鼠肝硬化门脉高压形成中和门奇静脉断流术后血胰岛素变化的研究

Insulin Change in Portal and Peripheral Venous Blood of Rats with Experimental Cirrhotic Portal Hypertension and after Porta-azygous Devascularization

本实验用四氯化碳(简称 CCl_4)诱发大鼠肝硬化,观察硬化形成过程中门脉和外周血胰岛素的变化,以及门奇静脉断流术后门脉和外周血中胰岛素变化情况。结果发现,随肝硬化程度加重,门静脉压力逐渐增高,门脉血中胰岛素和 C 肽浓度逐渐降低,外周血胰岛素浓度增高、C 肽浓度减低。断流术前后,门脉和外周血胰岛素和 C 肽浓度、门静脉压力均无明显改变。提示肝硬化时出现的高胰岛素血症主要原因是肝细胞受损,胰岛素降解减少。但断流术能维持门脉血胰岛素的含量,有利于受损肝细胞的恢复和正常肝细胞的再生。

To investigate the change of insulin concentration in rats' peripheral and portal venous blood in the course of experimental by carbon tetrachloride and after porta-azygous devascularization.Liver cir- rhosis was verified by histologic fintings.It was found that the portal venous pressure increaded and the concentration of insulin and C-peptide in portal venous blood decreased gradually,the insulin concen- trations in peripheral blood increased but that of C-peptide decreased with the extent of liver cirrhosis. Before and after porta-azygous devascularization,insulin and C-peptide concentrations in portal and peripheral venous blood in cirrhotic rats did not vary obviously.The results surgesf that the main cause of hyperinsulinemia in rats with liver cirrhosis is that liver cells are damaged and the degradation of in- sulin is decreased.Porta-azygous devascularization can maintain insulin contents in portal venous blood and promote recovery of damaged liver cells and regeneration of normal liver cells.