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Hypoxia and Relaxation

  • Winifred G. Nayler
  • Darren J. Buckley
  • Jennifer S. Elz

Abstract

Hypoxia has a profound effect on the myocardium. Early changes include a decline in peak developed tension [1], depletion of the endogenous adenosine triphosphate (ATP) and creatine phosphate (CP) [2) reserves, an accumulation of protons [3], and a gain in Na+ and loss of K+ [4]. As the duration of the hypoxic episode progresses, other changes occur, including a gradual but sustained increase in end-diastolic resting tension. Many factors, including extracellular pH [5], temperature [6], and the glucose content of the perfusion buffer [7], have been shown to affect the rate of onset and the magnitude of this hypoxia-induced increase in end-diastolic resting tension (hypoxic contracture). Nevertheless its precise cause is uncertain. Basically there are two schools of thought: that the contracture occurs because there is inadequate ATP to facilitate cross-bridge detachment [8]; or that the contracture occurs because of a raised cytosolic Ca2+ [9].

Keywords

Hypoxic Episode Perfusion Buffer Calcium Paradox Perfusion Sequence Aerobic Control 
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

© Martinus Nijhoff Publishing 1987

Authors and Affiliations

  • Winifred G. Nayler
  • Darren J. Buckley
  • Jennifer S. Elz

There are no affiliations available

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