Study of serum endotoxin and CD_(14) gene expression in a model of cerebrogenic multiple organ dysfunction syndrome

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 ( P0.001). CD 14mRNA expression also was found in multiple organs both in control group and sham-operative group. There was a significant difference in lung ( P0.01). Relative analysis indicated that there was a significant positive correlation between CD 14mRNA expression and plasma endotoxin level, especially in lung and intestine ( P0.01).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.