Michielsen P P
Division of Gastroenterology, Faculty of Medicine, University of Antwerp (U.I.A), Antwerpen-Wilrijk, Belgium.
Acta Gastroenterol Belg. 1996 Jul-Sep;59(3):191-7.
Ascites is a frequent complication of sinusoidal and postsinusoidal or posthepatic forms of portal hypertension. Its pathogenesis can be divided into factors favouring the efflux of fluid from the vascular to the peritoneal space, factors favouring the accumulation of fluid in the peritoneal compartment and factors responsible for the repletion of the intravascular volume and hence the continuous formation of ascites. In decompensated cirrhosis, this repletion is realized by renal retention of sodium and water due to activated neurohumoral systems. The peripheral vasodilation theory can explain most of the physiopathological events in cirrhosis with ascites. Some observations, however, oppose this theory. Hence, recently a modification of the theory was proposed in order to reconcile some apparently conflicting studies. The origin of the vasodilatory state in portal hypertension appears to be multifactorial. Most reports indicate that an increased vascular production of nitric oxide, a potent, locally acting vasodilator, plays an important role in the pathogenesis of the peripheral vasodilation in portal hypertension.
腹水是窦性和窦后性或肝后性门静脉高压症的常见并发症。其发病机制可分为有利于液体从血管内流向腹腔的因素、有利于液体在腹腔内积聚的因素以及负责补充血管内容量从而导致腹水持续形成的因素。在失代偿期肝硬化中，这种补充是通过激活的神经体液系统导致肾脏对钠和水的潴留来实现的。外周血管扩张理论可以解释肝硬化腹水的大多数生理病理事件。然而，一些观察结果反对这一理论。因此，最近有人提出对该理论进行修正，以调和一些明显相互矛盾的研究。门静脉高压症中血管扩张状态的起源似乎是多因素的。大多数报告表明，血管中一氧化氮（一种强效的局部血管扩张剂）生成增加在门静脉高压症外周血管扩张的发病机制中起重要作用。
