Heusch G, Schulz R
Abteilung für Pathophysiologie Zentrum für Innere Medizin Universitätsklinikum Essen.
Z Kardiol. 1998;87 Suppl 2:41-8. doi: 10.1007/s003920050532.
During moderate prolonged myocardial ischemia, the myocardium is dysfuctional but can remain viable. In such ischemic and dysfunctional myocardium, contractile function is reduced in proportion to the reduction in regional myocardial blood flow, i.e., a state of "perfusion-contraction matching" exists. The metabolic status of such myocardium improves over the first few hours, as myocardial lactate production is attenuated and creatine phosphate, after an initial reduction, returns to control values. Ischemic myocardium, characterized by perfusion-contraction matching, metabolic recovery and lack of necrosis, has been termed "short-term hibernating myocardium". "Short-term hibernating" myocardium can respond to an inotropic stimulation with increased contractile function, however, at the expense of a renewed worsening of the metabolic status. A role for endogenous adenosine in the development of hibernation has been excluded, since neither contractile function, metabolic parameters, nor viability are altered by increased catabolism of endogenous adenosine by infusion of adenosine deaminase. Also activation of ATP-dependent potassium channels is not responsible for "short-term hibernation". "Short-term hibernating" myocardium has, however, reduced calcium responsiveness.
在中度持续性心肌缺血期间，心肌功能失调但仍可存活。在这种缺血且功能失调的心肌中，收缩功能随局部心肌血流量的减少而成比例降低，即存在“灌注-收缩匹配”状态。在最初几个小时内，这种心肌的代谢状态会有所改善，因为心肌乳酸生成减少，磷酸肌酸在最初降低后又恢复至对照值。以灌注-收缩匹配、代谢恢复且无坏死为特征的缺血心肌被称为“短期冬眠心肌”。“短期冬眠”心肌可对正性肌力刺激作出反应，使收缩功能增强，然而，代价是代谢状态再次恶化。内源性腺苷在冬眠形成过程中的作用已被排除，因为通过输注腺苷脱氨酶增加内源性腺苷的分解代谢，既不会改变收缩功能、代谢参数，也不会影响心肌活力。而且，ATP依赖性钾通道的激活也与“短期冬眠”无关。然而，“短期冬眠”心肌的钙反应性降低。
