尼卡地平对缺氧/复氧心肌细胞损害及细胞内Ca^(2+)的影响

Effect of Nicardipine on Anoxia Reoxygenation Injury and Intracellular Calcium in Primary Culture Myocardial Cells

目的 :研究尼卡地平对缺氧 /复氧心肌细胞损害及细胞内Ca2 +的影响。方法 :培养 4～ 5天原代SD大鼠心肌细胞分为正常对照、单纯缺氧 /复氧以及低剂量和高剂量 (终浓度分别为 30ng/ml和 2 70ng/ml)的尼卡地平预防用药 2 0分钟后缺氧 /复氧四组。实验结束测定培养液乳酸脱氢氧酶 (LDH)和肌酸激酶 (CK)活性以及细胞内Ca2 +含量。结果 :缺氧复氧后 ,心肌细胞内游离Ca2 +浓度 ,以及培养液中LDH和CK活性显著升高。高剂量尼卡地平能明显减轻这种升高 ,而低浓度尼卡地平则无明显影响。结论 :高浓度尼卡地平减轻缺氧 /复氧心肌细胞Ca2 +超载 。

Objective:To study the effect of nicardipine on anoxia reoxygenation injury and intracellular calcium in primary culture myocardial cells.Methods:Myocardial cells,cultured in 1640 culture medium for 4 5 days,were assigned to control group,anoxia reoxygenation group and treating with nicardipine(30ng/ml or 270 ng/ml in final concentration) followed anoxia reoxygenation group.Intracellular free calcium in single cell and lactic dehydrogenase(LDH) and creatine kinase (CK) in culture medium were measured at the end of experiment.Results:High dose(270ng/ml) of nicardipine significantly attenuated the great increases of intracellular calcium,or LDH and CK in culture medium caused by anoxia reoxygenation, but low dose of it did not.Conclusion:High dose of nicardipine protects myocardium cells from anoxia reoxygenation injury at extent through decreasing intracellular calcium.