培养大鼠心肌细胞缺氧与复氧时H~+-Ca^(2+)交换的研究  被引量:5

STUDY OF H ̄+-Ca ̄(2+)EXCHANGE IN CULTURED HEART CELLS AFTER HYPOXIA AND REOXYGENATION

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作  者:张北奇[1] 马宁[1] 董力[1] 周锡英[1] 于占久[1] 伍贻经[1] 

机构地区:[1]河北省医学科学院生理室,北京医科大学病理生理教研室

出  处:《生理学报》1995年第1期54-58,共5页Acta Physiologica Sinica

基  金:国家自然科学基金

摘  要:大量研究表明:心肌细胞缺氧后再复氧,可因氧反常和pH反常造成细胞内Ca2+超载。通常认为,在心肌细胞发生pH反常后,H+-Na+和Na+-Ca2+交换加强是细胞内Ca2+超载的重要机制。本实验结果表明:阻断了H+-Na+和Na+-Ca2+交换后,仍有部分Ca2+进入细胞,Ca2+内流量与缺氧时间成正比关系。在无Na+溶液中也得到了同样结果,表明此时Ca2+内流是通过与Na+无关的通路进入细胞的。进一步实验表明这种Ca2+内流与细胞膜内外pH梯度差密切相关。当胞外pH升高即胞内相对H+浓度增加时,Ca2+内流量也增加。故推测:pH反常所致细胞内Ca2+超载的原因,除H+-Na+和Na+-Ca2+交换外,尚有H+-Ca2+交换机制。Reoxygenation is more serious for hypoxic myocardial cells because of the subscquence calcium overload. The calcium overload is known due to augmentation of H+-Na+, Na+-Ca2+, exchange during PH paradox. But the present experiment showedthat, when H+-Na+, Na+-Ca2+ exchange was inhibited, calcium could still enter myocardial cells after hypoxia or reoxygenation. Similar result was observed after usingNa+-Free solution, suggesting that calcium entance into the cell was unrelated to Na+channel. It was further shown that calcium accumulation was related to PH gradientacross the myocardial cell membrane, i. e., being increased with increase of H+ concentration in the cell. Therefore, it appears that, besides H+-Na+, Na+-Ca2+ exchange,H+-Ca2+ exchange is one of the reasens of calcium overload during intracellular pHparadox.

关 键 词:心肌细胞 心肌缺氧   病理生理学 

分 类 号:R541.402[医药卫生—心血管疾病]

 

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