Atucha N M, Cegarra M, Ramirez A, Quesada T, Garcia-Estañ J
Departamento de Fisiología, Facultad de Medicina, Murcia, Spain.
Am J Physiol. 1993 Dec;265(6 Pt 1):G1045-9. doi: 10.1152/ajpgi.1993.265.6.G1045.
Arterial hypotension in liver cirrhosis has been proposed as a major mechanism contributing to renal sodium and water retention. To evaluate kidney excretory responses at different levels of arterial pressure (AP), we have characterized the relationships between renal perfusion pressure (RPP) and sodium and water excretion in carbon tetrachloride cirrhotic rats. Experiments were performed in anesthetized control (n = 9) and cirrhotic rats with (Asc, n = 6) and without ascites (Cir, n = 6) by mechanically adjusting vascular resistance in animals with renal denervation and infused with main systemic hormones. Control and Cir animals showed similar glomerular filtration rates (GFR), renal blood flows, hematocrits (Hct), and plasma proteins (PP). However, Hct, PP, and GFR were significantly lower in the Asc rats. For the same level of RPP, both cirrhotic groups excreted significantly less water and sodium than controls. Then, the pressure diuresis and natriuresis relationships of the Cir animals were significantly depressed, but those of the Asc animals were more reduced than those of the Cir rats. These results indicate that the cirrhotic kidney is not able to normally increase the sodium and water excretion in response to changes in AP. Intrarenal mechanisms, and not mainly RPP, are likely mediators of the renal alterations of liver cirrhosis.
肝硬化患者的动脉低血压被认为是导致肾钠和水潴留的主要机制。为了评估在不同动脉压（AP）水平下肾脏的排泄反应，我们研究了四氯化碳诱导的肝硬化大鼠肾灌注压（RPP）与钠和水排泄之间的关系。实验在麻醉的对照大鼠（n = 9）以及有腹水（Asc，n = 6）和无腹水（Cir，n = 6）的肝硬化大鼠中进行，通过机械调节去肾神经大鼠的血管阻力并输注主要的全身激素。对照大鼠和Cir组大鼠的肾小球滤过率（GFR）、肾血流量、血细胞比容（Hct）和血浆蛋白（PP）相似。然而，Asc组大鼠的Hct、PP和GFR显著更低。对于相同水平的RPP，两个肝硬化组排泄的水和钠均明显少于对照组。然后，Cir组大鼠的压力利尿和利钠关系明显降低，但Asc组大鼠的这种关系比Cir组大鼠降低得更多。这些结果表明，肝硬化肾脏不能正常地响应AP变化而增加钠和水的排泄。肾内机制而非主要是RPP，可能是肝硬化肾脏改变的介导因素。
