Abstract: Objective: To discuss the relationship between gene expression of IL-1βand serum endotoxin in a animal model of cerebrogenic multiple organ dysfunction syndrome(CMODS) complicated by cerebral hemorrhage, and to investigate the pathogenesis of CMODS. Methods: Ninty-six Wistar rats were randomly divided into four groups: normal control group (n=6), sham-operative group (n=6) and model group 1 with 0.4U collagenase (n=42) and model group 2 with 0.8U collagenase cerebral (n=42). The content of endotoxin in plasma was evaluated with a test box. Gene expression of IL-1β was assayed using in situ hybridization. The area density and the optical density of positive staining expressing IL-1βmRNA were analyzed for the relative content of IL-1βmRNA using in situ hybridization and CMIA medical imaging analysis system. Results: Expression of IL-1βmRNA in lung, liver, intestines andkidney tissues started to increase at 12 hours in model groups, and reached the peak at 24-36 hours. This was markedly higher in model group 2 than in model group 1 at 24 hours(P＜0.01). Compared with normal control and shamoperative groups, expression of IL-1βmRNA was significantly higher at 12-48 hours in models groups(P＜0.01). There was endotoxemia administration after acute cerebral hemorrhage. Plasma endotoxin level of model group 2 was higher than that of model group 1(P＜0.01). It started to increase at 8 hours after hemorrhage andpeaked at 24 hours, then returned to the baseline value at 72 hours in model group 1, but still maintained high level in model group 2. Relative analysis indicated that there was significant positive correlation between the IL1βmRNA expression in lung, liver, kidney, intestine and plasma endotoxin level(P＜0.01). Conclusion: Endotoxemia occurres after cerebral hemorrhage, and the gene expression of IL-1βincreases, which implicate that endotoxemia irritates the release of inflammatory factor, and systemic inflammatory response syndrom(SIRS) developes. This is key process in generation of CMODS.

Key words: Multiple organ failure, Endotoxins, Interleukin-1β, Gene expression, Rat, Wistar