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门脉高压时腹水,主要因钠、水潴留所致。门脉高压患者由于肝脏的灭能作用削弱,伴有肾功障碍,肾小管对钠的重吸收增加,血浆容量扩充,加上肝窦压力增高和血浆胶体渗透压降低,就可引起腹腔容量扩大而导致腹水。另外,有效循环血量减少可促进醛固酮分泌,也使肾小管重吸收钠增加,加之利钠因子减少,致使钠的排出减少,当有效循环血量显著减少时,与钠、水潴留有关的抗利尿激素和肾素-血管紧张素-醛固酮系统释放,交感神经兴奋性增高,前列腺素及激肽系统形成减少,也可促使腹水形成。这种腹水的形成,与抗利尿激素分泌增加和肾小管回收滤液增多而引起肾排水障碍也有一
Portal hypertension when ascites, mainly due to sodium, water retention caused. Portal hypertension in patients with impaired liver function, with renal dysfunction, renal tubular reabsorption of sodium increased plasma volume expansion, coupled with increased sinusoidal pressure and decreased plasma colloid osmotic pressure, can cause increased abdominal capacity And cause ascites. In addition, the effective reduction of circulating blood volume can promote aldosterone secretion, but also to renal tubular reabsorption of sodium increased, coupled with reduced natriuretic factor, resulting in decreased sodium output, when the effective circulating blood volume decreased significantly, and sodium, water retention-related anti Release of the diuretic hormone and renin-angiotensin-aldosterone system, increased sympathetic excitability, decreased formation of prostaglandins and kinin systems, and promotion of ascites formation. This formation of ascites, with increased secretion of antidiuretic hormone and tubular reabsorption of filtrate increased renal drainage disorder also has a