| Background & Objective:Portal hypertension (PHT) is a common clinical syndrome characterized by a pathological increase in portal pressure. It is often present in patients with chronic liver diseases. The studies on pathogenesis of PHT demonstrate both "backward" and "forward" mechanisms play a role in it. According to "backward" mechanism, PHT is the result of an increase in vascular resistance due to extra-hepatic or intra-hepatic portal occlusion. On the basis of "forward" mechanism, PHT patients manifest hyperdynamic circulation. The increased splanchnic blood flow raises portal flow, which contributes to the maintenance of elevated portal pressure. So in PHT, high blood pressure and high blood flow constitute a special hemodynamic state in the portal venous system, which is different from that in hypertension disease. Stress, the force of unit area, can be induced by pressure and flow. The portal veins with thickened walls and enlarged lumens in patients with PHT show some arterial characters. The phenomena may be caused by stress in this special hemodynamic state. The increase of the portal vein contractility elevates portal resistance to flow, thus portal pressure becomes higher. The higher portal pressure is, the more arterial characters the vein has, and vice versa. Accordingly, the extent of severity and fatalness in complications of PHT is increased.Vascular remodeling, or vascular changes in function as well as in structure, can be caused either by high blood pressure such as hypertension disease or by high blood flow such as arteriovenous fistula. But their processes and mechanisms are different. The first is a positive feedback process: the thickener the vessel wall is, the higher theblood pressure is. Whereas high blood flow increases inner diameter and outer diameter of the vessel, then the flow decreases untile to a stable level. At present, the research on vascular remodeling of hypertension disease is a hot point all over the world, but little attention has been paid to vascular remodeling of PHT. In PHT, vascular remodeling must have its special properties in view of the special hemodynamic state in portal venous system. Furthermore, the increase in stress induced by blood pressure and flow results in changes of several vasoactive factors such as nitric oxide (NO) and endothlin-1 (ET-1). It is recognized by more and more scholars that some vasoactive factors may play a role in the pathogenesis of PHT. But it remains unclear which roles the vasoactive factors correlated with stress play in it.In this study, biomechanical properties of portal venous system in rats such as hemodynamics, structure and mechanical characteristics of the portal vein, dynamic changes of NO and ET-1 were observed both in the pathogenesis of portal hypertension and in the situation that portal resistance or flow inhibited by some drugs. The aim of the study is to investigate the effects of the special hemodynamic state characterized by high blood pressure and high blood flow in the portal venous system on vascular remodeling of the portal vein and NO and ET-1; to explore the pathogenesis of PHT through the changes of biomechanical properties in PHT; and to try to offer a new thought in selecting pharmacotherapy and evaluating its curative effect, for finding out a new pathway in the drug treatment for PHT.Methods:}. The models of prehepatic and intrahepatic PHT were established in SD rats by means of partial portal vein ligation (PVL) and 60% carbon tetrachloride (CCU) injection, respectively. PVL rats (n=120) were compared with sham operation (SO) rats (n=120) while CCLj injected rats (n=87) were compared with Olive-oil injected rats (n=75), normal rats (n=15, respectively) were also studied. Changes of several hemodynamic indexes such as portal venous pressure (PVP), portal venoxis flow (PVF), mean arterial pressure (MAP), portal vascular resistance (PVR) and splanchnicvasculai- resistance (SVR) were detected in 1,2, 4, 8, 12, 16, 20, 26 days after the operation and in 2, 4, 6, 8, 10 wee...
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