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The Cellular Basis of Stunned Myocardium

  • Hideo Kusuoka
  • Eduardo Marban
  • Myron L. Weisfeldt

Summary

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.

Keywords

Contractile Dysfunction Stun Myocardium Contractile Reserve Develop Pressure Reperfused Ischemic Heart 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Tokyo 1989

Authors and Affiliations

  • Hideo Kusuoka
    • 1
  • Eduardo Marban
    • 2
  • Myron L. Weisfeldt
    • 2
  1. 1.The First Department of MedicineOsaka University School of MedicineOsakaJapan
  2. 2.Division of Cardiology, Department of MedicineThe Johns Hopkins University School of MedicineBaltimoreUSA

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