The biology of myocardial hibernation

The biology of myocardial hibernation
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DOI:
10.1016/s1050-1738(00)00058-x
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发表时间:
2000-04-01
影响因子:
9.3
通讯作者:
Schulz, R
Schulz, R
中科院分区:
医学2区
文献类型:
--
作者:
Heusch, G;Schulz, R

文献摘要

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患有慢性冠状动脉疾病的患者经常具有收缩功能障碍,其在再灌注后恢复。心肌冬眠的概念将观察到的收缩功能的降低视为不是持续的能量不足的结果,而是用于维持心肌完整性和活力的适应性下调。在实验中,持续的灌注-收缩匹配、持续缺血期间能量和底物代谢的恢复、正性肌力储备的募集潜力、坏死的缺乏以及因此在再灌注时功能的恢复是冬眠的既定特征。除了钙反应性降低外,其潜在机制尚不清楚。在患者中,基线血流量减少与叠加重复性顿抑的重要性存在一定争议;然而,在大多数研究中,血流量减少,心肌必须经常缺血,足以发生持续性功能障碍。从形态学上看,冬眠心肌表现出去分化、心肌细胞和肌原纤维丢失以及变性、间质纤维化增加的特征。随着对冬眠的潜在机制的更好理解,这些对缺血的适应性反应可能被招募并加强冬眠以延迟即将发生的心肌梗死。(C)2001年,Elsevier Science Inc.
Patients with chronic coronary artery disease frequently have contractile dysfunction that recovers upon reperfusion, The concept of myocardial hibernation views the observed reduction in contractile function not as the result of an ongoing energetic deficit, but as an adaptive down-regulation that serves to maintain myocardial integrity and viability. In the experiment, sustained perfusion-contraction matching, recovery of energy and substrate metabolism during ongoing ischemia, the potential for recruitment of inotropic reserve, lack of necrosis, and therefore recovery of function upon reperfusion are established features of hibernation. Apart from reduced calcium responsiveness, the underlying mechanisms are still unclear. In patients, the importance of reduced baseline blood flow vs. that of superimposed repetitive stunning is somewhat controversial; however, in most studies blood flow is reduced and the myocardium must be ischemic often enough to have persistent dysfunction. Morphologically, hibernating myocardium displays features of dedifferentiation, with loss of cardiomyocytes and myofibrils, and of degeneration, with increased interstitial fibrosis, Patients with hibernating myocardium must be identified and undergo revascularization. With a better understanding of the underlying mechanisms of hibernation, these adaptive responses to ischemia can potentially be recruited and reinforced pharmacologically to delay impending myocardial infarction. (C) 2001, Elsevier Science Inc.