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目的 探讨缺氧对心肌细胞的损伤作用及其机制。方法 原代培养乳鼠心肌细胞 ,使其缺氧 5、10、2 0和 30分钟 ,分别检测各时相组心肌细胞内游离钙浓度 ([Ca2 + ]i)、ATP含量以及孵育液中 L DH含量 ;用流式细胞仪检测心肌细胞凋亡率 ;台盼蓝染色检测细胞活力 ;原位杂交检测 bcl- 2基因表达。结果 各缺氧组心肌细胞 [Ca2 + ]i、孵育液 L DH含量、凋亡率及活力明显增加 ,ATP含量明显降低 ,缺氧 10分钟组心肌细胞 bcl- 2 m RNA表达明显降低 ,与对照组相比差异有显著性 (P<0 .0 1)。结论 缺氧可引起乳鼠心肌细胞严重受损 ,bcl- 2基因在其损伤过程中起重要作用
Objective To investigate the effect of hypoxia on cardiomyocyte injury and its mechanism. Methods Primary cultured neonatal rat cardiomyocytes were exposed to hypoxia for 5, 10, 20 and 30 minutes, and the intracellular free calcium concentration ([Ca2 +] i), ATP content and L DH content; flow cytometry myocardial cell apoptosis rate; Trypan blue staining cell viability; bcl-2 gene expression was detected by in situ hybridization. Results The levels of [Ca2 +] i, L DH, the apoptotic rate and the viability of the cardiomyocytes in hypoxia group were significantly increased, while the ATP content was significantly decreased. The expression of bcl-2 mRNA in cardiomyocytes decreased significantly in hypoxia group There was significant difference between the two groups (P <0.01). Conclusion Hypoxia can cause severe damage to neonatal rat cardiomyocytes and bcl-2 gene plays an important role in the process of injury