Changes in Cytosolic Ca2+ Concentration of Single Rabbit Coronary Artery Smooth Muscle Cell during Ischemic Cardioplegic Period.
10.4070/kcj.1996.26.2.561
- Author:
Young Ho LEE
;
Gyu Bog CHOI
;
Soon Tae KIM
;
Bok Soon KANG
- Publication Type:Original Article
- Keywords:
Cytosolic [Ca2+];
Fura-2;
Ischemic-cardioplegia;
Smooth muscle
- MeSH:
Caffeine;
Cardioplegic Solutions;
Coronary Occlusion;
Coronary Vessels*;
Cytosol*;
Edema;
Endothelial Cells;
Fura-2;
Ischemic Contracture;
Muscle, Smooth*;
Myocardium;
Myocytes, Smooth Muscle*;
Nickel;
Nifedipine;
No-Reflow Phenomenon;
Reperfusion;
Sarcoplasmic Reticulum
- From:Korean Circulation Journal
1996;26(2):561-577
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: 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. METHODS: 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. RESULTS: 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 (5x10-7M 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. CONCLUSIONS: 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.
