门静脉高压症血流动力学改变的发病机理

门静脉高压症（PHT）与肝内循环、体循环和门体侧支循环的血流动力学改变有关。肝内阻力增加和高动力循环侧支血管的扩张在门静脉高压的发病机理中起到了重要作用。不同严重程度的肝硬化均存在能广泛影响人体的血流动力学紊乱。门静脉高压和高动力循环是肝硬化患者发病和死亡的主要原因。而血管结构重塑和血管新生是治疗门静脉高压症的重要目标。

Roles of hemodynamic alterations in portal hypertension and cirrhosis

Portal hypertension （PHT） is the most common cause of cirrhosis. Since portal pressure is dependent upon intrahepatic resistance and splanchnic blood flow, hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation can contribute to or be affected by its perturbation. Intrahepatic vascular regulation and development of intrahepatic resistance involve multiple cellular and molecu- lar mechanisms, such as hepatic stellate cells and sinusoidal endothelial cells and nitric oxide （NO） signaling, especially through the endo- thelial nitric oxide synthase （ eNOS）. Studies have implicated increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation as playing central roles in the pathogenesis of PHT. A detailed understanding of these processes in PHT is critical to developing effective treatment options and reducing the currently high rates of morbidities and mortality related to hemodynamic al- terations in patients with cirrhosis. In this review, the roles of PHT - related vascular remodeling on severity and complications （ including cardiac, kidney, and pulmonary） of cirrhosis, and of collateral circulation angiogenesis are discussed, as they represent potential targets for treatment of portal hypertension.