摘要
目的和方法:应用肝脏原位灌注模型,观察内皮素-1(endothelin-1,ET-1)对肝脏的损伤作用,以及一氧化氮(nitricoxide,NO)和前列环素(prostacyclin,PGI2)对ET-1生物学效应的调节作用。结果:ET-1能使肝细胞浊肿变性,增加脂质过氧化物生成和酶的漏出。NO合成抑制剂能使ET-1的肝损伤作用加重,PGI2和消炎痛能部分减轻ET-1的肝损伤作用。结论:NO。
AIM and METHOD:On the perfusion model of rat liver in situ, the effects of endothelin-1(ET-1) on hepatic damage was studied, the effect of nitric oxide and prostacyclin on regulation ET-1 biological function was observed. RESULTS:ET-1 significantly induced hepatic edema and increased production of lipid peroxidation and leakage of enzyme. An administration of LNNA, an inhibitor of NO(nitric oxide), augmented the hepatic damage induced by ET-1, prostacyclin and indomethacin partially decreased the hepatic damage induced by ET-1. CONCLUSION:NO and PGI2 may regulate ET-1 biological function.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1998年第4期419-423,共5页
Chinese Journal of Pathophysiology