Changes in intracellular Ca2+ concentration of rabbit coronary artery smooth muscle cell during ischemic cardioplegic period.
10.3349/ymj.1996.37.4.251
- Author:
Young Ho LEE
1
;
Gyu Bog CHOI
;
Duck Sun AHN
;
Bok Soon KANG
Author Information
1. Department of Physiology, College of Medicine, Yonsei University, Seoul, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Ischemic cardioplegia;
'no-reflow' phenomenon. [Ca2+]i;
coronary artery
- MeSH:
Animal;
Arteries/metabolism;
Calcium/*metabolism;
Coronary Vessels/*metabolism;
Female;
*Heart Arrest, Induced;
Intracellular Membranes/*metabolism;
Male;
Muscle, Smooth, Vascular/*metabolism/pathology;
Myocardial Ischemia/*metabolism/pathology;
Osmolar Concentration;
Rabbits;
Support, Non-U.S. Gov't
- From:Yonsei Medical Journal
1996;37(4):251-261
- CountryRepublic of Korea
- Language:English
-
Abstract:
To elucidate the possibility whether an elevation of intracellular Ca2+ concentration ([Ca2+]i) 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+] 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 x 10 (-1)M 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 25 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 cardioplegia-induced [Ca2+]i elevation.
