摘要
目的:探讨创伤脓毒症早期病理生理变化。方法:Wistar大鼠造成失血性休克(维持血压在30～35mmHg)持续2小时,休克末快速经颈静脉回输(15分钟内)失血和等量的林格氏液;复苏后6小时,以蠕动泵经尾静脉输入大肠杆菌内毒素2mg/kg。实验分成5组,分别观察致伤前、创伤失血休克末、复苏后及输注内毒素后2小时和24小时各器官功能的变化。结果:动物在创伤休克末和缺血再灌注后即有全身炎症反应出现,心、肝、肾、肺、肠等器官功能指标出现变化,创伤休克末ALT和AST较伤前增加1倍;心肌酶谱在输内毒素2h后大于正常值的3倍以上;病理学观察显示各器官组织出现不同程度的实质性损伤;实验动物总死亡率为39.6%,单个器官功能障碍发生率为64.7%,二个或二个以上器官功能不全为23.5%。结论:本实验较好地重现了创伤后脓毒症发生的诱因和临床特点;SIRS发生率较高,符合MODS标准的仅为23.5%,是较好的创伤脓毒症模型。
Objective:To investigate the pathophysiological changes during early stage of sepsis after trauma in rats. Methods: A rat model of hemorrhagic shock was established by bleeding and maintaining the blood pressure within 30-35mmHg for 2h, followed by rapid resuscitation with Ringer's lactate and shed blood. Endotoxin (E. coli O_(55) B_5) was infused at a dose of 2mg/kg through tail vein at 6h after resuscitation. Wistar rats were divided into five groups according to time intervals: prior to bleeding(n=10), end of hemorrhage (n=10), end of resuscitation (n=10),2h as well as 24h after resuscitation combined with endotoxin challenge(n=8 and 9). Results: It was revealed that inflammatory response in animals during early stage after hemorrhage/resuscitation, and organ function parameters including the heart, liver, kidneys, lungs and intestine were abnormal. ALT and AST were elevated by 2-fold compared to baseline values. Meanwhile, CK-MB increased by 3-fold at 2 h after endotoxin challenge. The pathological examination showed vital organ damage to certain extent. The total mortality rate of experimental animals was 39.6% and the incidence of single and two or more organ dysfunction was 64.7% and 23. 5%, respectively. Conclusion: Our data indicated that this model appears to simulate the clinical characteristics of sepsis associated with trauma. The incidence of SIRS in rats is high and that of MODS is 23.5%.
出处
《感染．炎症．修复》
2000年第2期93-96,共4页
Infection Inflammation Repair
