Yang J A, Chen X, Yu Y F
Department of Cardiovascular Surgery, PLA General Hospital, Beijing 100853, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2001 Aug;17(3):240-3.
To observe the effects of HOE642 (Cariporide) on intracellular free calcium in isolated immature rabbit ventricular myocytes induced by anoxia/reoxygenation, and to search the protective mechanism of the Na+/H+ exchange inhibitor on immature rabbit hearts.
The ventricular cardiomyocytes isolated from six New Zealand immature rabbit hearts were divided into three groups of each heart, which were attained by mean of collagenase (type II, 0.28 mg/ml) perfusion. All cells were incubated with calcium fluorescence indicator Fluo-3/AM, and then the intracellular free calcium was measured under the laser scanning confocal microscopy. As well as the creatine phosphokinase (CK) and lactic dehydrogenase (LDH) were measured. The baseline was measured after isolation without anoxia/reoxygenation. The control group received anoxic conditions for 60 minutes and reoxygenation for 30 minutes, then measured. The experiment group received the same conditions as control group with addition of HOE642 (1 micromol/L).
After anoxia/reoxygenation, the intracellular free calcium of isolated immature rabbit ventricular myocytes and CK, LDH in control group increased significantly than baseline (P < 0.01), there were no significant difference of immature myocardial [Ca+]i and CK, LDH between experiment group and baseline (P > 0.05), and the experiment group myocardial [Ca2+]i and CK, LDH reduced significantly than control (P < 0.01).
HOE642 (Cariporide) may reduce intracellular calcium overload and the enzymes level (CK, LDH) in isolated immature rabbit ventricular myocytes induced by anoxia/reoxygenation, so the protective mechanism of HOE642 on immature rabbit heart may be by inhibition of the intracellular free calcium overload.
