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.

A rat model of multicompartmental traumatic injury and hemorrhagic shock induces bone marrow dysfunction and profound anemia

Background:Severe trauma is associated with systemic inflammation and organ dysfunction.Preclinical rodent trauma models are the mainstay of postinjury research but have been criticized for not fully replicating severe human trauma.The aim of this study was to create a rat model of multicompartmental injury which recreates profound traumatic injury.Methods:Male Sprague-Dawley rats were subjected to unilateral lung contusion and hemorrhagic shock(LCHS),multicompartmental polytrauma(PT)(unilateral lung contusion,hemorrhagic shock,cecectomy,bifemoral pseudofracture),or na?ve controls.Weight,plasma toll-l ike receptor 4(TLR4),hemoglobin,spleen to body weight ratio,bone marrow(BM)erythroid progenitor(CFU-GEMM,BFU-E,and CFU-E)growth,plasma granulocyte colony-stimulating factor(G-CSF)and right lung histologic injury were assessed on day 7,with significance defined as p values<0.05(*).Results:Polytrauma resulted in markedly more profound inhibition of weight gain compared to LCHS(p=0.0002)along with elevated plasma TLR4(p<0.0001),lower hemoglobin(p<0.0001),and enlarged spleen to body weight ratios(p=0.004).Both LCHS and PT demonstrated suppression of CFU-E and BFU-E growth compared to naive(p<0.03,p<0.01).Plasma G-CSF was elevated in PT compared to both na?ve and LCHS(p<0.0001,p=0.02).LCHS and PT demonstrated significant histologic right lung injury with poor alveolar wall integrity and interstitial edema.Conclusions:Multicompartmental injury as described here establishes a reproducible model of multicompartmental injury with worsened anemia,splenic tissue enlargement,weight loss,and increased inflammatory activity compared to a less severe model.This may serve as a more effective model to recreate profound traumatic injury to replicate the human inflammatory response postinjury.

Effi cacy of partial and complete resuscitative endovascular balloon occlusion of the aorta in the hemorrhagic shock model of liver injury

BACKGROUND:Resuscitative endovascular balloon occlusion of the aorta(REBOA)can temporarily control traumatic bleeding.However,its prolonged use potentially leads to ischemia-reperfusion injury(IRI).Partial REBOA(pREBOA)can alleviate ischemic burden;however,its security and eff ectiveness prior to operative hemorrhage control remains unknown.Hence,we aimed to estimate the effi cacy of pREBOA in a swine model of liver injury using an experimental sliding-chamber ballistic gun.METHODS:Twenty Landrace pigs were randomized into control(no aortic occlusion)(n=5),intervention with complete REBOA(cREBOA)(n=5),continuous pREBOA(C-pREBOA)(n=5),and sequential pREBOA(S-pREBOA)(n=5)groups.In the cREBOA and C-pREBOA groups,the balloon was inflated for 60 min.The hemodynamic and laboratory values were compared at various observation time points.Tissue samples immediately after animal euthanasia from the myocardium,liver,kidneys,and duodenum were collected for histological assessment using hematoxylin and eosin staining.RESULTS:Compared with the control group,the survival rate of the REBOA groups was prominently improved(all P<0.05).The total volume of blood loss was markedly lower in the cREBOA group(493.14±127.31 mL)compared with other groups(P<0.01).The pH was significantly lower at 180 min in the cREBOA and S-pREBOA groups(P<0.05).At 120 min,the S-pREBOA group showed higher alanine aminotransferase(P<0.05)but lower blood urea nitrogen compared with the cREBOA group(P<0.05).CONCLUSION:In this trauma model with liver injury,a 60-minute pREBOA resulted in improved survival rate and was effective in maintaining reliable aortic pressure,despite persistent hemorrhage.Extended tolerance time for aortic occlusion in Zone I for non-compressible torso hemorrhage was feasible with both continuous partial and sequential partial measures,and the significant improvement in the severity of acidosis and distal organ injury was observed in the sequential pREBOA.

Resuscitative endovascular balloon occlusion of the aorta in the treatment of severe hemorrhagic shock caused by upper gastrointestinal bleeding

Hemorrhagic shock is a life-threatening disease often encountered in emergency departments(EDs).Hemorrhagic shock caused by extensive bleeding from multiple sites is often associated with high mortality and morbidity.In recent years,resuscitative endovascular balloon occlusion of the aorta(REBOA)has been widely used in traumatic hemorrhagic shock and is considered to be an effective resuscitation measure.[1]Some studies reported that REBOA was also effective for non-traumatic hemorrhage.[2,3]In this study,we report a case of hemorrhagic shock caused by acute upper gastrointestinal bleeding that was successfully treated and received REBOA to obtain a transition time.This report may provide feasible options for emergency physicians,gastroenterologists,or surgeons to more actively treat refractory gastrointestinal bleeding.

Effect of Hypertonic Versus Isotonic Saline Resuscitation on Heme Oxygenase-1 Expression in Visceral Organs Following Hemorrhagic Shock in Rats

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.

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.

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.

Effects of mineralocorticoid receptor antagonists on responses to hemorrhagic shock in rats

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.

Expression of Egr-1 in the liver of mice following hemorrhagic shock and resuscitation

Objective: To investigate the expression of early growth response gene-1(Egr-1) in the liver following hemorrhagic shock with or without resuscitation(HS or HSR). Methods: Mice were subjected to HS or HSR.Liver expression of Egr-1 mRNA was detected by Northern blotting.DNA binding activity of the Egr-1 protein in liver nuclear extracts(NE) was determined by electrophoretic mobility shift assay(EMSA).Western blot analysis was used to assess the induction of Egr-1 protein in the liver tissue,cytoplasma and NE. Results: Egr-1 mRNA was strongly expressed as early as 1 h after HS,and its level was decreased in the following 2.5 h but still higher than that in 1 h HS group.The Egr-1 DNA binding activity elevated in the liver NE of 2.5 h HS group and 2.5 h HS + 4 h R group,so did the Egr-1 protein in the liver and the liver NE of the same two groups.However,the maximal Egr-1 protein expression was found in the cytoplasma of liver following 2.5 h HS. Conclusion: Our data suggest that both Egr-1 mRNA and protein are strongly elevated and the binding activity of Egr-1 to its cognate DNA site is increased in the liver following HSR,indicating the increases of Egr-1 transcriptional and translational levels.This study provides evidence that Egr-1 gene is activated in the liver during HS and HSR.

Effects of plasma β-endorphin on hemorrhagic shock in acute hypoxic rats

Forty rots were randomized into 2 groups and naloxone or saline were injected to therats after they were inflicted with hemorrhagic shock at sea level and at a simulated altitude of4000m respectively to observe the effects of naloxone on left ventricular systolic pressure(LVSP),left ventricular diastolic pressure(LVDP),the maximal changing rate of LVSP(dp/dt max),heartrate(HR),and survival time of the animals.Plasma β-endorphin(β-EP)was determined beforeand after hemorrhage to observe the relationship between β-EP and hemorrhagic shock.It wasfound that the circulatory parameters of hemorrhagic shock changed more markedly at high alti-tude than at sea level,naloxone could restore these parameters and prolong the survival time inboth the animals of the sea level and high altitude groups,and plasma β-EP level was elevatedafter hemorrhage especially in those animals at high altitude.These findings indicate:(1)Hemorrhagic shock at high altitude is usually accompanied with severe clinical manifestations,rapid progression,and high mortality.(2)β-EP seems to participate in the pathologicalmanifestafions of hemorrhagic shock at high altitude,and its depressive action on myocardialcontraction may be one of the factors inducing hemorrhagic shock.(3)Naloxone possesses defi-nite property to comet hemorrhagic shock at high altitude.

A study of therapeutic effects of 7.5% NaCl-6% dextran 70 in small dosage on hemorrhagic shock at high altitude in dogs

The effects of 7.5％ NaCl-6％ dextran 70 in small dosage on the cardiovascular func-tion and the survival rate in hemorrhagic shock at a simnlated altitude of 4000 m were observedin dogs.The animals were bled from the femoral artery for 8 rain to reduce the mean arterialpressure to 5.73±0.1kPa,which was maintained for an hour.Then the dogs were intravenouslyinjected with 4ml/kg 0.9％ NaCL(NS group,n=7),7.5％ NaCl(HS group,n=6)and 7.5％Naa-6％ dextran 70(HSD group,n=6)respectively.In the 2-hour-period after injection,5out of 7 dogs of NS group died but only 1 out of the 6 of both the HS and HSD groupsdied.Significant increase of mean arterial pressure,left ventricular pressure,±dp/dt max of leftventricle,cardiac output,cardiac index and cardiac minute work index was observed in both theHS and HSD groups.Improvement of the cardiovascular function was even more marked inHSD group than in HS group,thougth the difference between the 2 groups was statisticallyinsignificant.There was a tendency for the pulmonary vascular resistance to decrease in HS andHSD groups as compared with the NS group.The percentage of plasma expansion of HSDgroup was larger than that of HS group(P【0.05)and of NS group(P【0.01),but nosignificant difference existed between the HS and NS groups.It is believed that intravenous injection of hypertonic saline alone or in combination with dextran is effective for the treatment ofhemorrhagic shock at high altitude and the combination of 7.5％ NaCl and 6％ dextran 70seems even more effective.

Effects of hemorrhagic shock on endotoxemia and its molecular mechanism

In order to investigate whether hemorrhgic shock (HS) can enhance an individual’s sensitivity to endotoxin and the mechanism of this sensitization if it occurs, the changes of arterial blood pressure, plasma level of lactate and β-glucuronidase (β-G) and mortality rate were observed in rabbits of HS, lipopolysaccharide (LPS) and HS＋LPS groups. In addition. the expression of CD14 was determined in peritoneal macrophages in mice with HS.It was found that after the Infusion of LPS in HS＋LPS group, arterial blood pressure was significantly decreased while plasma lactate and β-G increased. The changes of these 3 parameters in HS＋LPS group were significantlydifferent from those of HS or LPS group at all time points. All the rabbits in HS＋LPS group died and those of HSand LPS groups survived. The expression of CD14 elevated in the peritoneal macrophages of mice during HS andsubsequent resuscitation. It is concluded that HS can markedly increase an individual’s sensitivity to endotoxin.which might be due to the upregulation of CD14 expression after HS.

Role of transcription factor Egr-1 in liver injury following hemorrhagic shock and resuscitation

Objective: To investigate the role of transcription factor Egr-1 in liver injury following hemorrhagic shock (HS) /resuscitation (R). Methods: Both Egr-1 knockout (KO) and wild-type (WT) mice were subjected to HS and HSR injuries. The expressions of TNF-α, IL-6, G-CSF and ICAM-1 mRNAs in the liver were examined by RT-PCR, and their serum levels were measured by ELISA. The liver inflammatory infiltration and liver injury in both Egr-1 WT and KO mice following HS/R were evaluated by liver MPO content, serum ALT level and histological examination. Results: Egr-1 inhibition resulted in less mRNA expression of TNF-α, IL-6 , G-CSF and ICAM-1 in the liver, and lower serum levels of TNF-α, IL-6, G-CSF and ICAM-1 antigens in Egr-1 KO mice following HS/R. The liver inflammatory infiltration and liver injury were less severe in Egr-1 KO mice following HS/R, as evidenced by lower serum ALT level, lower hepatic MPO content and histological manifestations. Conclusion: Our data suggest that transcription factor Egr-1 is involved in regulating the expression of inflammatory response genes and plays a role in liver injury following HS/R.

Hemorrhagic shock due to ruptured lower limb vascular malformation in a neurofibromatosis type 1 patient:A case report

BACKGROUND Neurofibromatosis type 1(NF-1)is a common autosomal dominant genetic disorder.It is characterized by café-au-lait spots and cutaneous neurofibromas.Although NF-1 typically involves the skin,nerves,bones,and eyes,vascular manifestation in the form of devastating hemorrhage can occur rarely.CASE SUMMARY We present the case of a 47-year-old female with NF-1 who had a ruptured right lower limb arterial malformation.She presented with sudden right lower limb swelling for two hours and symptoms of hemorrhagic shock on admission.The physical examination revealed a right lower limb presenting as elephantiasis and visible dark-brown pigmentation over a large area.Computed tomography angiography showed right lower limb arteriovenous malformation.Therefore,the patient underwent emergency right lower limb digital subtraction angiography(DSA)and vascular embolization after blood transfusions.However,after DSA,vascular embolization,and repeated blood transfusions,the anemia and right lower limb swelling and tenderness did not improve.As a result,the patient underwent right lower extremity above-knee amputation.After amputation,the patient's hemoglobin level improved significantly without blood transfusion,and she was discharged from the hospital after the incision healed.Postoperative pathological examination suggested neurogenic tumors.No other complications had occurred 1-year follow-up.CONCLUSION Vascular malformation and rupture are fatal complications of NF-1.Embolization may not provide complete relief,the patient might need to undergo neurofibroma resection or amputation.

Effects of GLP on Intestinal Mucosal Injury and the Change of TNF-α Content in Hemorrhagic Shock Rabbits

Objective To observe the intestinal mucosal injury and the change of TNF-αcontent in rabbits with hemorrhagic shock/reperfusion(HS-R)and the effects of ganoderma Lcidum polysaccharide(GLP)on them.Methods 30rabbits were made into hemorrhagic shock,then reperfused with different liquids.These rabbits were divided by random number table into three groups:sham operation group(Sham group),reperfusion with normal saline group(NS group),reperfusion with 1%GLP group(LS group).Bacterial translocation of blood and TNF-αcontent in serum were respectively observed at the time before shock,40 min after shock,40 min and 90 min after.TNF-αcontent in intestinal mucosa and the degree of intestinal mucosal injury were examined at 90 min post-resuscitation.Results 1 With the extension of reperfusion time,the positive rate of blood bacteria increased gradually in NS group,which was significantly higher than that of Sham group and LS group(P<0.05),meanwhile the degree of intestinal mucosal injury in NS group was more severe than that of Sham group and LS group too(P<0.05).2TNF-αcontent in serum of NS group and LS group were increased obviously compared with that before shock and in Sham group(P<0.05).TNF-αcontent in serum was further increased after reperfusion with NS,which was distinctly higher than that in LS group.TNF-αcontent in intestinal mucosa of NS group was significantly higher than that in LS group and Sham group too(P<0.05).Conclusion GLP can protect intestinal mucosa against HS-R injury,and its effects may relate with the change of TNF-αin hemorrhagic shock rabbits.

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.

EFFECT OF HEMORRHAGIC SHOCK ON ENDOTOXININDUCED TNF PRODUCTION AND ITS MOLECULAR MECHANISM IN RATS

The present study was designed to investigate the production of tumor necrosis factor a (TNFα) in-duced by low-dose (1μg/kg) lipopolysaccharide (LPS) and its cellular source after hemorrhagic shock(HS) in rats, and to further analyze the mechanism for increased sensitivity to LPS through looking at ex-pression of lipopolysaccharide -binding protein (LBP ) mRN A in t he liver, lungs and kidneys. lt wa s foundin uiuo that plasma TNFa levels in the HS+LPS group were 20-fold higher than that in the HS group (P<0. 01 ), and 2. 7-fold higher than that in the LPS group (P<0. 05). lt was shown in ndro that the ca-pacity of peripheral white blood cells to produce TNFa in response to LPS stimulation was significantly de-creased by 126 % (P<0. 01 ) and 57% (P<0. 05) compared with pre-shock levels and the sham group re-spectively at the end of resuscitation following shock, and was still markedly decreased 3 hours after resus-citation, while the capacity of Kupffer Cells was significantly increased by 110% compared with the shamgroup (P<0. 01) after shock and resuscitation. Results from RT-PCR showed that expression of LBPmRNA in the liver, lungs and kidneys was increased after shock and resuscitation. It is suggested thathemorrhagic shock could significantly enhance endotoxin-induced TNFa production, which might be due toup-regulation of LBP expression in tissues after shock, and tissue macrophages might be the main source ofcytokine production.

THE CHANGE OF ARTERIOVENOUS CARBON DIOXIDE AND pH GRADIENTS DURING SEVERE HEMORRHAGIC SHOCK AND RESUSCITATION

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.