Cody R J, Covit A B, Schaer G L, Laragh J H, Sealey J E, Feldschuh J
J Clin Invest. 1986 May;77(5):1441-52. doi: 10.1172/JCI112456.
As the characteristics of sodium and water balance in heart failure remain undefined, we evaluated the hemodynamic, metabolic, and hormonal effects of balanced sodium intake in 10 patients with chronic congestive heart failure. We discontinued diuretics to avoid their confounding influence, and all patients received 1 wk of 10 meq and 100 meq balanced sodium intake and controlled free water. Comparing sodium intake of 10 with 100 meq, the following observations were made. There was weight gain (2.0 kg) and increased sodium excretion (11 +/- 3 to 63 +/- 15 meq/24 h), unaccompanied by increase of blood volume. Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. For both diets, plasma renin and urinary aldosterone excretion were correlated with urinary sodium excretion (r = -0.768, r = -0.726, respectively; P less than 0.005). Systemic hemodynamics were minimally changed with increased sodium intake. However, reversal of vasoconstriction by captopril during the 10 meq diet, and its ineffectiveness during the 100 meq diet, indicated a renin-dependent mechanism in the former, and a renin-independent mechanism in the latter diet. There were two subgroups of response to the 100 meq diet: one group (n = 5) achieved neutral balance, while the second (n = 5) avidly retained sodium and water. Renin-angiotensin system activity was significantly higher in the latter group, and the mechanism for differences in sodium excretion for the subgroups could not be identified by blood volume or hemodynamic parameters. Orthostatic hypotension during tilt was greater during the 10 meq sodium diet, and in all cases, related to ineffective hemodynamic and hormonal compensatory responses.
由于心力衰竭中钠和水平衡的特征尚未明确，我们评估了10例慢性充血性心力衰竭患者摄入平衡钠后的血流动力学、代谢及激素效应。我们停用了利尿剂以避免其混杂影响，所有患者均接受了为期1周的10毫当量和100毫当量平衡钠摄入并控制自由水。比较10毫当量与100毫当量的钠摄入量，得出以下观察结果。体重增加（2.0千克）且钠排泄增加（从11±3增至63±15毫当量/24小时），但血容量未增加。在10毫当量饮食期间，肾素-血管紧张素系统和交感神经系统活性均较高，而在100毫当量钠饮食时受到抑制。对于两种饮食，血浆肾素和尿醛固酮排泄均与尿钠排泄相关（分别为r = -0.768，r = -0.726；P < 0.005）。随着钠摄入量增加，全身血流动力学变化极小。然而，在10毫当量饮食期间卡托普利可使血管收缩逆转，而在100毫当量饮食期间则无效，这表明前者存在肾素依赖性机制，后者存在肾素非依赖性机制。对100毫当量饮食有两个反应亚组：一组（n = 5）达到中性平衡，而另一组（n = 5）则大量潴留钠和水。后一组的肾素-血管紧张素系统活性显著更高，且通过血容量或血流动力学参数无法确定亚组间钠排泄差异的机制。在10毫当量钠饮食期间，倾斜试验时的直立性低血压更明显，且在所有病例中均与无效的血流动力学和激素代偿反应有关。
