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目的 探讨脑缺血模型内毒素受体CD1 4mRNA在肺、肝、肠和肾组织的表达变化规律及并发多器官功能障碍综合征 (MODS)的机制。方法 通过阻断双侧颈总动脉 30min建立急性前脑缺血模型 ,随机将 54只大鼠分为正常对照组、假手术组及缺血后 5个亚组 ( 1 2h、2 4h、36h、4 8h、72h组 ) ,依据全身炎症反应综合征 (SIRS)、MODS的诊断标准判断SIRS、MODS的发生率 ,采用原位杂交技术检测缺血后肺、肝、肠和肾脏器CD1 4的基因表达。结果 大鼠急性前脑缺血后SIRS发生率为 1 0 0 % ,MODS发生率为 53 1 % ;缺血后 1 2h、2 4h、36h、4 8h、72h时相点动物肺、肝、肠和肾组织均有不同程度的损害 ,以肺脏和小肠改变为著 ;缺血后 1 2h肺、肝、肠和肾组织CD1 4mRNA表达升高 ,2 4～ 36h达高峰 ,4 8h后下降 ,以肺脏变化最显著 (P <0 0 0 1 ) ;正常对照组和假手术组中肺、肝、肠和肾组织CD1 4mRNA均有不同程度的表达 ,其中两组肺脏CD1 4mRNA的表达有显著性差异 (P <0 0 0 1 )。结论 脑缺血后肺、肠、肝和肾组织CD1 4mRNA的异常表达和病理改变为肠道内毒素易位和内毒素血症的发生提供条件 ,为研究脑缺血后MODS的发生机制提供客观依据
Objective To investigate the expression of endotoxin receptor CD14 mRNA in lung, liver, intestine and kidney and the mechanism of multiple organ dysfunction syndrome (MODS) in cerebral ischemia model. Methods Acute forebrain ischemia models were established by blocking bilateral common carotid arteries for 30 min. 54 rats were randomly divided into normal control group, sham operation group and 5 subgroups after ischemia (12h, 24h, 36h, 48 h and 72 h groups). The incidence of SIRS and MODS was determined according to the diagnostic criteria of SIRS and MODS. The expression of CD14 in lung, liver, intestine and kidney was detected by in situ hybridization expression. Results The incidence of SIRS in acute forebrain ischemic rats was 100% and the incidence of MODS was 53.1%. The lung, liver and intestine of rats at 12h, 24h, 36h, 48h and 72h after ischemia And kidney tissue were different degrees of damage to the lungs and small intestine as the change; 12h after ischemia, CD14 mRNA expression in lung, liver, intestine and kidney tissue increased from 24 to 36h and reached the peak at 48h (P <0.01). The expression of CD14 mRNA in lung, liver, intestine and kidney in normal control group and sham operation group were all different, and the expression of CD14 mRNA in both groups had significant difference (P <0 0 0 1). Conclusions The abnormal expressions of CD14 mRNA in lung, intestine, liver and kidney tissue and the pathological changes after cerebral ischemia provide conditions for the development of intestinal endotoxin translocation and endotoxemia and provide an objective basis for studying the pathogenesis of MODS after cerebral ischemia