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目的探讨匹那地尔对高钾停搏液处理后大鼠离体心肌细胞内游离钙与舒缩功能的影响。方法SD大鼠心室肌细胞酶解分离静息1~2 h后随机分为对照组,高钾停搏液组,匹那地尔强化组,格列苯脲拮抗组。四组细胞均在24℃下保存2 h,此后对细胞进行复氧、复灌20 m in并测定细胞收缩、[Ca2+]i瞬态、肌浆网内贮钙释放功能。结果匹那地尔使心肌细胞在缺血再灌注中收缩功能,[Ca2+]i瞬态,肌浆网内贮钙释放能力明显优于高钾停搏液组(P<0.01〉及细胞内钙释放后的钙峰回落时间明显短于高钾停搏液组(P<0.01〉。结论匹那地尔通过维持良好的肌浆网和细胞膜Na+/Ca2+交换体功能来调节钙瞬态变化,减少细胞内钙超载从而改善心肌细胞缺血后收缩功能,同时避免了高钾停搏液的负面效应。
Objective To investigate the effect of pinacidil on the intracellular free calcium and systolic and diastolic function in isolated rat myocardial cells treated with high-potassium cardioplegia. Methods SD rat ventricular myocytes were isolated by enzymolysis for 1 ~ 2 h and then randomly divided into control group, hyperkalemia cardioplegia group, pinacidil group and glibenclamide antagonist group. All four groups of cells were stored at 24 ℃ for 2 h, after which the cells were reoxygenated, reperfused for 20 min, and the cell contraction, [Ca2 +] i transient, and calcium release in sarcoplasmic reticulum were measured. Results Pinacidil induced cardiomyocyte contraction during ischemia / reperfusion. The transient release of Ca2 + in sarcoplasmic reticulum was significantly better than that in hyperkalemic cardioplegia (P <0.01) and intracellular calcium The release time of calcium peak was significantly shorter than that of hyperkalemia cardioplegia group (P <0.01) .Conclusion Pinacidil modulates the transient changes of calcium by maintaining good sarcoplasmic reticulum and cell membrane Na + / Ca2 + exchanger function, reducing Overloading of intracellular calcium improves myocardial contractile function after ischemia and avoids the negative effects of hyperkalemic cardioplegia.