Riegger G A, Liebau G, Kochsiek K
Am J Med. 1982 Jan;72(1):49-52. doi: 10.1016/0002-9343(82)90576-9.
In advanced heart failure, severe edema develops associated with hyponatremia. In 20 patients with severe congestive heart failure, we studied plasma antidiuretic hormone (ADH) concentrations related to hemodynamics and plasma osmolality. Prazosin was used to test the acute response to changes in atrial receptors and hemofiltration to test the response to changes in volume receptors. One group of the patients had inappropriately high ADH values (14.5 +/- 8.8 pg/ml) in relation to their plasma osmolality, which was well below normal values (276 +/- 23 mosmol/kg water) with no apparent osmoregulatory control. The other group showed a normal relationship of ADH and plasma osmolality (3.9 +/- 1.0 pg/ml; 289 +/- 8 mosmol/kg water), Only in the normal regulating group did lowering of left atrium pressure by prazosin result in a rise in ADH related to the decrease in pressure. Inappropriately high ADH secretion could be reversed by hemofiltration. This suggests that the syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli; however, it cannot be ruled out that associated hemodynamic effects in the kidney or other intrarenal or hormonal factors contribute to this mechanism.
在晚期心力衰竭中,会出现与低钠血症相关的严重水肿。我们对20例严重充血性心力衰竭患者的血浆抗利尿激素(ADH)浓度与血流动力学及血浆渗透压的关系进行了研究。使用哌唑嗪来测试心房受体变化的急性反应,使用血液滤过来测试容量受体变化的反应。一组患者的ADH值(14.5±8.8 pg/ml)相对于其血浆渗透压而言过高,其血浆渗透压远低于正常值(276±23 mosmol/kg水),且无明显的渗透压调节控制。另一组患者的ADH与血浆渗透压呈正常关系(3.9±1.0 pg/ml;289±8 mosmol/kg水)。只有在正常调节组中,哌唑嗪降低左心房压力才会导致ADH随压力降低而升高。血液滤过可逆转不适当的高ADH分泌。这表明严重充血性心力衰竭中的“稀释性低渗综合征”可能是由不适当的高ADH分泌引起的,其中渗透压感受器系统受非渗透压刺激主导;然而,不能排除肾脏中的相关血流动力学效应或其他肾内或激素因素对这一机制有影响。