脓毒症小鼠肝肺损伤机制的研究

Mechanism of liver and lung injury in septic mice

目的:利用盲肠结扎穿孔伴严重腹腔感染造成的脓毒症模型,探讨脓毒症肝、肺损伤的机制。方法:24只雄性昆明小鼠随机分为2组,盲肠结扎穿孔(cecal ligation and puncture,CLP)组和假手术对照组。于术后3 h和12 h检测肝、肺微血管通透性改变、组织含水量以及髓过氧化物酶(myeloperoxidase,MPO)活性的改变,并检测肝窦内皮细胞和肺微血管内皮细胞的凋亡情况。结果:肝、肺微血管的通透性在CLP后12 h明显高于对照组(P<0.01)。CLP同时造成肝、肺组织的含水量和MPO活性明显高于对照组。另外,在CLP组12 h肺微血管内皮细胞的凋亡率为(5.03±0.92)%,对照组为(3.48±1.21)%。两者比较差异有显著性意义(P<0.01)。结论:脓毒症可引起严重的肝、肺组织损伤,肺微血管内皮细胞凋亡可能是导致脓毒症肺微血管通透性增高并引起肺损伤的重要原因。

Objective：To investigate the mechanism of liver and lung injury in mouse septic models. Methods： Twenty-four male Kunming mice were subjected to cecal ligation and puncture （CLP） or sham operation. The permeability of microvasculature, water contents, activities of myeloperoxidase （MPO） and the apoptosis of microvascular endothelial cells in lung microvasculature and liver sinus were examined 3 h and 12 h after operation. Results： Both the liver and lung showed a significant increase in microvessel permeability at 12 h in CLP group compared with sham operation group. MPO activity and water content in CLP group were obviously higher than those in the sham operation group. The apoptosis of lung microvascular endothelial cells at 12 h in CLP group （5.03±0.92）% was significantly higher than that of control group （3.48±1.21）% （P〈0.01）. Conclusion： Sepsis can lead to severe injury to the liver and lung. Apoptosis in lung microvascular endothelial cells might cause alteration of microvascular permeability, finally resulting in the injury of lung.