INCREASED PLASMA ARGININE VASOPRESSIN LEVELS IN PATIENTS WITH CONGESTIVE HEART-FAILURE
INCREASED PLASMA ARGININE VASOPRESSIN LEVELS IN PATIENTS WITH CONGESTIVE HEART-FAILURE
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DOI：
10.1016/s0735-1097(83)80040-0
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发表时间：
1983-01-01
影响因子：
24
通讯作者：
COHN, JN
中科院分区：
文献类型：
--
作者：
GOLDSMITH, SR;FRANCIS, GS;COHN, JN
抗利尿激素精氨酸加压素可能导致充血性心力衰竭患者常见的血管收缩和水处理功能受损。为了确定在这种情况下的基础水平加压素，血浆加压素测定放射免疫法在一组31例晚期充血性心力衰竭患者。同时，还测定了血浆去甲肾上腺素、血浆肾素活性和许多血流动力学变量。在一个亚组的患者中，加压素的反应引起的硝普钠输注和抑制肾素-血管紧张素系统与卡托普利的血流动力学变化进行了研究。并与51例正常老年人进行比较。平均加压素水平（±.平均值的标准误差）为9.5 ±。0.89 pg/ml，而4.7 ±。0.66（概率P < 0.001）。血清钠为137 ±。0.56 meq/l。血管加压素水平与任何血流动力学变量无关，在心脏指数低和正常的患者中增加到相同的程度。加压素水平未能与血清钠，并类似地增加低和正常血清钠的患者。加压素与血浆去甲肾上腺素无相关性，但加压素与血浆肾素活性呈中度相关（r = 0.53，P < 0.02）。由硝普钠引起的急性血流动力学变化不影响血管加压素水平，也没有类似的变化伴随着抑制肾素-血管紧张素系统与卡托普利。因此，在稳态条件下测量的血管加压素水平通常在充血性心力衰竭患者中增加。这种增加不依赖于心脏指数的降低。在某些人中，加压素和血清钠之间的关系似乎存在异常，加压素对急性血流动力学变化无反应，无论是否抑制肾素-血管紧张素系统。导致血管加压素水平升高的机制及其在充血性心力衰竭中的生物学意义仍有待确定。
The antidiuretic hormone arginine-vasopressin could contribute to both the vasoconstriction and impaired water handling frequently found in patients with congestive heart failure. In order to determine basal levels for vasopressin in this condition, plasma vasopressin was measured by radioimmunoassay in a group of 31 patients with advanced congestive heart failure. At the same time, plasma norepinephrine, plasma renin activity and numerous hemodynamic variables were also measured. In a subgroup of patients, the response of vasopressin to hemodynamic changes induced by nitroprusside infusion and to inhibition of the renin-angiotensin system with captopril was studied. The basal vasopressin levels in the patients were compared with those obtained from 51 comparably aged normal subjects. The mean vasopressin level (.+-. standard error of the mean) in the patients was 9.5 .+-. 0.89 pg/ml as compared with 4.7 .+-. 0.66 (probability P < 0.001) in the normal subjects. Serum Na was 137 .+-. 0.56 meq/l. The vasopressin level did not correlate with any hemodynamic variable and was increased to the same degree in patients with both low and normal cardiac index. The vasopressin level failed to correlate with serum Na, and was similarly increased in patients with low and normal serum Na. There was no correlation of vasopressin and plasma norepinephrine, but vasopressin did correlate modestly with plasma renin activity (r = 0.53, P < 0.02). Acute hemodynamic changes induced by nitroprusside did not influence vasopressin levels, nor did comparable changes accompanied by inhibition of the renin-angiotensin system with captopril. Thus, vasopressin levels measured under steady state conditions are usually increased in patients with congestive heart failure. The increase is not dependent on reduced cardiac index. There appears to be an abnormality in the relation between vasopressin and serum Na in some persons and vasopressin does not respond to acute hemodynamic changes with or without the inhibition of the renin-angiotensin system. The mechanisms causing increased vasopressin levels and their biologic importance in congestive heart failure remain to be defined.