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目的研究“钾异心”停搏液对缺血心肌的保护作用并探讨其机理。方法用原代培养的乳鼠心肌细胞为材料，缺糖缺氧处理３ｈ造成缺血损伤，以培养液中乳酸脱氢酶（ＬＤＨ）活性及细胞含钙量为指标，比较高钾、钾异心停搏液对缺血心肌的保护作用。结果“钾异心”停搏液能显著降低缺血处理的心肌细胞培养液的ＬＤＨ活性及细胞含钙量，与高钾停搏液相比效果显著。结论“钾异心”停搏液保护缺血心肌的效果优于高钾液，其机理与降低细胞含钙量有关。
Objective To study the protective effect of “potassium heterostime” cardioplegia on ischemic myocardium and to explore its mechanism. Methods Primary cultured neonatal rat cardiomyocytes were used as materials. Hypoxia and hypoxia for 3 hours resulted in ischemic injury. LDH activity and calcium content in the culture medium were used as indexes. Protective effect of cardioplegia on ischemic myocardium. Results “Disodium potassium” cardioplegia can significantly reduce LDH activity and cell calcium content in ischemic cardiomyocyte culture medium, which is significant compared with high potassium cardioplegia solution. Conclusion The effect of “potassium heterostime” cardioplegia on ischemic myocardium is better than that of high potassium fluid, and its mechanism is related to reducing the calcium content of cells.