摘要
多数研究资料表明:在心肌细胞发生氧反常和pH反常后,H ̄+一Na ̄+、Na ̄+一Ca ̄(2+交换加强是细胞内Ca ̄(2+)超载的重要机制。我们的研究表明,造成细胞Ca ̄(2+)超载的原因,除H ̄+一Na ̄+、Na ̄+一Ca ̄(2+)交换外,尚有H ̄+一Ca ̄(2+)交换参加.本实验证实,在细胞缺氧10、20、30和40min时,经H ̄+一Ca ̄(2+)交换进入细胞的Ca2+量占同一时点细胞摄Ca ̄(2+)总量的比率分别为(%):10.1±0.5、124±0.7、11.8±0.4和11.2±0.5、平均值为(%):11.4±0.9.当缺氧细胞再复氧后,这一比率显著增加。各时点的比率分别为(%):23.7±0.6、22.3±0.5、22.1±0.7和20.5±0.8、平均值为(%):22.2±12。这一结果表明:在pH反常所致Ca ̄(2+)超载过程中,H ̄+一Ca ̄(2+)交换的作用不容忽视。
Reoxygenation is more serious to hypoxic myocardial eells because it followedwith calcium o verload.It is already kno wn that the calcium overload is due toaugmentation of H+ 一Na+, Na+ 一Ca2+ exchanges during pH paradox. Our past experimentshowed that,besides H+ 一Na+,Na+ 一Ca+ exchanges,H+ 一Ca2+ exchange was also one ofthe reasons of calcium overload.The present experiment showed that H+ 一Ca2+ exchangecaused 11.4 per eent of total Ca2+uptake of myocardial cells after hypoxia, and the per- eentage was risen to 22.2 per cent after reoxygenation.It was suggested that duringintraeellular calcium overload the action of H+ 一Ca2+ exchange sho uld not be neglected.
出处
《中国病理生理杂志》
CSCD
北大核心
1996年第6期587-590,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
关键词
钙
心肌缺氧
复氧
氢
Calcium.Mvocardium.Cells. culture