ABSTRACT
Preparations of heart cells viable under physiological conditions offer a less complex model system for studying the consequences of anoxia and reoxygenation. Elongated heart cells shorten rapidly and spontaneously when subjected to prolonged anoxia. The “oxygen paradox” resulting from reoxygenation of hypoxic heart or reperfusion of the ischemic tissue involves an abrupt uptake of Ca2+, release of intracellular enzymes, some tissue disruption, and a gradual recovery of coordinated mechanical function after an episode of arrhythmic behavior. In any case, the fine-structure of the response is more evident if the behavior of cardiomyocytes is monitored on an individual basis. On the basis of identifying cell shortening with hypoxic contracture in the myocardium, a more fundamental approach to reducing the vulnerability of the heart to interruptions in its oxygen supply would be to delay the onset of rigor.
