不同复苏液体对二次打击致MODS血管内皮细胞损伤研究
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摘要
目的:研究失血性休克不同液体复苏再二次打击致多脏器功能障碍综合征(MODS)时血管内皮细胞(EC)损伤影响。方法: SD大鼠84只,随机分为正常对照组、生理盐水复苏组、7.5%高渗盐水复苏组、万汶复苏组4组,每组21只。除正常对照组腹腔注入等量生理盐水外,其余3组SD大鼠失血性休克维持1h,进行不同液体复苏,复苏成功30min后3组腹腔注射内毒素。分别在注射内毒素后24、48、72h四组随机取7只大老鼠抽取静脉血检测各组EC生化指标循环内皮细胞(CEC)、一氧化氮(NO)、内皮素(ET-1)。结果:复苏再二次内毒素打击致MODS中,CEC数量生理盐水复苏组最高,对照组最低(P<0.05),7.5%高渗复苏组明显低于生理盐水复苏组(P<0.05)。NO含量以7.5%高渗复苏组最高,并随时间延长数量逐渐增加,高于生理盐水复苏组及万汶复苏组(P<0.05)。ET-1含量7.5%高渗复苏组低于生理盐水复苏组及万汶复苏组(P<0.05)。各检测指标随时间变化无明显改变(P>0.05)。镜下观察7.5%高渗盐水复苏组脏器标本切片病理改变比生理盐水复苏组轻。结论:失血性休克不同复苏液体内毒素二次打击致MODS血管内皮细胞损伤程度不同,7.5%高渗盐水复苏具有抗血管内皮细胞损伤作用。同时能够减轻重要脏器损伤,改善MODS预后。
Objective: To study the influence of blood vessel endothelium cell of MODS rats which resuscitated hemorrhagic shock by different liquid and strike with the endotoxin again. Methods:84 SD rats were randomly divided into four average groups(n=21)which named Normal conrol group, Resuscitated by 0.9% normal saline group, Resuscitated 7.5% hypertonic saline group and Resuscitated by Hydroxyethyl Starch (130/0.4) group。Beside Normal conrol group abdominal cavity pours into 0.9% normal saline(2ml/100g), the other three group of SD rats all had been kept hemorrhagic shock for one hour, then resuscitated by different liquid.and after 30 minutes during accomplish anabiosis , the three groups rats were injected into antrum of abdomen with the endotoxin again. After it the blood of vein which was taken out from different 7 rats got randomly from the four groups on 24、48、72h was tested about the level of CEC、NO、ET-1. Results: Of the MODS rats which resuscitated hemorrhagic shock by different liquid and strike with the endotoxin again , the CEC quantity of Resuscitated by 0.9% normal saline group is the highest and the control group the lowest (P <0.05). the CEC quantity of 7.5% hypertonic saline group is lower than Resuscitated by 0.9% normal saline group (P <0.05 ).The content of NO to 7.5% hypertonic resuscitation group is the highest with time a gradual increase in quantity, and is higher than Resuscitated by 0.9% normal saline group, and Resuscitated by Hydroxyethyl Starch (130/0.4) group (P <0.05) The ET-1 content of 7.5% hypertonic saline group is lower than the Resuscitated by 0.9% normal saline group and Resuscitated by Hydroxyethyl Starch (130/0.4) group (P <0.05) .Detect the target over time no significant change (P> 0.05).Endoscopic observation,pathological changes of the heart,liver,kidney of the recovery of 7.5% hypertonic saline group is lighter than the normal saline resuscitation group . Conclusions: It is different the influence of blood vessel endothelium cell of rats model which resuscitated hemorrhagic shock by different liquid and strike with the endotoxin again. 7.5% hypertonic saline resuscitation has anti-vascular endothelial cell injury,at same time to reduce important organ damage and improve the prognosis of MODS.
Objective: To study the influence of blood vessel endothelium cell of MODS rats which resuscitated hemorrhagic shock by different liquid and strike with the endotoxin again. Methods:84 SD rats were randomly divided into four average groups(n=21)which named Normal conrol group, Resuscitated by 0.9% normal saline group, Resuscitated 7.5% hypertonic saline group and Resuscitated by Hydroxyethyl Starch (130/0.4) group。Beside Normal conrol group abdominal cavity pours into 0.9% normal saline(2ml/100g), the other three group of SD rats all had been kept hemorrhagic shock for one hour, then resuscitated by different liquid.and after 30 minutes during accomplish anabiosis , the three groups rats were injected into antrum of abdomen with the endotoxin again. After it the blood of vein which was taken out from different 7 rats got randomly from the four groups on 24、48、72h was tested about the level of CEC、NO、ET-1. Results: Of the MODS rats which resuscitated hemorrhagic shock by different liquid and strike with the endotoxin again , the CEC quantity of Resuscitated by 0.9% normal saline group is the highest and the control group the lowest (P <0.05). the CEC quantity of 7.5% hypertonic saline group is lower than Resuscitated by 0.9% normal saline group (P <0.05 ).The content of NO to 7.5% hypertonic resuscitation group is the highest with time a gradual increase in quantity, and is higher than Resuscitated by 0.9% normal saline group, and Resuscitated by Hydroxyethyl Starch (130/0.4) group (P <0.05) The ET-1 content of 7.5% hypertonic saline group is lower than the Resuscitated by 0.9% normal saline group and Resuscitated by Hydroxyethyl Starch (130/0.4) group (P <0.05) .Detect the target over time no significant change (P> 0.05).Endoscopic observation,pathological changes of the heart,liver,kidney of the recovery of 7.5% hypertonic saline group is lighter than the normal saline resuscitation group . Conclusions: It is different the influence of blood vessel endothelium cell of rats model which resuscitated hemorrhagic shock by different liquid and strike with the endotoxin again. 7.5% hypertonic saline resuscitation has anti-vascular endothelial cell injury,at same time to reduce important organ damage and improve the prognosis of MODS.
引文
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[10]FanJ Shek PN, Suntress ZE, et al. Liposomal antioxidants provide proonged prote- ction against acuter spiratory distress syndrome [J].Surgery, 2000, 128:332-33381.
[11]Michael AM, Guy AZ, Charles E, etal Future research directions in acute lung injury.summary of a national heart lung and blood institute working groop[J].AM J Respir Crit Care Med, 2003, 167(7):1027-1035.
[12]Balibrea JL, Arias-Dlaz J.Acute respiratory distress syndrome inthe septic surgical patient.World J Surg, 2003, 27:1275-1284.
[13]Crimi E, Sluts AS. Inflammation and the acute respiratory distress syndrome. Best Practice Res Clin Anaesth, 2004, 18(3):477-492.
[14]Kshdu FU C, Karim T.Acute respiratory distress syndrome [J].Am Fam Physician, 2003, 67:315-322.
[15]Nagase T, UozumiN, T shiiS, etal.Acute lung injury by sepsisandacid aspiration:akerole forcy to solicphospholiaseA2[J]. NatImmunol, 2000, 1(1):42 246.
[16]张亚瑞,唐方.中医药对肠屏障功能保护作用的研究概况[J].浙江中医杂志, 2005, 3( 3):133.
[17]徐杰.危币重病患者肠黏膜屏障的变化与肠内营养[J].中国中西医结合急救杂志, 2004, 6( 11):385
[18]Chakravortty D, Kumark SN.Modulation of barrier function of small intestinal epithelial cells by laminapropria fibroblasts in response to lip opolysaccharide:Possible role in TNFa in inducing barrier dysfunction[J].M icrobioll Mm unol, 1999, 43(6):527.
[19]蒋建新,田昆全,陈惠孙,等.家兔创伤性休克后血浆内毒素、TNF-α和IL-6的动态变化.中华麻醉学杂志, 1997, 17:171.
[20]Deitch EA.Multiple organ failure:Pathophysiology and potential future therap[J].Ann Surg, 1992, 216:117.
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[22]姚宁,方国恩,杜成辉,等.猪多器官功能障碍模型的建立.[J]中华实验外科杂志, 2005, 22(1):108-109.
[23]方积乾,孙振球.卫生统计学.人民卫生出版社, 2005, (5):131-133.
[24]Ashbaugh DG, Bigelow DB, Petty, et al. Acute respiratory duress in adults. Lancet, 1967, 2: 319-323.
[25]HeumannD, GlauserMP, CalandraT. Molecular basis of host-Pathogen interaction in septic shock[J].Curr Opin Microbiol, 1998, 1(1):49.
[26]Trautmann M, Lauterbacher F, Mricke A . Endotoxin-Freisetzung durch piperacillin-tazobactam imvergleichmit Ceftazidim [J].Chemother J, 2000, 9:126.
[27] Liao W, Rudling M, Angelin B.Endoutoxin suppresses rat Hepatic low-density lipoprotein receptor expression [J].Biochem, 1996, 313:873.
[28]Condliffe AM, Chilvers ER, Haslett C, et al.Priming differentially regulates neutrophil adhesion molecule expression/function [J] Immunology, 1996, 89: 105-111.
[29]Drost EM, Macnee W. Potential role of IL-8, platelet-activating factor and TNF-a in the sequestration of neutrophils in the lung: effects on neutrophil deformability, adhesion receptor expression, and chemotaxis. [J] Eur J Immunol, 2002, 32: 393-03.
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[32]Ghosh S, Latimer RD, Gray BM, et al. Endotoxin-induced organ injury. Crit Care Med, 1993, 21: S19-S24.
[33]Kabir K, Gelinas JP, Chen M, et al. Characterization of a marine model of endotoxin-induced acute lung injury. Shock, 2002, 17: 300-303.
[34]Bhatia M, Moochala S. Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. [J] Pathol, 2004, 202: 145-156.
[35]朱华栋周玉淑等.内毒素血症细胞因子一氧化氮在重度失血性休克发展中的作用[J].中国急救医学1999 Vol.19 No.11
[36] Lee WL, Downey GP. Neutrophil activation and acute lung injury. [J] Curr Opin Crit Care, 2001, 7: 1-7.
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