大鼠急性前脑缺血致MODS模型血清内毒素水平及意义

Serum endotoxin level and significance in rat acute forebrain ischemia MODS models

目的:建立大鼠急性前脑缺血致MODS模型,监测其血清内毒素水平,探讨急性前脑缺血致MODS的发病机制。方法:采用阻断大鼠双侧颈总动脉后再灌注法制作大鼠急性前脑缺血模型,根据相关指标判断MODS发病率,应用微量内毒素鲎试剂盒检测各组大鼠内毒素含量。结果:急性前脑缺血后大鼠MODS发病率为53.1%;大鼠急性前脑缺血后存在明显的内毒素血症,血清内毒素在缺血后12h升高,24h达高峰,72h基本恢复正常。结论:以急性前脑缺血为致伤因素可成功建立急性前脑缺血致MODS的大鼠实验动物模型,急性前脑缺血后出现明显的内毒素血症,提示内毒素致炎性细胞因子过度表达,可能是急性前脑缺血致MODS的机制之一。

Objective： To establish a rat model of acute forebrain ischemia complicated with multiple organ dysfunction syndrome （MODS）, determine the serum endotoxin level and discuss the pathogenesis of acute forebrain ischemia complicated with MODS. Methods： Rat acute forebrain ischemia models were established by blocking bilateral common carotid artery occlusion followed by reperfusion, the incidence of MODS was calculated according to relevant indexes, the content of serum endotoxin was evaluated by trace endotoxin limulus kit. Results： The incidence of MODS was 53.1% after acute forebrain ischemia. There was an obvious endotoxemia after acute forebrain ischemia, serum endotoxin level was markedly increased 12 hours after ischemia, then reached its peak after 24 hours, and returned to normal level after 72 hours. Conclusion： The experimental animal models of MODS can be successfully established by acute forebrain ischemia, the endotoxemia occurred after acute forebrain ischemia suggests that the excessive expression of inflammatory cytokines caused by endotoxemia may be one of the pathophysiological mechanisms of MODS caused by acute forebrain ischemia.