Hodsman G P, Kohzuki M, Howes L G, Sumithran E, Tsunoda K, Johnston C I
University of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Australia.
Circulation. 1988 Aug;78(2):376-81. doi: 10.1161/01.cir.78.2.376.
In chronic cardiac failure, various neurohumoral mechanisms are activated to sustain blood volume, blood pressure, and organ perfusion. Using the coronary artery ligation model of heart failure in the rat, we have measured changes in vasoactive hormone secretion and related these changes to salt and water status during a 1-month period. When compared with controls, rats with infarction had a marked rise in plasma atrial natriuretic peptide (294 +/- 59 vs. 79 +/- 10 pg/ml, p less than 0.001) although there was no increase in total exchangeable body sodium. Plasma renin activity and plasma aldosterone concentrations were the same for both rats with infarction and controls. Similarly, there were no significant differences in plasma arginine vasopressin, plasma osmolality, or plasma sodium concentration in rats with infarction. Ventricular norepinephrine levels were reduced in animals with infarction (p less than 0.01). Plasma atrial natriuretic peptide levels were raised in this model of chronic left ventricular failure. However, there was no salt retention and little stimulation of the renin-angiotensin-aldosterone system or vasopressin. The results suggest that high circulating atrial natriuretic peptide levels may prevent or limit salt and water retention, either directly or indirectly, by inhibiting the renin-angiotensin-aldosterone system.
在慢性心力衰竭中，多种神经体液机制被激活以维持血容量、血压和器官灌注。我们利用大鼠冠状动脉结扎所致心力衰竭模型，在1个月期间测量了血管活性激素分泌的变化，并将这些变化与盐和水的状态相关联。与对照组相比，梗死大鼠血浆心钠素显著升高（294±59对79±10 pg/ml，p<0.001），尽管总体可交换钠没有增加。梗死大鼠和对照组的血浆肾素活性及血浆醛固酮浓度相同。同样，梗死大鼠的血浆精氨酸加压素、血浆渗透压或血浆钠浓度也无显著差异。梗死动物的心室去甲肾上腺素水平降低（p<0.01）。在这种慢性左心室衰竭模型中，血浆心钠素水平升高。然而，没有盐潴留，肾素-血管紧张素-醛固酮系统或加压素也几乎未受刺激。结果提示，循环中高水平的心钠素可能直接或间接通过抑制肾素-血管紧张素-醛固酮系统来预防或限制盐和水的潴留。
