Left ventricular remodeling after myocardial infarction - Pathophysiology and therapy
Left ventricular remodeling after myocardial infarction - Pathophysiology and therapy
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DOI：
10.1161/01.cir.101.25.2981
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发表时间：
2000-06-27
期刊：
影响因子：
37.8
通讯作者：
Sharpe, N
中科院分区：
文献类型：
--
作者：
Sutton, MGS;Sharpe, N
血管紧张素-醛固酮系统，并刺激心房和脑钠肽（ANP和BNP）的产生。10交感神经刺激引起的缩短和心率增加导致非梗死心肌运动过度和暂时性循环代偿。此外，利钠肽降低血管内容量和全身血管阻力，使心室充盈正常化，并改善泵功能。
renin-angiotensin-aldosterone system, and stimulates the production of atrial and brain natriuretic peptides (ANP and BNP). 10 Augmented shortening and increased heart rate from sympathetic stimulation result in hyperkinesis of the noninfarcted myocardium and temporary circulatory compensation. In addition, the natriuretic peptides reduce intravascular volume and systemic vascular resistance, normalize ventricular filling, and improve pump function.