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充血性心力衰竭中的神经体液轴。

The neurohumoral axis in congestive heart failure.

作者信息

Francis G S, Goldsmith S R, Levine T B, Olivari M T, Cohn J N

出版信息

Ann Intern Med. 1984 Sep;101(3):370-7. doi: 10.7326/0003-4819-101-3-370.

DOI:10.7326/0003-4819-101-3-370
PMID:6147109
Abstract

The incidence of congestive heart failure is increasing in the United States. This common syndrome is characterized not only by impaired ventricular function but also by an increase in some endogenous vasoconstrictor substances, including norepinephrine, angiotensin II, and arginine vasopressin. Although activation of the systems that release these substances is presumed to be compensatory (to maintain perfusion pressure during inadequate flow), the sympathetic nervous system, renin-angiotensin-aldosterone system, and arginine vasopressin may contribute to the pathogenesis of the syndrome. The excessive vasoconstriction present in heart failure likely produces a further burden on the failing myocardium. New strategies in therapy are being developed to counteract the activation of vasoconstrictor forces in congestive heart failure. Data indicate that selective blockade of the renin-angiotensin system is useful. Preliminary data suggest that inhibition of the sympathetic nervous system may be helpful, and inhibition of vasopressin in animals with heart failure is being studied. New and more selective therapy for heart failure may come from these studies.

摘要

在美国,充血性心力衰竭的发病率正在上升。这种常见综合征不仅以心室功能受损为特征,还表现为一些内源性血管收缩物质增加,包括去甲肾上腺素、血管紧张素II和精氨酸加压素。尽管释放这些物质的系统激活被认为具有代偿作用(在血流不足时维持灌注压),但交感神经系统、肾素-血管紧张素-醛固酮系统和精氨酸加压素可能会促进该综合征的发病机制。心力衰竭中存在的过度血管收缩可能会给衰竭的心肌带来进一步负担。目前正在开发新的治疗策略来对抗充血性心力衰竭中血管收缩力的激活。数据表明,肾素-血管紧张素系统的选择性阻断是有用的。初步数据表明,抑制交感神经系统可能会有帮助,并且正在研究对心力衰竭动物的加压素抑制作用。心力衰竭的新的、更具选择性的治疗方法可能来自这些研究。

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1
The neurohumoral axis in congestive heart failure.充血性心力衰竭中的神经体液轴。
Ann Intern Med. 1984 Sep;101(3):370-7. doi: 10.7326/0003-4819-101-3-370.
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Neurohumoral mechanisms involved in congestive heart failure.
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Neurohumoral control mechanisms in congestive heart failure.充血性心力衰竭中的神经体液控制机制。
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