摘要
目的 观察急性前脑缺血致多器官功能障碍综合征(MODS)模型血清内毒素含量及其受体在 各脏器基因表达的规律,分析脑源性多器官功能障碍综合征(CMODS)的发生机制。方法 随机将54只 Wistar大鼠分为正常对照组(6只)、假手术组(8只)和前脑缺血组(40只),后者又被随机分为12h、24h、36 h、48h和72h时相点的5个亚组,每亚组各8只;建立大鼠急性前脑缺血模型;分别测定肺、肝、肠和肾组织 CD14mRNA水平;检测CD14mRNA的相对含量。结果 大鼠急性前脑缺血后12h血清内毒素升高,24h达高 峰,72h基本恢复至正常水平;肺、肝、肠和肾组织CD14mRNA的表达也在缺血后12h升高,24h～36h达高 峰,48h后下降,并以肺变化最显著(P<0.001);正常对照组和假手术组CD14mRNA在各脏器均有不同程度 的表达,其中肺的表达差异有显著性(P<0.01)。内毒素与其受体在各脏器的表达均存在显著相关性(均P< 0.01),其中与肠、肺组织CD14mRNA表达相关最显著(P<0.001)。结论 急性前脑缺血致MODS大鼠存在 内毒素血症;急性脑血管病→应激反应→肠道黏膜屏障损害→内毒素易位→内毒素血症→内脏器官功能障 碍→MODS是CMODS发生的重要过程,肠道机制是CMODS发生的重要机制之一。
Objective To investigate the changes of serum endotoxin and its receptor CD 14 gene expression in multiple organs in models of acute forebrain ischemia complicated with multiple organ dysfunction syndrome (MODS), and the pathogenesis of cerebrogenic multiple organ dysfunction syndrome (CMODS). Methods 54 Wistar rats were randomly divided into normal control group ( n=6), sham-operative group ( n=8) and forebrain ischemic group ( n=40). The rats in forebrain ischemic group were randomly divided into 5 subgroups: 12, 24, 36, 48, and 72 h (8 rats in each group). The contents of endotoxin in plasma were determined after models of acute forebrain infarction established. The area density and optical density of positive staining expressing CD 14mRNA in lung, liver, intestine and kidney were analyzed for the relative content of CD 14mRNA using in situ hybridization and CMIA medical image analysis system.Results Plasma endotoxin level was markedly high at 12 hours after acute forebrain ischemia, peaked at 24 hours and somewhat decreased at 72 hours. The CD 14mRNA expression in lung, liver, intestine, and kidney tissues increased after brain ischemia, reached the peak at 24~36 h, and decreased after 48 hours. The highest change of CD 14mRNA expression was found in lung ( P<0.001). CD 14mRNA expression also was found in multiple organs both in control group and sham-operative group. There was a significant difference in lung ( P<0.01). Relative analysis indicated that there was a significant positive correlation between CD 14mRNA expression and plasma endotoxin level, especially in lung and intestine ( P<0.01).Conclusions Acute forebrain ischemia may cause endotoxemia in rat with MODS. The progression (acute cerebrovascular diseases → stress → injure of intestinal mucosa → endotoxin translocation → endotoxemia → injure of organs → MODS) is the key process in development of CMODS. Intestinal mechanism is one of the important pathogenesis of CMODS.
出处
《临床神经病学杂志》
CAS
北大核心
2005年第1期48-50,共3页
Journal of Clinical Neurology
基金
山东省"九五"攻关重大课题(编号:1997CA3CAA7)
关键词
脑源性多器官功能障碍综合征
内毒素
CD14肠道
cerebrogenic multiple organ dysfunction syndrome
endotoxin
cluster of differentiation 14
Intestinal
