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采用荧光探针ＢＣＥＣＦ／ＡＭ结合计算机图像处理技术测定不同时间的缺氧和缺氧复氧单心肌细胞内ｐＨ的变化以及Ｃａ２＋通道阻滞剂Ｖｅｒａｐａｍｉｌ和Ｎａ＋－Ｃａ２＋交换抑制剂Ｍｎ２＋对其的影响。结果显示随着缺氧时间的延长，细胞内ｐＨ也逐渐降低。复氧开始４０ｍｉｎ内，细胞内ｐＨ并未恢复正常。Ｖｅｒａｐａｍｉｌ能减轻缺氧细胞内酸化程度并使其接近正常水平（Ｐ＞０．０５），却未能减轻缺氧复氧细胞内的酸化。无论是缺氧或缺氧复氧心肌细胞，Ｍｎ２＋均未能减轻细胞内的酸化程度。本实验结果提示缺氧和缺氧复氧时细胞内酸化途径并非完全一致。ＶｅｒａＰａｍｉｌ抑制缺氧细胞内ｐＨ下降是其保护缺氧心肌作用的机制之一。
Fluorescence probe BCECF / AM combined with computer image processing technique was used to determine the changes of pH in hypoxia and hypoxia-reoxygenation cardiomyocytes at different time and the effects of Ca 2+ channel blockers Verapamil and Na + -Ca 2+ exchange inhibitor Mn 2+. The results showed that with the hypoxia time, the intracellular pH also gradually decreased. Within 40 minutes of reoxygenation, the intracellular pH did not return to normal. Verapamil can reduce the level of acidification in hypoxic cells and bring it to near normal level (P> 0.05), but it can not reduce the acidification in hypoxia-reoxygenation cells. Both hypoxia and hypoxia-reoxygenation myocardial cells, Mn2 + failed to reduce the degree of intracellular acidification. The experimental results suggest that hypoxia and hypoxia and reoxygenation intracellular acidification pathway is not exactly the same. VeraPamil inhibition of hypoxic cell pH drop is one of its mechanisms of protection of hypoxic myocardium.