Changes in Intracellular Ca2+ Concentration of Rabbit Coronary Artery Smooth Muscle Cell during Ischemic Cardioplegic Period

Abstract

To elucidate the possibility whether an elevation of intracellular Ca2+ concentration ([Ca2+]) in rabbit coronary artery myocytes during ischemic cardioplegic period may serve as one of the mechanisms of the 'no-reflow' phenomenon or not, the changes in [Ca2+]i were measured under ischemic cardioplegia conditions using a fluorescent Ca2+ indicator, fura 2/AM. When single cells were perfused with cardioplegic or ischemic cardioplegic solutions, [Ca2+]i was significantly increased and the degree of [Ca2+]i elevation was further augmented by the ischemic cardioplegic solution. Pretreatment of a sarcoplasmic reticulum emptying agent, 20 mM caffeine, had no effect on ischemic cardioplegia-induced [Ca2+]i changes, but application of a Ca2+ channel blocker, 5 × 10-7M nifedipine, or an antagonist of Na+/Ca2+ exchange, 5 mM Ni2+, significantly inhibited the [Ca2+]i elevation, respectively. The magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate in the range of 0 and 2.5 mM. When Ni2+ was added to the reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with the controls. It is concluded that ischemic cardioplegia-induced [Ca2+]i elevation may serve as one of the mechanisms of the 'no-reflow' phenomenon in rabbit coronary artery smooth muscle, cells. We propose that Na+/Ca2+ exchange may serve as a key function in ischemic cardiopelgia-induced [Ca2+]i elevation.