Calcium and the Injured Cardiac Myocyte

  • Winifred G. Nayler
  • M. J. Daly
Part of the Developments in Cardiovascular Medicine book series (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.

Keywords

Intercalate Disc Ischemic Episode High Energy Phosphate Massive Influx Passive Permeability 
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 Science+Business Media Dordrecht 1984

Authors and Affiliations

  • Winifred G. Nayler
  • M. J. Daly

There are no affiliations available

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