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Cardiovascular Research 1999 43(2):285-287; doi:10.1016/S0008-6363(99)00164-9
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Understanding the temporal relationship of ATP loss, calcium loading, and rigor contracture during anoxia, and hypercontracture after anoxia in cardiac myocytes

David F. Stowe, M.D., Ph.D.

Professor of Anesthesiology and Physiology, Cardiovascular Research Center, The Medical College of Wisconsin, Milwaukee, Wisconsin, USA

Received 27 April 1999; accepted 27 April 1999

The first 150 words of the full text of this article appear below.

See article by Ladilov et al. [9] (pages 408–416) in this issue.

Much research effort has been directed toward understanding the pathogenesis of cardiac ischemia reperfusion injury and developing methods to ameliorate the degree of damage. The interesting discover by Murry et al., reported 13 years ago, that a brief period of ischemia and reperfusion can partially protect the heart from reperfusion damage after a subsequent period of ischemia has sparked intense interest in the area of cardioprotection [1]. Hans Michael Piper and his collaborators, working mostly at the University of Dusseldorf and Justus-Liebig University, have contributed substantially to our knowledge of the pathophysiology of ischemia and reperfusion. They are mostly using a model of simulated ischemia (anoxia, acidosis, and substrate depletion) in which cell shortening of isolated cardiomyocytes during anoxia (rigor contracture) and during re-oxygenation (hypercontracture) are measured temporally with indices of metabolism and myocyte ion concentrations. They . . . [Full Text of this Article]


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