Alterations in alpha adrenoreceptor density and localization after mechanical left ventricular unloading with the jarvik flowmaker left ventricular assist device
Alterations in alpha adrenoreceptor density and localization after mechanical left ventricular unloading with the jarvik flowmaker left ventricular assist device
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DOI：
10.1016/j.healun.2004.03.005
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发表时间：
2005-05-01
影响因子：
8.9
通讯作者：
Bick, RJ
中科院分区：
文献类型：
--
作者：
Grigore, A;Poindexter, B;Bick, RJ
已知心脏α 1肾上腺素受体（α（1）AR）介导人心室肌的正性肌力作用。1，2在心力衰竭的早期阶段，心室收缩力通过肾上腺素能刺激、肾素-血管紧张素激活和其他神经激素和细胞因子系统反应来维持。3，4然而，随着疾病的进展，这些代偿机制不再提供益处;心室扩张和纤维化发生，心脏功能恶化。当心室收缩力变得严重抑制并且不再对正性肌力支持有反应时，插入左心室辅助装置（LVAD）可以允许左心室休息、重塑和恢复一些收缩功能。我们以前的工作已经证明，心肌有能力在卸载期间进行自我修复，5，6之后，一些患者能够恢复正常的生活方式，不再需要心脏移植。(c)2005年，国际心脏和肺移植学会。
Cardiac alpha one adrenoreceptors (alpha(1) AR) are known to mediate positive inotropism in human ventricular myocardium. 1,2 In the early stages of heart failure, ventricular contractility is maintained by adrenergic stimulation, rennin-angiotensin activation, and other neurohormonal and cytokine system responses. 3,4 As the disease progresses, however, these compensatory mechanisms cease to provide benefit; ventricular dilation and fibrosis occur and cardiac function deteriorates. When ventricular contractility becomes severely depressed and is no longer responsive to inotropic support, insertion of a left ventricular assist device (LVAD) may allow the left ventricle to rest, remodel, and recover some contractile function. Our previous work has demonstrated that the myocardium has the capacity to repair itself during a period of unloading, 5,6 after which some patients are able to resume a normal lifestyle and no longer need a cardiac transplant. (c) 2005 by the International Society for Heart and Lung Transplantation.