缺氧、再给氧对培养大鼠心肌细胞的损伤和尼可地尔的保护作用

本实验观察缺氧、再给氧对培养大鼠心肌细胞的损伤和尼可地尔(Nicorandil)的保护作用。缺氧组和缺氧加Nicorandil组给予充氮生长液;正常组和正常加Nicorandil组给予正常生长液。各组在实验9h时均用正常生长液置换原生长液。缺氧组心肌细胞在3h后搏幅减弱,频率变慢,节律失常。9h后约有1/3细胞停搏,细胞形态改变,上清液内乳酸脱氢酶(LDH)和肌酸激酶(CK)明显增高。更换正常生长液后15h内细胞病变和酶谱变化更趋严重,停搏细胞持续增加。缺氧加Nicorandil组内在Nicorandil剂量为0.5～2mg/ml时,细胞形态基本正常,很少节律失常,上清液内LDH和CK明显低于缺氧组。正常组和正常加Nicorandil组细胞搏动频率、节律和上清液内LDH、CK均无明显改变。

HYPOXIA AND HYPOXIA-REGENERATION INDUCED INJURY ON CULTURED RAT HEART CELLS AND THE PROTECTIVE EFFECTS OF NICORANDIL

Hypoxia-reoxygenation induced injuries on cultured rat beating heart cells and the protective effects of nicorandil on such injuries were studied. Normal growth medium with PO2 over 46.47kPn was used for tho normal and nicorandil control groups. Growth medium with P0, equal to 5.33kPa was used for hypoxia and hypoxia plus nicorandil treated, groups. In the hypoxin group, the rate of heart cell beating decreased and arrhythmias appeared at 3 hours. 9 hours after hypoxia, pathological changes appeared in cells, lactic acid dehydrogenase (LDH) and creatine kinase (CK) levels in the culture medium significantly increased and 1/3 of the cells ceased beating. The hypoxia growth medium was then replaced by normal growth medium, the pathological changes in the heart cells and increase in LDH and OK levels in the culture medium became still more significant, and the number of non-beating cells gradually increased during the next 15 hours after reoxygenation. In the hypoxia plus nicorandil (in 0.5-2mg/ml doses) treated group, the heart cells showed no or slight hypoxia and reoxygenation injury, arrhythmias occurred less frequently than in the hypoxia group. No significant changes in the rate and rhythm of cell beat or LDH and CK levels in the culture medium were observed in the normal and nicorandil control groups.