Gentile S, Bologna E, Terracina D, Angelico M
Department of Medicine, Fatebenefratelli Hospital, Isola Tiberina, Rome, Italy.
Life Sci. 1994;54(21):1585-93. doi: 10.1016/0024-3205(94)90030-2.
Taurine is a non-protein sulfur amino acid widely distributed in mammalian tissues, with poorly understood functions. Taurine administration has a variety of hemodynamic effects, including improvement of cardiac function and suppression of sympathetic activity. Increased urinary volume and sodium excretion have been reported in taurine-fed hamsters. Since patients with ascitic liver cirrhosis have severe hemodynamic and renal abnormalities potentially sensitive to taurine feeding, we evaluated the effects of the i.v. infusion of taurine on urinary flow and sodium excretion and on the hormones involved in the control of hydrosaline homeostasis. Eight cirrhotic patients with tense ascites were given an i.v. bolus of taurine (16 mumoles in 40 ml of saline). The next day patients were given saline only, as a control. Diuresis, urinary sodium and plasma renin activity, aldosterone, atrial natriuretic peptide and arginine vasopressin were measured for the following 6 hrs. Plasma taurine increased ten fold after infusion, then decreased exponentially. No side effects were recorded. After taurine, but not after saline, there was a prompt and significant increase in both urinary volume and sodium excretion. Diuresis increased from 340 +/- 43 to 817 +/- 116 microliters/min (p < 0.01); urinary sodium from 13.8 +/- 3 to 26.3 +/- 4 mumoles/min (p < 0.05). Both values returned to normal after 2-3 hrs. Taurine infusion caused a concomitant significant decrease in plasma renin activity (from 7.7 +/- 2.2 to 4.3 +/- 1.9 ng/ml/hr, p < 0.05) and aldosterone (from 588 +/- 47 to 348 +/- 89 pg/ml, p < 0.05), but no changes in atrial natriuretic peptide and arginine vasopressin. We conclude that i.v. taurine infusion in ascitic cirrhosis promotes a transient diuresis and natriuresis, apparently through the inhibition of the renin-aldosterone axis.
牛磺酸是一种非蛋白质含硫氨基酸，广泛分布于哺乳动物组织中，其功能尚不清楚。给予牛磺酸具有多种血流动力学效应，包括改善心脏功能和抑制交感神经活动。据报道，喂食牛磺酸的仓鼠尿量和钠排泄增加。由于腹水型肝硬化患者存在严重的血流动力学和肾脏异常，可能对喂食牛磺酸敏感，我们评估了静脉输注牛磺酸对尿流和钠排泄以及对参与水盐平衡控制的激素的影响。八名有张力性腹水的肝硬化患者静脉推注牛磺酸（40ml生理盐水中含16微摩尔）。第二天仅给予患者生理盐水作为对照。在接下来的6小时内测量利尿、尿钠以及血浆肾素活性、醛固酮、心房利钠肽和精氨酸加压素。输注后血浆牛磺酸增加了10倍，然后呈指数下降。未记录到副作用。给予牛磺酸后而非生理盐水后，尿量和钠排泄迅速且显著增加。利尿从340±43微升/分钟增加到817±116微升/分钟（p<0.01）；尿钠从13.8±3微摩尔/分钟增加到26.3±4微摩尔/分钟（p<0.05）。这两个值在2 - 3小时后恢复正常。输注牛磺酸导致血浆肾素活性（从7.7±2.2降至4.3±1.9纳克/毫升/小时，p<0.05）和醛固酮（从588±47降至348±89皮克/毫升，p<0.05）同时显著降低，但心房利钠肽和精氨酸加压素无变化。我们得出结论，在腹水型肝硬化患者中静脉输注牛磺酸可促进短暂的利尿和利钠作用，显然是通过抑制肾素 - 醛固酮轴实现的。
