Simón M A, Díez J, Prieto J
Department of Medicine, Hospital Miguel Servet, Zaragoza, Spain.
Gastroenterology. 1991 Nov;101(5):1354-60. doi: 10.1016/0016-5085(91)90088-3.
It has been proposed that in liver cirrhosis portal hypertension causes splanchnic vasodilation and this induces blood volume expansion to maintain blood pressure. The current study was designed to explore the homeostatic response to sodium restriction, a maneuver aiming to contract blood volume, in compensated cirrhosis. Mean blood pressure, sympathetic nervous activity, and proximal sodium reabsorption were evaluated in 16 healthy control and 21 nonazotemic cirrhotic patients (11 without ascites and 10 with ascites) under two experimental conditions: after 4 days on a free sodium diet (basal condition) and after 4 days on a restricted sodium diet (40 mmol/day). No differences were observed in basal conditions in the above parameters between control and cirrhotic patients without ascites. However, cirrhotic patients with ascites showed lower basal values of mean blood pressure and higher basal levels of both plasma norepinephrine and fractional proximal sodium reabsorption than controls. Neither control nor cirrhotic patients with ascites showed significant changes in the measured parameters after sodium restriction. In contrast, in nonascitic patients, this maneuver induced an elevation in plasma norepinephrine concentration (164.4 +/- 24.6 vs. 270.1 +/- 24.9 pg/mL; mean +/- SEM; P less than 0.005) and in fractional proximal sodium reabsorption (86.4 +/- 2.1 vs. 91.8% +/- 0.5%; P less than 0.01). In addition, the nonascitic cirrhotic patients became hypotensive compared with controls (80.9 +/- 1.6 vs. 88.5 +/- 4.8 mm Hg; P less than 0.05) when subjected to the low-sodium diet. In patients without ascites, under conditions of sodium restriction, the decrease in mean arterial pressure correlated inversely with the increase in plasma norepinephrine concentration (r = -0.713; P less than 0.05), whereas the levels of plasma norepinephrine correlated directly with fractional proximal sodium reabsorption (r = 0.893; P less than 0.01). These findings suggest that ineffective circulatory volume is detected in nonascitic cirrhotic patients only under conditions of sodium restriction, but it is always present in cirrhotic patients with ascites, irrespectively of the amount of sodium in the diet. These results are compatible with the existence of fixed arterial vasodilation in cirrhosis.
有人提出，在肝硬化中，门静脉高压会导致内脏血管舒张，进而引起血容量扩张以维持血压。本研究旨在探讨代偿期肝硬化患者对钠限制（一种旨在收缩血容量的措施）的稳态反应。在两种实验条件下，对16名健康对照者和21名非氮质血症肝硬化患者（11名无腹水，10名有腹水）的平均血压、交感神经活动和近端钠重吸收进行了评估：自由钠饮食4天后（基础状态）和限制钠饮食4天（40 mmol/天）后。在基础状态下，对照者和无腹水的肝硬化患者在上述参数上未观察到差异。然而，有腹水的肝硬化患者的平均血压基础值较低，血浆去甲肾上腺素水平和近端钠分数重吸收基础水平均高于对照者。钠限制后，对照者和有腹水的肝硬化患者的测量参数均未出现显著变化。相比之下，在无腹水的患者中，这种措施导致血浆去甲肾上腺素浓度升高（164.4±24.6对270.1±24.9 pg/mL；平均值±标准误；P<0.005）以及近端钠分数重吸收增加（86.4±2.1对91.8%±0.5%；P<0.01）。此外，无腹水的肝硬化患者在接受低钠饮食时与对照者相比出现低血压（80.9±1.6对88.5±4.8 mmHg；P<0.05）。在无腹水的患者中，在钠限制条件下，平均动脉压的降低与血浆去甲肾上腺素浓度的升高呈负相关（r=-0.713；P<0.05），而血浆去甲肾上腺素水平与近端钠分数重吸收呈正相关（r=0.893；P<0.01）。这些发现表明，无效循环血容量仅在钠限制条件下在无腹水的肝硬化患者中被检测到，但在有腹水的肝硬化患者中始终存在，与饮食中的钠含量无关。这些结果与肝硬化中存在固定的动脉血管舒张现象相符。
