Short-term hemodynamic effects of vasopressin V1-receptor inhibition in chronic right-sided congestive heart failure.
Short-term hemodynamic effects of vasopressin V1-receptor inhibition in chronic right-sided congestive heart failure.
复制标题
加压素 V1 受体抑制对慢性右侧充血性心力衰竭的短期血流动力学影响。
DOI：
10.1161/01.cir.78.5.1251
复制
发表时间：
1988
期刊：
影响因子：
37.8
通讯作者：
HoodJr,WB
中科院分区：
文献类型：
--
作者：
Stone,CK;Liang,CS;Imai,N;Sakamoto,S;Sladek,CD;HoodJr,WB
精氨酸加压素在充血性心力衰竭时升高。为了确定精氨酸加压素对全身血流动力学和局部血流量的影响，我们给15只患有三尖瓣撕脱和进行性肺动脉收缩引起的慢性右心衰竭的狗施用了加压素血管作用的特异性抑制剂[1-（β-巯基-β，β-环戊亚甲基丙酸），2-（O-甲基）-酪氨酸]-精氨酸加压素[d（CH 2）5 Tyr（Me）AVP]。动物显示血浆精氨酸加压素和去甲肾上腺素水平升高。加压素抑制增加心输出量和左心室dP/dt和dP/dt/P，并降低总外周血管阻力，而平均主动脉压没有显着变化。同时，骨骼肌、肾脏、皮肤和左右心室心肌的血流量增加。血浆儿茶酚胺也增加。用心得安和哌唑嗪预处理可消除加压素抑制引起的心输出量和左心室功能的增加。预处理还导致血管加压药抑制后平均主动脉压降低。与此相反，d（CH）2）5 Tyr（Me）AVP给药11假手术动物或给药生理盐水9假手术和8个心力衰竭的狗是没有效果，无论是在存在或不存在肾上腺素能受体阻滞剂。因此，精氨酸加压素参与控制右侧充血性心力衰竭的循环，对血管具有直接收缩作用，并通过抑制交感神经系统而间接起作用。
Arginine vasopressin is elevated in congestive heart failure. To determine the effect of arginine vasopressin upon systemic hemodynamics and regional blood flows, we administered the specific inhibitor of the vascular action of vasopressin [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)-tyrosine]-arginine vasopressin [d(CH2)5Tyr(Me)AVP] to 15 dogs with chronic right-heart failure produced by tricuspid avulsion and progressive pulmonary artery constriction. The animals exhibited increased plasma arginine vasopressin and norepinephrine levels. Vasopressin inhibition increased cardiac output and left ventricular dP/dt and dP/dt/P, and it decreased total peripheral vascular resistance, whereas mean aortic pressure did not change significantly. Simultaneously, blood flow increased to skeletal muscle, kidneys, skin, and right and left ventricular myocardium. Plasma catecholamines also increased. Pretreatment with propranolol and prazosin abolished the increases in cardiac output and left ventricular function produced by vasopressin inhibition. Pretreatment also led to a decrease in mean aortic pressure after vasopressor inhibition. In contrast, administration of d(CH)2)5Tyr(Me)AVP to 11 sham-operated animals or administration of normal saline to nine sham-operated and eight heart-failure dogs was without effect either in the absence or in the presence of adrenergic receptor blockade. Thus, arginine vasopressin participates in the control of the circulation in right-sided congestive heart failure, with both a direct constrictor action on blood vessels and an indirect action by inhibition of the sympathetic nervous system.