A study of serum endotoxin and its gene expression in a model of cerebrogenic multiple organ dysfunction syndrome

Objective To study changes of serum endotoxin and its receptor CD14 gene expression in lung, liver, intestines, kidney tissues in model of acute forebrain ischemia complicated by multiple organ dysfunction syndrome(MODS), and to investigate the pathogenesis of cerebrogenic MODS. Methods 54 Wistar rats were randomly divided into seven groups: normal control group(n=6)、sham-operative group(n=8) and 5 ischemia groups(n=40)including 12 h, 24 h, 36 h, 48 h, 72 h five time points. Model of cerebral infarction was established. The content of endotoxin in plasma was evaluated with a test kit. The area density and optical density of positive staining of CD14mRNA expressing were analyzed for the relative content of CD14mRNA using in-situ hybridization and CMIA medical imaging analysis system. Results Plasma endotoxin level were markedly high at 12 h (0.184±0.055)Eu/L after acute forebrain ischemia, peaking at 24 h (0.639±0.064)Eu/L and it was somewhat decreased at 72 (0.117±0.024)Eu/L. The CD14mRNA expression in lung, liver, intestines, kidney tissues increased after brain ischemia, reaching the peak at the 24~36 h, and decreased after 48 h. The highest change of CD14mRNA expression was found in lung(P0.001). Compared with normal control group, the CD14mRNA expression significantly elevated in pulmonary tissue of sham-operative group(P0.01). Relative analysis indicated that there was significant positive correlation between the CD14mRNA expression in lung、liver、kidney and intestine and plasma endotoxin level(P0.01). Conclusions There was endotoxemia after acute forebrain ischemia. acute cerebrovascular diseases → stress → injure of intestinal mucosa → endotoxin translocation → endotoxemia → injure of organs → MODS is key process in generation of CMODS. Intestinal mechanism is one of the important pathogenesis of CMODS.