The Cellular Basis of Stunned Myocardium
Contractility is decreased after ischemia, even when there is no histologic evidence of irreversible injury; myocardium so afflicted has come to be known as ‘stunned.’ The contractility lesion in stunned myocardium might affect at least one of three major factors in force generation; the [Ca2+] transient, myofilament Ca2+-sensitivity and maximal Ca2+-activated force. Our results indicate that contractile dysfunction in stunned myocardium is characterized by a decline in maximal force and a shift to higher Ca in the myocardial sensitivity to extracellular Ca. The latter may reflect either a decrease in myofilament Ca2+-sensitivity or a decrease in the [Ca2+] transient. Reperfusion with a solution of low Ca concentration or an acidic solution ameliorated functional recovery, indicating that calcium entry upon reperfusion plays a major role in the pathogenesis of myocardial stunning. Recent research suggests that the lower intramyocardial level at ATP may be an epiphenomenon and not a causal factor in stunning. Thus, we favor the hypothesis that calcium is the crucial mediator of reversible post-ischemic dysfunction.
KeywordsContractile Dysfunction Stun Myocardium Contractile Reserve Develop Pressure Reperfused Ischemic Heart
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