VA WNY Health Care System, Buffalo, USA.
J Mol Cell Cardiol. 2012 Apr;52(4):822-31. doi: 10.1016/j.yjmcc.2011.08.019. Epub 2011 Aug 26.
A large body of evidence has demonstrated that there is a close coupling between regional myocardial perfusion and contractile function. When ischemia is mild, this can result in the development of a new balance between supply and energy utilization that allows the heart to adapt for a period of hours over which myocardial viability can be maintained, a phenomenon known as "short-term hibernation". Upon reperfusion after reversible ischemia, regional myocardial function remains depressed. The "stunned myocardium" recovers spontaneously over a period of hours to days. The situation in myocardium subjected to chronic repetitive ischemia is more complex. Chronic dysfunction can initially reflect repetitive stunning with insufficient time for the heart to recover between episodes of spontaneous ischemia. As the frequency and/or severity of ischemia increases, the heart undergoes a series of adaptations which downregulate metabolism to maintain myocyte viability at the expense of contractile function. The resulting "hibernating myocardium" develops regional myocyte cellular hypertrophy as a compensatory response to ischemia-induced apoptosis along with a series of molecular adaptations that while regional, are similar to global changes found in advanced heart failure. As a result, flow-function relations become independently affected by tissue remodeling and interventions that stimulate myocyte regeneration. Similarly, chronic vascular remodeling may alter flow regulation in a fashion that increases myocardial vulnerability to ischemia. Here we review our current understanding of myocardial flow-function relations during acute ischemia in normal myocardium and highlight newly identified complexities in their interpretation in viable chronically dysfunctional myocardium with myocyte cellular and molecular remodeling. This article is part of a Special Issue entitled "Coronary Blood Flow".
大量证据表明，局部心肌灌注和收缩功能之间存在紧密的耦合关系。当缺血程度较轻时，这可能导致供应和能量利用之间建立新的平衡，使心脏在数小时内适应，从而保持心肌存活，这种现象称为“短期冬眠”。在可逆性缺血后再灌注时，局部心肌功能仍然受到抑制。“顿抑心肌”在数小时到数天内自发恢复。慢性反复性缺血的心肌情况更为复杂。慢性功能障碍最初可能反映出反复性顿抑，在自发缺血发作之间心脏没有足够的时间恢复。随着缺血的频率和/或严重程度增加，心脏经历一系列适应，下调代谢以牺牲收缩功能来维持心肌细胞活力。由此产生的“冬眠心肌”会发生局部心肌细胞肥大，作为对缺血诱导的细胞凋亡的代偿反应，同时还会发生一系列分子适应，尽管是局部的，但与晚期心力衰竭中发现的全球变化相似。因此，血流-功能关系会独立受到刺激心肌再生的组织重塑和干预的影响。同样，慢性血管重塑可能以增加心肌对缺血易感性的方式改变血流调节。在这里，我们回顾了在正常心肌急性缺血期间对心肌血流-功能关系的现有理解，并强调了在具有心肌细胞和分子重塑的慢性功能障碍的存活心肌中，对其解释的新出现的复杂性。本文是“冠状动脉血流”特刊的一部分。
