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代偿良好的肝硬化患者对下体负压的肾交感神经及肾素-血管紧张素反应

The renal sympathetic and renin-angiotensin response to lower body negative pressure in well-compensated cirrhosis.

作者信息

Wong F, Sniderman K, Blendis L

机构信息

Department of Medicine, Toronto Hospital, University of Toronto, Ontario, Canada.

出版信息

Gastroenterology. 1998 Aug;115(2):397-405. doi: 10.1016/s0016-5085(98)70206-9.

DOI:10.1016/s0016-5085(98)70206-9
PMID:9679045
Abstract

BACKGROUND & AIMS: Certain antinatriuretic hormonal systems may be involved in the subclinical sodium handling abnormality in preascitic cirrhosis. The aims of this study were to determine the following in preascitic cirrhosis: (1) basal activity of the renal sympathetic and renin-angiotensin systems and (2) the relationship between the response of these systems to lower body negative pressure and sodium excretion.

METHODS

Seven preascitic cirrhotic patients and 9 age- and sex-matched controls were studied on a 150 mmol sodium per day diet. Systemic and renal hemodynamics, renal neurohormonal secretion rates, and sodium excretion were assessed before, during increasing levels of, and after lower body negative pressure, each for 30 minutes.

RESULTS

Both groups responded with a significant decrease in central venous pressure (P < 0.01) that remained higher in the cirrhotics than in the controls throughout the study. Cirrhotics showed significant increases compared with controls in renal renin and angiotensin II secretion rates at -20 mm Hg of lower body negative pressure, which was associated with significant renal sodium retention (96 +/- 17 micromol/min vs. 218 +/- 21 micromol/min at baseline, P < 0.05), but there was no change in renal sympathetic activity.

CONCLUSIONS

In preascitic cirrhosis, sodium retention occurs in response to lower body negative pressure, which was associated with increased renal renin-angiotensin activity. Stimulation of the intrarenal renin-angiotensin system may be the initial renal pathophysiological change causing sodium retention in cirrhosis.

摘要

背景与目的

某些利钠激素系统可能参与了腹水前期肝硬化患者亚临床期钠代谢异常。本研究的目的是确定腹水前期肝硬化患者的以下情况:(1)肾交感神经和肾素 - 血管紧张素系统的基础活性;(2)这些系统对下体负压的反应与钠排泄之间的关系。

方法

7例腹水前期肝硬化患者和9例年龄及性别匹配的对照者采用每日150 mmol钠的饮食进行研究。在下体负压增加前、增加过程中及增加后各30分钟,评估全身和肾脏血流动力学、肾脏神经激素分泌率及钠排泄情况。

结果

两组患者的中心静脉压均显著降低(P < 0.01),且在整个研究过程中,肝硬化患者的中心静脉压始终高于对照组。在 -20 mmHg下体负压时,肝硬化患者的肾脏肾素和血管紧张素II分泌率与对照组相比显著增加,这与显著的肾脏钠潴留相关(基线时为96 ± 17 μmol/min,而对照组为218 ± 21 μmol/min,P < 0.05),但肾脏交感神经活性无变化。

结论

在腹水前期肝硬化患者中,下体负压会引起钠潴留,这与肾脏肾素 - 血管紧张素活性增加有关。肾内肾素 - 血管紧张素系统的激活可能是肝硬化患者钠潴留的初始肾脏病理生理变化。

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