No-reflow is a specific type of vascular damage occuring when removal of coronary occlusion dose not lead to restoration of coronary flow. There are three major explanations for the no-reflow phenomenon such as endothelial cell edema, microvascular plugging by platelets or thrombi and coronary occlusion by ischemic contracture of the myocardium. But detailed mechanisms of no-reflow phenomenon are not known. The objects of this study are to elucidate the possibility whether elevation of cytosolic Ca²⁺ concentration during ischemic cardioplegic period is mechanism of no-reflow phenomenon or not.

Changes in cytosolic Ca²⁺ concentration were measured under varying experimental condition. Free [Ca²⁺] in the cytosole [Ca²⁺]_i of single rabbit coronary artery cells was measured with fluorescent Ca²⁺ indicator, Fura-2.

Resting [Ca²⁺]_i was 134.2±34 nM (n=43). When single cells were perfused with cardioplegic or ischemic cardioplegic solution, [Ca²⁺]_i was significantly increased and degree of [Ca²⁺]_i elevation was further augmented by ischemic cardioplegic solution. Pretreatment of sarcoplasmic reticulum emptying agent (20mM caffeine) had no effect on cardioplegia-induced [Ca²⁺]_i change, but application of Ca²⁺ channel blocker (5×10^-7M nifedipine) or an antagonist of Na+/Ca²⁺ exchange (5mM Ni²⁺ ) partially (nifedipine) or completely (nickel) inhibited the [Ca²⁺]_i elevation. Pretreament of caffeine had no effect on ischemic cardioplegia-induced [Ca²⁺]_i change, but application of nifedipine or nickel partially inhibited the [Ca²⁺]_i elevation. Magnitude of ischemic cardioplegia-induced [Ca²⁺]_i elevation was dependent on the Ca²⁺ concentration of perfusate from 0 to 2.5mM. When Ni²⁺ was added to reperfusion solution, recovery of ischemic cardioplegia-induced [Ca²⁺]_i elevation was very rapid compared with control.

From the above results, it may be speculated that ischemic cardioplegia-induced [Ca²⁺]_i elevation may act as one of the mechanism of no-reflow phenomenon in rabbit coronary artery.