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.

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.

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.

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.

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.

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.

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.

Effect of abdominal trauma on hemorrhagic shock-induced acute lung injury in rats

TO evaluate the effects of abdominal trauma on hemorrhagic shock-induced acute lung injury in rats. METHODS： Five groups were allocated （n = 8） in the study. Group Ⅰ was taken as the control group, group Ⅱ as the hemorrhagic shock group, group Ⅲ as hemorrhagic shock ＋ laparotomy, group Ⅳ as hemorrhagic shock ＋ splenectomy and group V as splenectomy ＋ omentectomy ＋ hemorrhagic shock group. Hemorrhagic shock was induced by drawing blood and reducing mean arterial pressure （MAP） to 40 mmHg within 10 min. After a hypotensive period of 1 h, animals were resuscitated. Bronchoalveolar lavage （BAL） was performed to recover cells from the alveolar space with 40 mL of BAL fluid after resuscitation malondialdehyde （MDA） and L-γ-glutamyl-L-cysteinylglycine （GSH） levels were measured in serum, erythrocytes and lung tissue. RESULTS： Serum, erythrocyte, lung tissue MDA and GSH levels were significantly increased in hemorrhagic shock groups Ⅱ-Ⅴ （P 〈 0.05）. Lymphocyte, neutrophil and alveolar macrophage counts in BAL fluid indicated a significant difference between control and shock groups （P 〈 0.05）. CONCLUSION： The degree of trauma increases hemorrhagic shock-induced acute lung injury.

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

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.

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.

Can albumin administration relieve lung injury in trauma/hemorrhagic shock?

AIM: To study the effect of albumin administration on lung injury in trauma/hemorrhagic shock (T/HS). METHODS: Sixty experimental animals were randomly divided into three groups: rats undergoing laparotomy without shock (T/SS); rats with T/HS and resuscitation with blood plus twice the volume of shed blood as Ringer’s lactate (RL), and rats with T/HS and resuscitation with blood plus additional 3 mL of 50 g/L human albumin. Expression of polymorphonuclear neutrophil (PMN) CD11b/CD18, intercellular adhesion molecule-1 (ICAM-1) of jugular vein blood and the severity of lung injuries [determined mainly by measuring activity of lung tissue myeloperoxidase (MPO) and lung injury score (LIS)] were measured after a 3-h recovery period. RESULTS: All three groups showed a significant difference in the expressions of CD11b/CD18, ICAM-1, and severity of lung injury. The expressions of CD11b/ CD18 in T/SS group, T/HS + RL group, T/HS + albumin group were 17.76% ± 2.11%, 31.25% ± 3.48%, 20.36% ± 3.21%, respectively (F = 6.25, P < 0.05). The expressions of ICAM-1 (U/mL) in T/SS group, T/ HS + RL group, T/HS + albumin group were 258.76 ± 98.23, 356.23 ± 65.6, 301.01 ± 63.21, respectively (F = 5.86, P < 0.05). The expressions of MPO (U/g) in T/SS group, T/HS + RL group, T/HS + albumin group were 2.53 ± 0.11, 4.63 ± 1.31, 4.26 ± 1.12, respectively (F = 6.26, P < 0.05). Moreover, LIS in T/HS + RL group, T/HS + albumin group was 2.62 ± 0.23, 1.25 ± 0.24, respectively. The expressions of CD11b/CD18, ICAM-1 and MPO in T/HS + RL group were significantly increased compared to T/SS group (P = 0.025, P = 0.036, P = 0.028,respectively). However, administration of 3 mL of 50 g/L albumin significantly down-regulated the expressions of CD11b/CD18, ICAM-1 and lung injury index (MPO and LIS) when compared with the T/HS + RL rats (P = 0.035, P = 0.046, P = 0.038, P = 0.012, respectively). CONCLUSION: The infusion of albumin during resuscitation period can protect lung from injury and decrease the expressions of CD11b/CD18, ICAM-1 in T/ HS rats.

Immunoprotective effects of HSH resuscitation on rats with hemorrhagic shock

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.

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 different infusion volumes on hemo-dynamics of portal hypertension canines after hemorrhagic shock

BACKGROUND: Portal hypertension ( PHT) with upper gastrointestinal hemorrhage as its chief complication is a very common disease with great harm to humans. The effects of infusion volume, speed, and type on hemody- namics in case of cirrhosis, PHT esophageal variceal bleed- ing, and their mechanism should be clarified. This study was designed to assess the effects of different infusion vo- lumes on hemodynamics of PHT canines after hemorrhagic shock (HS). METHODS: PHT canine models were made by chronic embolization via coarctating half of the main portal vein with silk suture. Two weeks later, the models were subjec- ted to hemorrhagic shock by quick femoral artery venesec- tion. The canines were divided into two groups to resusci- tate : one to receive a large volume of infusion (n =6) (large volume infusion group) and the other to receive a small vo- lume of infusion (n =6) (small volume infusion group). Hemodynamic indexes of PHT canines after HS and infu- sion were observed closely. RESULTS: The PHT canines showed a series of hemody- namical changes in hemorrhagic shock stage, which aggra- vated hemodynamical disorder in PHT. After quick infu- sion, mean arterial pressure (MAP), inferior vena cava pressure (IVCP), portal venous pressure ( PVP), portal vein pressure gradient ( PVPG), portal vein blood flow ( PVBF), hepatic artery blood flow ( HABF) and hepatic blood flow (HBF) increased significantly. These indexes in the large volume infusion group were higher than those in the small volume infusion group. Portal vascular resistance (PVR), splanchnic vascular resistance ( SVR), hepatic arte- rial resistance ( HAR) decreased significantly, but PVP, PVPG, PVBF, HABF and HBF showed a rebounding in- crease above the baseline values in the large volume infu- sion group. The changes of PVP, PVPG, PVBF, HABF and HBF were in parallel with those of MAP and inferior vena cava pressure (IVCP), without a rebounding increase in the small volume infusion group. In the large volume in- fusion group PVPG increased earlier and more significantly than did PVP; moreover PVPG exceeded the baseline by 13% , making the possibility of rebleeding great. In the small volume infusion group, PVPG was lower than the baseline by more than 22% , indicating a small possibility of rebleeding. SVR and HAR were lower in the large volume infusion group. PVP, PVPG, PVBF, HABF and HBF were positively correlated with accumulated volume of vein infusion. PVR showed a positive correlation with accumu- lated volume of vein infusion in the small volume infusion group. HAR was negatively correlated with accumulated volume of vein infusion in the large volume infusion group. CONCLUSIONS: PHT canines after HS, resuscitated by vein infusion, may show a rebounding increase of PVP, PVPG, PVBF, HABF and HBF above the baseline values in the large volume infusion group but not in the small vol- ume infusion group. A large volume infusion causes PVP, PVPG, PVBF, HABF and HBF to increase higher than does a small volume infusion.

EXPRESSION OF TNFα IL-1β、IL-6 mRNA, RELEASE OF TNFα IN VITAL ORGANS AND THEIRRELATIONSHIP WITH ENDOTOXIN TRANSLOCATION FOLLOWING HEMORRHAGIC SHOCK

This study was designed to systematically investigate expression of TNF α,IL-1β,I1-6 mRNA in the liver,lungs and kidneys, release of TNF α in the above tissues,their relationship with hepatic, pulmonary and renal dysfunction,and distribution of endogenous endotoxin in tissues after hemorrhagic shock in mice and rats, with reverse-transcription-polymerase chain reaction, ELISA, etc, to elucidate the kinetics of expression and release of major cytokines in vital organs,their role and mechanism of production in shock. The results were: ①expression of TNF α, IL-1 β, IL-6 mRNA in vital organs successively increased after hemorrhagic shock and resuscitation,and TNF α expression was the first to appear followed by IL-1β. Though expression of IL-6 mRNA appeared late,it persisted longer;②TNF α levels in the liver,lungs and kidneys were all elevated but to different degrees after shock and resuscitation. At 3 hours after resuscitation,TNF α levels in the three above tissues were still significantly high,while plasma TNF α levels were already decreased to control levels; ③hepatic,pulmonary and renal functions were damaged to different degrees after hemorrhagic shock,with hepatic dysfunction being the most severe; ④endotoxin levels in the liver, lungs and kidneys were markedly increased after shock and resuscitation,and paraIleled the expression of cytokine genes. In addition,there was slgniflcant correlatlon between changes in endotoxin level in tissues and TNF α release in tissues during early shock. lt is suggested that expression and release of cytokines in vital organs might play an important role in local organ damage after hemorrhagic shock,and production of cytokines is related to endotoxin translocation.

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.