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- W2056711683 abstract "In patients with advanced cirrhosis and portal hypertension, the regulation of extracellular fluid volume is often abnormal and results in the accumulation of fluid as ascites, pleural effusion, or edema. The mechanisms responsible for ascites formation include alterations in the splanchnic circulation and functional renal abnormalities that favor sodium and water retention.7, 33, 49 Renal abnormalities occur in the setting of marked changes of the systemic circulation characterized by increased cardiac output, reduced total vascular resistance, and activation of neurohormonal vasoactive systems. This circulatory dysfunction, which is caused by an intense arterial vasodilation in the splanchnic circulation, is currently considered a primary factor in the pathogenesis of ascites and is the basis for the forward theory of ascites formation. During the past decade, significant progress has been made in identifying factors involved in the pathogenesis of arterial vasodilation in patients with cirrhosis. In particular, a convincing body of evidence indicates that nitric oxide (NO) is a major factor responsible for these abnormalities." @default.
- W2056711683 created "2016-06-24" @default.
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- W2056711683 date "2000-05-01" @default.
- W2056711683 modified "2023-10-01" @default.
- W2056711683 title "MECHANISMS OF ASCITES FORMATION" @default.
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- W2056711683 doi "https://doi.org/10.1016/s1089-3261(05)70118-5" @default.
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