Hypoxia and Relaxation

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


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].


Hypoxic Episode Perfusion Buffer Calcium Paradox Perfusion Sequence Aerobic Control 
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© 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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