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作 者:王军[1] 张佩瑾[1] 章鲁[1] 齐建华[1] 魏丕敬[1] 顾培坤[1] 金正均[1]
机构地区:[1]上海第二医科大学药理教研室,上海第二医科大学计算机教研室,上海第二医科大学电生理教研室
出 处:《中国药理学通报》1996年第1期68-70,共3页Chinese Pharmacological Bulletin
摘 要: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。Fluorescent probe BCECF/AM combined with computer image processing technique was used to investigate intracellular pH (pHi)variation in various stages of hypoxic and reoxygenated myocytes and the effects of calcium channel blocker, verapamil,and Na+-Ca2+exchange inhibitor Mn2+on this variation.Results indicated that intracellular pH decreased gradually along with the prolongation of hypoxia. During 40 min of reoxygenation, the pHi did not return to normal.Verapamil inhibited pHi decrease during hypoxia but had no significant effect on pHi during reoxygenbation.The effect of Mn2+ on intracellular pH during both hypoxia and reoxygenation was not significant.Our study suggested that the mechanism of intracellular acidosis induced by hypoxia may not be the same as one induced by reoxygenation and one of the protective effects of verapamil on hypoxic myocytes is its inhibition of decrease in intracellular pH in myocytes.
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