Recruitment of an Inotropic Reserve in Hibernating and Stunned Myocardium

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Myocardial ischemia has been characterized as an imbalance between energy supply and demand. In the initial seconds after a sudden reduction of coronary blood flow, the energy demand (determined by contractile function) of the myocardium most certainly exceeds the reduced energy supply (determined by coronary blood flow). This temporary mismatch between regional contractile function and reduced blood flow, however, is an inherently unstable condition because regional contractile dysfunction ensues. The mechanisms responsible for the rapid reduction in contractile function in the acutely ischemic myocardium are still poorly understood. If some residual blood flow exists, a state of “perfusion-contraction matching” can be maintained without the development of irreversible damage, and the metabolic status of such hypoperfused myocardium improves as myocardial lactate production is attenuated and creatine phosphate, after an initial reduction, returns towards control values. Despite the decrease in baseline contractile function, the hypoperfused myocardium can respond to inotropic stimulation by dobutamine. The recruitment of an inotropic reserve implies increased energy utilization. In fact, during inotropic stimulation myocardial glycogen is further reduced and the partially normalized lactate production is again increased. Creatine phosphate is also decreased again, indicating that this energy reservoir is utilized more rapidly than it is being replenished. Apparently, the inotropic challenge once again precipitates a supply—demand imbalance, which had been at least partially corrected by the ischemia-induced decrease of regional contractile function. A chronic reduction in contractile function which normalizes upon reperfusion has been termed “hibernation.”