less than in the SMAO group （P 〈 0.05）. CONCLUSION： MLR exacerbated brain injury in a rat model of SMAO shock, which correlated with the intestinal lymphatic pathway. MLR decreased DA levels, but increased AChE activity, in a rat model of SMAO shock.

Arterial vs venous blood gas differences during hemorrhagic shock

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.

Early Aerobic Exercise Promotes Neurological Function Recovery of Rats after Cerebral Ischemia/Reperfusion by Upregulating the Expression of Heat Shock Protein A5

Objective The neuroprotective function of heat shock protein A5(HSPA5)in ischemic stroke has been confirmed.This study aimed to investigate the effects of early aerobic exercise on neurological function recovery from cerebral ischemia/reperfusion and to determine whether these effects are associated with the expression level of HSPA5 in the ischemic penumbra.Methods A total of 72 male Sprague-Dawley rats were randomly assigned to the ischemia and exercise group[middle cerebral artery occlusion(MCAO)-Ex,n=18],ischemia and sedentary group(MCAO-St,n=18),sham-surgery and exercise group(Sham-Ex,n=18),or sham-surgery and sedentary group(Sham-St,n=18).The MCAO-Ex and MCAO-St groups were subjected to MCAO for 60 min,whereas the Sham-Ex and Sham-St groups were subjected to an identical operation without MCAO.Rats in the MCAO-Ex and Sham-Ex groups then ran on a treadmill for 30 min once a day for 5 consecutive days.After reperfusion,the motor function of the rats was scored by the Bederson neurological function test,balance beam test,and screen test.Nissl staining was conducted to assess morphological and structural change of nerve cells in the ischemic penumbra.The reverse transcription-quantitative polymerase chain reaction was applied to detect the mRNA expression of HSPA5.Western blot analysis was conducted to determine the protein expression of HSPA5.Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL)staining was carried out in the ischemic penumbra after MCAO.Results Rats receiving early treadmill exercise had lower Bederson neurological function,balance beam,and screen test scores on the 3rd,7th,and 14th days after MCAO;in addition,more neurons survived in the ischemic penumbra after MCAO,and higher mRNA and protein expression of HSPA5 and fewer TUNEL-positive stained cells were observed.Conclusion Our study demonstrated that early aerobic exercise can improve neurological function recovery after ischemia/reperfusion.Furthermore,the increased level of HSPA5 in the ischemic penumbra might be one of the mechanisms of enhanced neurological function recovery.

Effects of three fluid resuscitation methods on apoptosis of visceral organs in rats with hemorrhagic shock

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.

Heat shock pretreatment improves stem cell repair following ischemia-reperfusion injury via autophagy

AIM: To investigate whether heat shock pretreatment(HSP) improves mesenchymal stem cell(MSC) repair via autophagy following hepatic ischemia-reperfusion injury(HIRI).METHODS: Apoptosis of MSCs was induced by 250 m M hydrogen peroxide(H2O2) for 6 h. HSP was carried out using a 42 ℃ water bath for 1, 2 or 3 h. Apoptosis of MSCs was analyzed by flow cytometry, and Western blot was used to detect Bcl-2, Bax and cytochrome C expression. Autophagy of MSCs was analyzed by flow cytometry and transmission electron microscopy, and the expression of beclin Ⅰ?and LC3-Ⅱ was detected by Western blot. MSCs were labeled in vivo with the fluorescent dye, CM-Dil, and subsequently transplanted into the portal veins of rats that had undergone HIRI. Liver levels of proliferating cell nuclear antigen(PCNA) were quantified by fluorescent microscopy. Serum aminotransferase activity and the extent of HIRI were also assessed at each time point.RESULTS: HSP for 2 h reduced apoptosis of MSCs induced by H2O2 as seen by a decrease in apoptotic rate, a decrease in Bax and cytochrome C expression and an increase in Bcl-2 expression(P < 0.001). In addition, HSP for 2 h induced autophagy of MSCs exposed to H2O2 as shown by an increase in acidic vesicular organelle-positive cells, beclin 1 and LC3-Ⅱ expression, and autophagosome formation(P < 0.05). Treatment with 3-methyladenine attenuated HSPinduced autophagy and abolished the protective effects of HSP on the apoptosis of MSCs. Rapamycin failed to have additional effects on either autophagy or apoptosis compared with HSP alone. The phosphorylation of p38 MAPK was significantly elevated and the phosphorylation of m TOR was downregulated in heat shock pretreated MSCs. Treatment with the p38 MAPK inhibitor, SB203580, reduced HSP-induced autophagy in MSCs. In vivo studies showed that the transplantation of HSP-MSCs resulted in lower serum aminotransferase levels, lower Suzuki scores, improved histopathology and an increase in PCNA-positive cells(P < 0.05).CONCLUSION: HSP effectively induces autophagy following exposure to H2O2 via the p38MAPK/m TOR pathway, which leads to enhanced MSC survival and improved MSC repair following HIRI in rats.

Biliary tract external drainage protects against intestinal barrier injury in hemorrhagic shock rats

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.

Hemorrhagic shock due to submucosal esophageal hematoma along with mallory-weiss syndrome:A case report

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.