肝动脉血流及一氧化氮、内皮素浓度与肝硬化门脉高压症发病机制的实验研究

目的:探讨肝动脉血流动力学指标和肝脏中一氧化氮(NO)、内皮素(ET-1)浓度的变化在肝硬化门脉高压症发生机制中的作用。方法:建立四氯化碳(CCl4)诱导的大鼠肝硬化门脉高压症模型,应用微电磁流量计测定肝硬化时肝动脉血流量(HABV)、肝动脉脉搏(PI)、肝动脉平均峰值(HAI)。应用RT-PCR技术检测肝组织中iNOSmRNA和ET-1mRNA的表达水平。硝酸还原酶法检测肝组织和门静脉血液中NO含量。放免法测定门静脉血中ET-1浓度。结果:肝硬化组肝组织中iNOSmRNA和ET-1mRNA的表达水平较正常组显著升高(P<0.05)。正常组大鼠肝组织NO、门静脉血中NO和ET-1浓度都很低,在肝硬化门脉高压组显著升高(P<0.05)。肝硬化门脉高压组肝动脉HABV、PI、HAI呈显著性升高(P<0.05)。结论:肝脏微循环中扩血管物质NO和缩血管物质ET-1浓度的比值改变是肝硬化门脉高压症形成过程中非常重要的因素,可能与门静脉系统高动力血流状态,血管渗透性增加等发生有密切关系。同时肝动脉血流量增加,一方面促进NO/ET-1比值的失衡,另一方面通过肝动脉缓冲作用,导致肝内门静脉循环受阻。

The study of hepatic arterial hemodynamics and NO, ET-1 in liver cirrhosis with portal hypertension

Objective : To observe the changes of hemodynamics of hepatic artery and NO, ET-1 in liver tissue in the process of portal hypertension, and to, discuss the relative mechanism of liver cirrhosis and portal hypertension. Methods: Using the carbon tetrachloride-induced cirrhosis rats, HABV, PI and HAI were detected by micro- electromagnetic flowmeter during open procedure. Concentration of NO was detected by Nitrate reductase methods and ET-1 was detected by radio-immunity technique. Results: iNOSmRNA and ET-1mRNA were up-regulated in portal hypertension group significantly(P<0. 05). In normal liver, the concentrations of NO and ET-1 were minimal, in contrast to portal hypertension, these indexes were markedly higher than normal (P<0. 05). In the same time, HABV, PI and HAI of hepatic artery were significantly higher than normal group(P<0. 05). Conclusion: The odds of NO and ET-1 may be the important index in the procession of portal hypertension, resulting in hyperkinesis of portal vein and increased blood vessel permeability. Furthermore, enlarged hepatic artery blood flow might promote this effect and cause the obstruction of in-hepatic microcirculation through hepatic artery buffer effect.