Toledo C, Ginés P, Arroyo V
Unidad de Hepatología, Hospital Clínic i Provincial, Barcelona, España.
Rev Med Chil. 1992 Feb;120(2):180-7.
The accumulation of ascites in cirrhosis has been classically attributed to the transudation of fluid from the splanchnic vascular bed to the peritoneal cavity due to the presence of portal hypertension. This transudation of fluid would induce hypovolemia responsible for the renal abnormalities frequently observed in these patients. Recent studies, however, indicate that the pathophysiology of ascites in cirrhosis is far more complex. Cirrhotic patients with ascites usually have profound disturbances in systemic hemodynamics and renal function and an activation of the endogenous vasoactive systems that contribute to the formation of ascites. In the present article the pathogenesis of these disturbances and their possible contribution to the formation of ascites are discussed.
在肝硬化中,腹水的积聚传统上被归因于由于门静脉高压的存在,液体从内脏血管床漏入腹腔。这种液体渗漏会导致血容量减少,进而引发这些患者中常见的肾脏异常。然而,最近的研究表明,肝硬化腹水的病理生理学要复杂得多。有腹水的肝硬化患者通常存在全身血流动力学和肾功能的严重紊乱,以及内源性血管活性系统的激活,这些都促使腹水的形成。在本文中,将讨论这些紊乱的发病机制及其对腹水形成的可能作用。