罕见病因引起消化道出血8例

目的对8例罕见病因消化道出血进行回顾性研究．方法由胃Dieulafoy溃疡引起上消化道大出血5例，均因大量呕血不同程度休克急诊手术．术中切开胃探查，发现在贲门远侧6cm以内有直径不超过1cm的浅表溃疡，动脉裸露，直径约1．2mm，其中3例有活动性出血，另2例血凝块附着，轻拭之有活动性出血．1例缝扎后作近端胃部分切除术．另4例作出血血管两端的可靠缝扎止血．2例小肠上段平滑肌瘤，位于系膜侧，突入肠腔内，瘤表面粘膜小缺损，凹陷累及血管破裂出血，急诊手术．作连同瘤体在内的小肠部分切除术．另有1例为小场中段粘连，粘连面溃疡出血，术前曾有5次反复大量便血史．手术将粘连段肠管切除．结果罕见病因的消化道出血在诊断和治疗上都很困难．多数术前诊断不明，因此主要依靠术中探查．本组8例术中仔细探查后诊断准确处理正确，均获完全治愈．要求经治医师掌握多方面的新知识，术中探查应注意系统性、逻辑性，注意新技术的应用．结论罕见病因消化道出血的诊断和治疗需具备丰富知识和经验的医师的手术探查．

失血性休克对内毒素的增敏作用及其分子机制

目的探讨失血性休克对内毒素的增敏作用及其机制，为失血性休克的治疗提供理论依据。方法采用生化、逆转录ＰＣＲ（ＲＴ－ＰＣＲ）及细胞原位杂交技术，观察了失血性休克条件下低剂量内毒素的作用及其可能机制，以及大鼠肝、肺、肾组织内脂多糖结合蛋白（ＬＢＰ）ｍＲＮＡ的表达。结果输入脂多糖（ＬＰＳ）后，失血性休克（ＨＳ）＋ＬＰＳ组家兔血压持续显著下降，血浆乳酸、β葡萄糖醛酸酶水平显著升高，与单纯ＬＰＳ或ＨＳ组比差异有显著意义。休克后２４小时，ＨＳ＋ＬＰＳ组动物全部死亡，而其余两组动物存活；ＲＴ－ＰＣＲ结果显示，休克及复苏后，大鼠肝、肺、肾组织内ＬＢＰｍＲＮＡ表达相继增多；细胞原位杂交结果表明，休克及复苏后，小鼠腹腔巨噬细胞内ＣＤ１４ｍＲＮＡ表达也明显增加。结论失血性休克能增敏内毒素的作用，其机制可能与休克上调ＬＢＰ／ＣＤ１４的表达有关。

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.

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 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.

Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury

Inducible heat shock protein 70 kD (HSP-70i) has been shown to protect cells, tissues, and organs from harmful assaults in in vivo and in vitro experimental models. Hemorrhagic shock followed by resuscitation is the principal cause of death among trauma patients and soldiers in the battlefield. Although the underlying mechanisms are still not fully understood, it has been shown that nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression play important roles in producing injury caused by hemorrhagic shock including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B4 (LTB4) generation. Moreover, transcription factors responsible for iNOS expression are also altered by hemorrhage and resuscitation. It has been evident that either up-regulation of HSP-70i or down-regulation of iNOS can limit tissue injury caused by ischemia/reperfusion or hemorrhage/resuscitation. In our laboratory, geldanamycin, a member of ansamycin family, has been shown to induce HSP-70i overexpression and then subsequently to inhibit iNOS expression, to reduce cellular caspase-3 activity, and to preserve cellular ATP levels. HSP-70i is found to couple to iNOS and its transcription factor. Therefore, the complex formation between HSP-70i and iNOS may be a novel mechanism for protection from hemorrhage/resuscitation-in-duced injury.

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.

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.

Effects of seawater immersion on the functions of mitochondria of myocardium and hepatocyte in hemorrhagic shock rats

Objective: To investigate the effects of seawater immersion on the function of myocardium and hepatocyte mitochondria in experimental hemorrhagic shock rats. Methods: Twenty-four male Wistar rats were divided into three groups (n=8 in each group): control group, HSL group (hemorrhagic shock group on land) and HSS group (hemorrhagic shock group in seawater). The hemodynamic parameters, activities of H+-ATPase (adenosinetriphosphatase), succinate dehydrogenase (SDH) and Ca 2+-Mg 2+-ATPase, the calcium contents in myocardium and hepatocyte mitochondria were measured and the changes of proton translocation across the inner mitochondrial membrane were analyzed. Results: The hemodynamic indexes and the activities of H+-ATPase, SDH, Ca 2+-Mg 2+-ATPase in HSS group were significantly lower than those in control group and HSL group (P< 0.05). In HSS group the calcium levels in tissue and mitochondria of myocardium and hepatocyte were elevated significantly compared with control group and HSL group(P< 0.05). There was no significant difference in proton translocation among three groups. Conclusions: This investigation demonstrates that seawater immersion can aggravate the conditions of hemorrhagic shock rats.

Effects of two fluid resuscitations on the bacterial translocation and inflammatory response of small intestine in rats with hemorrhagic shock

Objective： To investigate the effects of two fluid resuscitations on the bacterial translocation and the inflammatory factors of small intestine in rats with hemorrhagic shock. Methods： Fifty SD healthy male rats were randomly divided into 5 groups （ n = 10 per group） ： Group A （ Sham group）, Group B （ Ringer＇ s solution for 1 h ）, Group C （Ringer＇ s solution for 24 h ）, Group D （ hydroxyethyl starch for 1 h ） and Group E （（ hydroxyethyl starch for 24 h）. A model of rats with hemorrhagic shock was established. The bacterial translocation in liver, content of tumor necrosis factor-α （TNF-α） and changes of myeloperoxidase enzyme （MPO） activities in small intestine were pathologically investigated after these two fluid resuscitations, respectively. Results ： The bacterial translocation and the expression of TNF-α in the small intestine were detected at 1 h and 24 h after fluid resuscitation. There were significant increase in the number of translocated bacteria, TNF-α and MPO activities in Group C compared with Group B, significant decrease in Group E compared with Group D and in Group B compared with Group D. The number of translocated bacteria and TNF-α expression significantly decreased in Group E as compared with Group C. Conclusions： The bacterial translocation and the expression of TNF-α in the small intestine exist 24 h after fluid resuscitation. 6 % hydroxyethyl starch can improve the intestinal mucosa barrier function better than the Ringer＇ s solution.

The ATP sensitive K^+ channel and membrane potential in the pathogenesis of vascular hyporeactivity in severe hemorrhagic shock

To elucidate the mechanism of vascular hyporeactivity following severe hemorrhagic shock (HS) by studying the changes of ATP sensitive potassium channels (K ATP ) properties and membrane potential of mesenteric arteriolar smooth muscle cells. Methods: Single channel currents were studied on cell attached and inside out patches of enzymatically isolated mesenteric arteriolar smooth muscle cells (ASMCs). Membrane potentials of arteriolar strips and ASMCs were recorded by intracellular membrane potential recording method and confocal microscopy, respectively. Results: K ATP channels in ASMCs were activated, which induced smooth muscle hyperpolarization following vascular hyporeactivity in HS. Conclusions: Hyperpolarizing effect of K ATP channel activation plays an important role in low vasoreactivity during severe hemorrhagic shock.

Protective effect of albumin on lung injury in traumatic/hemorrhagic shock in rats

Objective. To determine the effect of albumin administration on lung injury in traumatic/hemorrhagic shock （T/HS） rats. Methods： Forty-eight adult Sprague-Dawley rats were divided into three groups randomly （ n = 16 in each group） ： Group A, Group B, Group C. In Group A, rats underwent laparotomy without shock. In Group B, rats undergoing T/HS were resuscitated with their blood plus lactated Ringer＇s （twice the volume of shed blood ）. In Group C, rats undergoing T/HS were resuscitated with their shed blood plus additional 3 ml of 5% human albumin. The expression of polymorphonuclear neutrophils CD18/CD11b in jugular vein blood was evaluated. The main lung injury indexes （the activity of myeloperoxidase and lung injury score） were measured. Results： Significant differences of the expression of CD18/11b and the severity degree of lung injury were found between the three groups. （P〈0.05）. The expression of CD18/CD11b and the main lung injury indexes in Group B and Goup C incresed significantly compared with those in Group A （P 〈0.05）. At the same time, the expression of CD18/CD11b and the main lung injury indexes in Group C decreased dramatically, compared with those in Group B （ P 〈0.05 ）. Conclusions ： The infusion of albumin during resuscitation period can protect lungs from injury and decrease the expression of CD18/CD11b in T/HS rats.

Beneficial effects of fructose 1,6 diphosphate on hemorrhagic shock in rats

Objective: To investigate the effects of fructose 1,6 diphosphate (FDP) on experimental hemorrhagic shock in rats. Methods: Sixty rats were randomly divided into three groups: the normal saline control group (group A), the 5% glucose solution control group (group B) and the 5% FDP solution treated group (group C). Shock models were made by bloodletting until the mean arterial pressure (MAP) reduced to 39.75 mmHg (1 mmHg=0.133 kPa) for 60 minutes, and then normal saline, 5% glucose and FDP were given to the rats, respectively. Results: FDP could significantly increase MAP and the survival rate, elevate pH value, partial oxygen pressure (PaO 2) and superoxide dismutase (SOD) activity, and decrease partial carbon dioxide pressure (PaCO 2) and malondialdehyde (MDA) in arterial blood of the shocked animals. Conclusions: It suggests that FDP has a good protective effect on hemorrhagic shock by improving tissue metabolism and preventing acidosis and tissue injury caused by free radicals.

Opioid receptors associated with cardiovascular depression following traumatic hemorrhagic shock in rats

Objective: To elucidate which one of μ, δ and κ opioid receptors is involved in the cardiovascular depression following traumatic hemorrhagic shock. Methods: With traumatic hemorrhagic shock rat models, the changes of myocardial and brain μ, δ and κ opioid receptors and cardiovascular functions and their relationship with hemodynamic parameters were observed. The effects of δ and κ opioid receptor antagonists on hemodynamic parameters of traumatic hemorrhagic shock rats were observed. Results: Following traumatic hemorrhagic shock, the number of myocardial and brain δ and κ opioid receptors significantly increased, their affinity did not alter, and the increased number of δ and κ opioid receptors was significantly associated with the decreased hemodynamic parameters. However, μ opioid receptor in heart and brain did not obviously change. δ opioid receptor antagonist ICI174,864 and κ opioid receptor antagonist Nor binaltorphimine (50 μg, Icv) could significantly reverse those decreased hemodynamic parameters. Conclusions: It suggests that opioid receptors, especially δ and κ opioid receptors are closely related to the pathogenesis of traumatic hemorrhagic shock, and they play important roles in the depression of cardiovascular function following traumatic hemorrhagic shock.