硫代乙酰胺诱导的门静脉高压大鼠肝脏超微结构观察

目的 该研究以硫代乙酰胺复制门脉高压大鼠模型,对成模后的大鼠肝脏超微结构进行观察,探讨门脉高压大鼠肝脏超微结构的变化.方法 50只大鼠分为造模组(40只)和正常对照组(10只).造模组采取前5周使用0.03%的硫代乙酰胺,后5周使用0.04%硫代乙酰胺作为其饮用水,共诱导10周成模.对成模大鼠测定肠系膜上静脉压力,取硬化后肝脏标本,对收集后标本行HE染色,同时行电子显微镜观察肝脏超微结构变化.结果 模型组内皮细胞窗孔数量明显少于对照组,同时,门静脉压力明显高于对照组.结论 肝窦毛细血管化在硫代乙酰胺诱导的肝硬化门脉高压发生中起重要作用,肝窦内皮细胞窗孔减少并减小,内皮细胞下基底膜形成使肝细胞与外界物质交换减少,导致细胞缺氧、代谢产物聚集,肝细胞坏死,最终导致门脉高压的发生.

Ultrastructural changes in TAA induced hepatic cirrhosis in rats

Objective To observe the ultrastructural changes in liver after portal hypertension in rats.Methods A total of 50 rats were divided into the model groups(40)and control groups(10).The rats in the model group accepted 0.03% TAA administration.Five weeks later,the concentration of TAA was changed to 0.04% for induction for 10 weeks to establish the model of portal hypertension.The pressure of superior mesenteric vein was determined and cirrhotic liver samples obtained.The ultrastructuraI changes of were observed under electron microscope.Results The fenestra quantity of endothelial cells was significantly lower in the model group(P＜0.01).The portal vein pressure was markedly higher in the control group(P＜0.01).Conclusion Hepatic sinusoid capillarization plays an important role in occurrence of portal hypertension.The fenestra of endothelial cells in hepatic sinusoid reduces and the diameter of fenestra decreases.The formation of basement membrane impaires the substance exchange between blood and hepatic cells,which results in oxygen deficiency,metabolic product accumulation and cell necrosis.