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Calcium and the Injured Cardiac Myocyte

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Book cover Physiology and Pathophysiology of the Heart

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 34))

Abstract

Injured cardiac myocytes accumulate Ca2+. It does not seem to matter whether the injury is due to reperfusion after prolonged periods of normothermic ischemia [1, 2], sustained hypoxia [3], a naturally occurring cardiomyopathy, or the reintroduction of Ca2+ after only a few minutes of Ca2+-free perfusion [4–6], the end result is the same—that is, the cells become overloaded with Ca2+. The primary aim of this chapter is to establish why the injured myocytes accumulate Ca2+, and then to define the route by which this Ca2+ enters. Finally we will consider the consequences of the resultant Ca2+ overloading.

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Authors
  1. Winifred G. Nayler
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  2. M. J. Daly
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Editor information

Editors and Affiliations

  1. Department of Physiology, University of Cincinnati Medical Center, 231 Bethesda Avenue, 45267, Cincinnati, Ohio, USA

    Nicholas Sperelakis

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© 1984 Springer Science+Business Media Dordrecht

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Nayler, W.G., Daly, M.J. (1984). Calcium and the Injured Cardiac Myocyte. In: Sperelakis, N. (eds) Physiology and Pathophysiology of the Heart. Developments in Cardiovascular Medicine, vol 34. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1171-4_22

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  • DOI: https://doi.org/10.1007/978-1-4757-1171-4_22

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-1173-8

  • Online ISBN: 978-1-4757-1171-4

  • eBook Packages: Springer Book Archive

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