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目的 探讨肝缺血再灌注损伤的作用机制。方法 采用大鼠部分肝缺血再灌注模型 ,将健康雄性SD大鼠 2 4只随机分为三组 :A组 (手术对照 ) ,B组 (肝缺血 90min) ,C组 (肝缺血 90min再灌注 1 2 0min)。观察每一动物肝组织病理切片 ;分别检测血浆谷草转氨酶 (AST)、谷丙转氨酶(ALT)、乳酸脱氢酶 (LDH)、肿瘤坏死因子 (TNF α)、白介素 1 β(IL 1 β)浓度 ;测定肝组织中髓过氧化物酶 (MPO)含量。结果 肝缺血再灌注后 ,光镜下大鼠肝组织有明显的肝血窦和中央静脉瘀血 ,内皮细胞及肝细胞普遍水肿变性 ;C组肝细胞坏死较B组明显 ;血浆中肝功能酶学指标显著升高 ,(B、C组与A组比及C组比B组P均 <0 0 1 ) ;肝组织中MPO活性升高 ,以再灌注 1 2 0min组为著 (C组比A组P <0 0 1 ) ;与血浆中TNF α、IL 1 β的变化趋势相同 (TNF α :C组比A组P <0 0 5 ,IL 1 β:B、C组比A组P均 <0 0 1 )。结论 肝脏微循环障碍是肝缺血再灌注损伤的病理基础 ;TNF α、IL 1 β介导中性粒细胞参与的肝缺血再灌注损伤过程
Objective To investigate the mechanism of hepatic ischemia-reperfusion injury. Methods 24 male Sprague-Dawley rats were randomly divided into three groups: group A (operation control), group B (liver ischemia 90 min), group C (liver ischemia 90 min Reperfusion 120min). The pathological sections of liver of each animal were observed. The concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), tumor necrosis factor (TNF), interleukin 1β ; Determination of liver tissue myeloperoxidase (MPO) content. Results After hepatic ischemia and reperfusion, hepatic sinusoid and central venous blood stained obviously, and the edema and denudation of endothelial cell and hepatocyte became obvious. The necrosis of hepatocyte in group C was more obvious than that in group B, (P <0.01). The activity of MPO in liver tissue was increased in group B and group C, and the level of MPO in group C was (P0.01) than in group B (P <0.01) in group A, P <0.01 compared with group A), but similar to that of plasma TNFα and IL 1 β All <0 0 1). Conclusions Liver microcirculation disturbance is the pathological basis of hepatic ischemia-reperfusion injury. TNF α and IL 1 β mediate the process of hepatic ischemia-reperfusion injury mediated by neutrophils