Open AccessHypoxia Delays the Intracellular Ca2+Clearance by Na+- Ca2+Exchanger in Human Adult Cardiac Myocytes
Author(s) -
Seung-Il Park,
Eun Ju Park,
Nak-Hyun Kim,
Wan Ki Baek,
Young Tak Lee,
Cheol Joo Lee,
Chang Kook Suh
Publication year - 2001
Publication title -
yonsei medical journal/yonsei medical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.702
H-Index - 63
eISSN - 1976-2437
pISSN - 0513-5796
DOI - 10.3349/ymj.2001.42.3.333
Subject(s) - intracellular , myocyte , sodium–hydrogen antiporter , intracellular ph , sodium calcium exchanger , ischemia , acidosis , hypoxia (environmental) , chemistry , medicine , biophysics , cytosol , cardiology , endocrinology , biochemistry , biology , sodium , oxygen , organic chemistry , enzyme
Transient myocardial ischemia during cardiac surgery causes a loss of energy sources, contractile depression, and accumulation of metabolites and H+ ion resulting in intracellular acidosis. The reperfusion following ischemic cardioplegia recovers intracellular pH, activates Na+-H+ exchange and Na+-Ca2+ exchange transports and consequently produces Ca2+ overload, which yields cell death. Among the various Ca2+ entry pathways, the Na+-Ca2+ exchanger is known to play one of the major roles during the ischemia/reperfusion of cardioplegia. Consequently, information on the changes in intracellular Ca2+ activities of human cardiac myocytes via the Na+-Ca2+ exchanger is imperative despite previous measurements of Ca2+ current of human single myocytes. In this study, human single myocytes were isolated from the cardiac tissues obtained during open-heart surgery and intracellular Ca2+ activity was measured with cellular imaging techniques employing fluorescent dyes. We report that the Na+-Ca2+ exchanger of adult cardiac myocytes is more susceptible to hypoxic insult than that of young patients.