Effect of hypothermic cardioplegia on cardiac protection--I. Effect of hypothermic cardioplegia on the cytosolic Ca2+ concentration in rat ventricular myocytes.
10.3349/ymj.1994.35.2.162
- Author:
Duck Sun AHN
1
;
Young Ho LEE
;
Doo Hee KANG
;
Bok Soon KANG
Author Information
1. Yonsei University College of Medicine, Department of Physiology, Seoul, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Rat myocyte;
cardioplegia;
Na+/Ca2+ exchange;
hypothermia;
ischemia;
fura-2
- MeSH:
Animal;
Calcium/*metabolism;
Cytosol/metabolism;
*Heart Arrest, Induced;
Heart Ventricle/metabolism;
Hypothermia, Induced;
Myocardial Ischemia/metabolism/*prevention & control;
Myocardium/*metabolism;
Rats;
Support, Non-U.S. Gov't
- From:Yonsei Medical Journal
1994;35(2):162-176
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cytosolic Ca2+ concentration of rat ventricular cells was measured under varying experimental conditions by using a fluorescent Ca2+ indicator, Fura-2. Resting [Ca2+]i of rat myocyte was 150 +/- 30 nM (n = 39), and this value was compatible with others. The Perfusion of cardioplegic solution significantly increased [Ca2+]i, and this effect was further augmented by hypothermia (p<0.05). Application of nifedipine (5 x 10(-7) M) to the perfusate or pretreatment of caffeine (10 mM) had no apparent effect on this cardioplegia-induced [Ca2+]i change. But Ni2+ (5 mM), an antagonist of Na+/Ca2+ exchange mechanism, prevented the [Ca2+]i change during cardioplegia (p<0.05). Magnitude of cardioplegia-induced [Ca2+]i increase was also dependent on the Ca2+ concentration of cardioplegic solution. These results suggest that Na+/Ca2+ exchange may play an important role in cardioplegia-induced [Ca2+]i change. To rule out the possibility whether the protective effect of hypothermic cardioplegia is due to the preservation of high-energy phosphate store or decreasing the transmembrane ionic fluxes by phase transition, we exhausted a energy store of cardiac cell by application of 2,4 dinitrophenol to the bath and measured its effect on [Ca2+]i change during cardioplegia. Hypothermic cardioplegia delayed the onset of [Ca2+]i increase and decreased its amplitude compared to those of normothermic cardioplegia. From the above results, hypothermic cardioplegia may protect the cardiac cells from ischemic insult by preserving a high-energy phosphate store. Application of Ni2+ to the cardioplegic solution or reduction of external Ca2+ concentration also had some protective effect, since it prevented [Ca2+]i increase during cardioplegia.
