Hypoxia and Relaxation

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].