Pathogenesis and the role of Ca2+ overload during myocardial ischemia/reperfusion.
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 microM 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+], 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.
Hayashi
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Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University, Japan. hayashi@riem.nagoya-u.ac.jp
D000818:Animals; D000963:Antimetabolites / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D048429:Cell Size / Q000187:drug effects; D004734:Energy Metabolism; D006168:Guinea Pigs; D066298:In Vitro Techniques; D017136:Ion Transport / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D000963:Antimetabolites; D012964:Sodium; D002118:Calcium