Jalan R, Hayes P C
Department of Medicine, Royal Infirmary of Edinburgh, UK.
Lancet. 1997 Nov 1;350(9087):1309-15. doi: 10.1016/S0140-6736(97)07503-X.
The first abnormality leading to sodium and water retention in cirrhosis is the renal tubular defect that is related to deteriorating liver function and hyperaldosteronism. With progression of liver disease and portal hypertension, renal blood flow declines because of the hepatorenal reflex, and is then maintained by the vasoactive hormonal systems. With increasing peripheral vasodilatation, intrarenal factors for maintenance of renal perfusion cause intense cortical vasoconstriction. The systemic vasoactive factors are predominantly compensatory; any attempts to counteract their action risk circulatory collapse. Future studies should be directed at intrarenal factors. The ideal drug for the treatment of portal hypertension would reduce portal pressure, increase renal blood flow, and produce insignificant changes in arterial pressure.
肝硬化导致钠水潴留的首要异常是与肝功能恶化及醛固酮增多症相关的肾小管缺陷。随着肝脏疾病和门静脉高压的进展，由于肝肾反射，肾血流量下降，随后由血管活性激素系统维持。随着外周血管扩张加剧，维持肾灌注的肾内因素导致强烈的皮质血管收缩。全身血管活性因子主要起代偿作用；任何对抗其作用的尝试都有循环衰竭的风险。未来的研究应针对肾内因素。治疗门静脉高压的理想药物应能降低门静脉压力、增加肾血流量，并使动脉压产生微小变化。
