Hypoxia delays the intracellular Ca2+ clearance by Na+-Ca2+ exchanger in human adult cardiac myocytes

Transient myocardial ischemia during cardiac surgery causes a loss of energ y sources, contractile depression, and accumulation of metabolites and H+ i on resulting in intracellular acidosis. The reperfusion following ischemic cardioplegia recovers intracellular pH, activates Na+-H+ exchange and Na+-C a2+ exchange transports and consequently produces Ca2+ overload, which yiel ds cell death. Among the various Ca2+ entry pathways, the Na+-Ca2+ exchange r is known to play one of the major roles during the ischemia/reperfusion o f cardioplegia. Consequently, information on the changes in intracellular C a2+ activities of human cardiac myocytes via the Na+-Ca2+ exchanger is impe rative despite previous measurements of Ca2+ current of human single myocyt es. In this study, human single myocytes were isolated from the cardiac tis sues obtained during open-heart surgery and intracellular Ca2+ activity was measured with cellular imaging techniques employing fluorescent dyes. We r eport that the Na+-Ca2+ exchanger of adult cardiac myocytes is more suscept ible to hypoxic insult than that of young patients.