Physiopathology of ascites in portal hypertension.
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.
Michielsen
P P
PP
Division of Gastroenterology, Faculty of Medicine, University of Antwerp (U.I.A), Antwerpen-Wilrijk, Belgium.
D001201:Ascites / Q000503:physiopathology*; D004487:Edema / Q000503:physiopathology; D006801:Humans; D006975:Hypertension, Portal / Q000503:physiopathology*; D007668:Kidney / Q000378:metabolism; D008103:Liver Cirrhosis / Q000503:physiopathology; D010529:Peritoneal Cavity; D012084:Renin-Angiotensin System / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D013152:Splanchnic Circulation / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014664:Vasodilation
D012964:Sodium