Pathogenesis of ascites in cirrhosis and portal hypertension.
Disturbance of the circulatory system frequently occurs in patients with cirrhosis. Cardiac index and plasma volume increase whereas mean arterial blood pressure and systemic vascular resistance decrease. Marked disturbance in vasoconstrictor and natriuretic systems also exist with activation mediators such as plasma renin, plasma noradrenaline, antidiuretic hormone and endothelin. Renal factors contribute to the pathogenesis of ascites formation although the exact mechanisms are yet to be elucidated. Several theories exist in relation to pathogenesis although none to date fully explain all of the findings observed in clinical practice. In this review, we examine the mechanisms that contribute to the development of ascites in patients with cirrhosis and portal hypertension.
Heneghan
M A
MA
Academic Department of Hepatology, Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE5 9PJ, England.
Harrison
P M
PM
D001158:Arteries / Q000503:physiopathology; D001201:Ascites / Q000209:etiology* / Q000503:physiopathology; D001810:Blood Volume / Q000502:physiology; D004231:Diuresis; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006530:Hepatorenal Syndrome / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006975:Hypertension, Portal / Q000150:complications* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000150:complications* / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology; D008954:Models, Biological; D009318:Natriuresis; D012079:Renal Circulation; D014661:Vasoconstriction