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血管加压素在充血性心力衰竭患者血管收缩中的作用:与肾素-血管紧张素系统及交感神经系统的比较

Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system.

作者信息

Creager M A, Faxon D P, Cutler S S, Kohlmann O, Ryan T J, Gavras H

出版信息

J Am Coll Cardiol. 1986 Apr;7(4):758-65. doi: 10.1016/s0735-1097(86)80333-3.

Abstract

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在血流动力学监测期间,对10例晚期充血性心力衰竭患者使用精氨酸加压素V1拮抗剂进行治疗,以确定加压素在该病症中对血管收缩的作用。在血浆加压素大于4.0 pg/ml的3例患者中(该组平均为2.4±0.6),加压素拮抗剂导致全身血管阻力降低。血浆加压素浓度与全身血管阻力降低百分比相关(r = 0.70,p<0.025)、与血清钠相关(r = 0.72,p<0.02)以及与血清肌酐相关(r = 0.85,p<0.005)。为了比较加压素、肾素 - 血管紧张素系统和交感神经系统的相对作用,这些患者还接受了卡托普利和酚妥拉明治疗。卡托普利使全身血管阻力降低20%(p<0.05),主要是在血浆肾素活性高的患者中。血浆肾素活性水平在每小时1至46 ng/ml之间(平均14.7±5.7),并与血清钠相关(r = 0.77,p<0.025)、与血清肌酐相关(r = 0.73,p<0.025)以及与右心房压力相关(r = 0.67,p<0.05)。酚妥拉明使所有患者的全身血管阻力降低(平均34%,p<0.01),但降低幅度与治疗前去甲肾上腺素浓度无关。所有患者的去甲肾上腺素水平均升高(694±110 pg/ml),并与基线每搏量指数相关(r = 0.75,p<0.025)以及与血浆肾素活性相关(r = 0.67,p<0.05)。(摘要截断于250字)

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