@article{oai:nagoya.repo.nii.ac.jp:00003927, author = {Hayashi, Hideharu}, issue = {3-4}, journal = {Nagoya Journal of Medical Science}, month = {Nov}, note = {To study the regulation of [Na+]i and [Ca2+]i during myocardial ischemia/reperfusion, [Na+]i and [Ca2+]i were measured simultaneously using guinea pig ventricular myocytes which were dual-loaded with SBFI/AM and fluo-3/AM. It was suggested that: (1) [Na+]i increased during metabolic inhibition (MI: 3.3 mM amytal and 5 μM CCCP) by both the activated Na+ influx via Na+/H+ exchange and the suppressed Na+ extrusion via the Na+/K+ pump; (2) Na+/Ca2+ exchange was inhibited during MI, causing the dissociation between [Na+]i and [Ca2+]I; (3) Na+/Ca2+ exchange could be reactivated by energy repletion, resulting in a significant increase in [Ca2+]i, Furthermore, a Ca2+ influx via the reverse-mode of Na+/Ca2+ exchange may play a key role in the mechanism of Ca2+ overload on reoxygenation; and (4) cell contracture during MI was related to rigor due to energy depletion, while cell contracture after energy repletion was likely to be related to Ca2+ overload.}, pages = {91--98}, title = {Pathogenesis and the role of Ca2+ overload during myocardial ischemia/reperfusion}, volume = {63}, year = {2000} }