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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 金正均[1]
机构地区:[1]上海第二医科大学药理教研室
出 处:《中国病理生理杂志》1996年第1期95-98,共4页Chinese Journal of Pathophysiology
摘 要:本文采用荧光探针Fura-2结合计算机图像处理技术观察不同时间的缺氧及复氧单心肌细胞内游离Ca ̄(2+)含量的变化以及Ca ̄(2+)通道阻滞剂及Na ̄+-Ca ̄(2+)交换抑制剂对其的响。结果显示随着缺氧和缺氧复氧时间的延长,细胞内Ca ̄(2+)浓度逐渐增加。缺氧复氧时细胞内Ca ̄(2+)增加幅度较单纯缺氧大。Mn ̄(2+)及维拉帕米均能降低缺氧时心肌细胞内Ca ̄(2+)超负荷(P<0.05)。Mn ̄(2+)同时也能降低缺氧复氧时细胞内Ca ̄(2+)含量(P<0.05),而维拉帕米降钙作用不明显(P>0.05)。本文提示缺氧和缺氧复氧时细胞内Ca ̄(2+)超负荷的机制并非完全一致。Fluorescent probe Fura-2 combined with computer image processing techiuquewas used to investigate the intracellular free calcium alterations in various stages of hypoxicand reo xygenated myo cytes and the effects of calcium channel blo cker andNa+-Ca ̄(2+) exchange inhibitor on it were studied.The results indicated that freeCa ̄(2+) oncentration gradually elevated with the increasing time of hypoxia andre0 xygenation. The elevating magintudes in imxygenation were higher than that inhypoxia. Both verapamil and Mn ̄(2+) lowered free Ca ̄(2+) concentration induced by hypoxia(P<0.05 respectively). Mn ̄(2+) diminished calcium-overioad caused by reoxygenation(P<0.05)but verapamil’s effect was not significant(P>0.05).These results suggested that the mecha-nisms of calcium overload induced by hypoxia and reoxygenation in myocytes were not thesame.
分 类 号:R541.402[医药卫生—心血管疾病]
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