一氧化氮合酶抑制剂对肝硬变鼠肝内阻力的影响

目的:探讨一氧化氮合酶(NOS)抑制剂对肝硬变大鼠肝内阻力的影响。方法:采用肝硬变大鼠原位肝脏灌注模型,观察NOS抑制剂硝基精氨酸(L-NNA)及一氧化氮(NO)合成底物L-精氨酸(L-arg)对大鼠门静脉去甲肾上腺素(NE)反应的影响。结果:应用L-NNA后,正常及肝硬变动物门静脉压力均较单用NE时显著升高,肝硬变动物门静脉压力的升高程度明显小于正常动物。L-arg可以消除L-NNA的作用。结论:NO参与正常及肝硬变动物门静脉压力的调节。肝硬变时,肝内NO合成减少,使肝内阻力进一步升高。

Effects of Nitric Oxide Synthase Inhibitor on Intrahepatic Resistance in Cirrhotic Rats

Objective: To evaluate the effects of nitric oxide synthase(NOS) inhibitor Nw-nitro-L-arginine(L-NNA) and nitric oxide(NO) substrate L-arginine(L-arg) on portal resistance in cirrhotic rats. Methods: The effects of L-NNA(10-4M) and L-arg(10-3M) on portal venous pressure(PVP) to increasing doses of norepinephrine(NE,10-8M~10-4M) were observed in an in situ liver perfusion model in cirrhotic rats. Results: L-NNA significantly enhanced the PVP responsiveness to NE in both cirrhotic and normal rats. However, the magnitude of PVP increase was more marked in normal rats than in cirrhotic ones. The increased PVP responsiveness to NE by L-NNA in both cirrhotic and normal rats was abolished by L-arg. Conclusions: NO plays a role in the regulation of intrahepatic portal circulation in both normal and cirrhotic rats. Diminished NO release in the liver results in a further increase of intrahepatic re-sistance in cirrhotic rats.