Hypoxia has a profound effect on the myocardium. Early changes include a decline in peak developed tension , depletion of the endogenous adenosine triphosphate (ATP) and creatine phosphate (CP) [2) reserves, an accumulation of protons , and a gain in Na+ and loss of K+ . 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 , temperature , and the glucose content of the perfusion buffer , 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 ; or that the contracture occurs because of a raised cytosolic Ca2+ .
KeywordsHypoxic Episode Perfusion Buffer Calcium Paradox Perfusion Sequence Aerobic Control
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