肝硬化门脉高压的病理生理机制

Pathophysiological Mechanism of Portal Hypertension in Cirrhosis

门脉高压是肝硬化的重要并发症之一,也是引起许多临床并发症的病理因素,目前没有理想的药物可以控制门脉高压的进展,所以逆转和控制肝硬化进展变得尤为困难,特别是肝内与肝外的两者截然不同的表现,肝内表现为血流阻力增加,血管收缩加剧,舒张减弱,而肝外体循环阻力下降,血管舒张,引起一系列的严重并发症,如难治性腹水,肝性脑病等,肝内外的动态因子亦存在很大的差异,如一氧化氮(NO)和内皮素受体(ETR)等,因此控制门脉高压而不引起体循环改变存在一定的难度。在此,对肝硬化门脉高压的肝内、外病理机制做一综述,研究其病理机制有助于找到新的治疗靶点,具有深刻的临床意义。

Portal hypertension(PHT) is one of the important complications of liver cirrhosis,and it is also a pathological factor causing many clinical complications.At present,there is no ideal drug to control the progress of portal hypertension,and so it is particularly difficult to reverse and control the progress of liver cirrhosis.In particular,theintrahepatic and extrahepaticmanifestationsare very different.In intrahepatic tissue,the blood flow resistance is increased and vasodilation is decreased.In extrahepatic tissue,systemic resistance decreased and vasodilationaggravated,causing a series of serious complications.For example,refractory ascites,hepatic encephalopathy and the dynamic factors such as NO and endothelin receptor(ETR) inside and outside the liver are also very different and so it is difficult to control portal hypertension without causing systemic circulation changes.In this paper,thepathological mechanisms of intrahepatic and extrahepatic PHT(in cirrhosis) were reviewed.Studying its pathological mechanism is helpful to find out a new therapeutic target,and has profound clinical significance.