梗阻性黄疸肝脏超微结构改变及其损伤机制

目的:通过观察梗阻性黄疸肝脏超微结构改变进一步探讨其损伤机制。方法:Wistar大鼠72只随机分为胆总管结扎组、假手术组和正常对照组，每组24只，胆总 管结扎组大鼠制成梗阻性黄疸动物模型,利用透射电子显微镜和7150型全自动生化分析仪观察各组大鼠肝组织超微结构及其功能改变。结果:实验组肝细胞核形态异常、固缩,线粒体脊断裂，内质网减少且肿胀,毛细胆管扩张,内有胆泥淤积。生化检测肝功能胆红素、血胆汁酸、丙氨酸转氨酶和天冬氨酸转氨酶与假手术组和对照组比较差异有显著性（P<0.01）。结论:梗阻性黄疸肝脏损伤可能与内毒素、胆汁酸血症、肝细胞缺血和Kupffer细胞功能受损有关。

Study on changes of ultrastructure and injury mechanisms in liver with obstructive jaundice

Objective Through observation of liver ultrastrutures in obstructive jaundice to study its injury mechanisms. Methods Seventy-two Wistar rats were randomly divided into 3 groups: experiment, sham and normal groups (n = 24). Wistar rat models with obstructive jaundice were made in experiment group. The liver ultrastructure in three groups were observed by the transmission electron microscope. The changes of the liver function were analyzed with 7150 autobiochemistry analytic instrument. Results The nucleus morphology of the hepatocytes was abnormal, the nucleus was pyknotic> the mitochondria crista was broken. The endoplasmic reticulum was reduced and swelled. Bile stasis was present within dilatation canaliculi. The results of biochemistry measurement of liver function indicated that the differenes of TBIL, TRA, ALT, and AST were statistically significant between experiment and sham, normal groups (P<0. 01). Conclusion Endotoxemia, bile acidemia, hepoemdia of the liver and Kupffer cells function injury may relate with the liver injury of obstructive jaundice.