mitoKATP和肌浆网钙ATP酶在心肌缺血预适应的作用及机制

目的探讨肌浆网钙ATP酶在心肌细胞缺氧预适应模型上的作用以及其与mitoKATP开放的相关性。方法原代培养的新生大鼠心肌细胞,随机分为4组正常培养组、缺氧/复氧损伤组、缺氧预适应组、5 HD(mitoKATP阻断剂)合并缺氧预适应组。测定各组细胞上清中LDH的释放量,细胞存活率及肌浆网钙ATP酶活性。结果缺氧预适应组与缺氧复氧组比较,LDH的释放显著下降(P <0 0 1) ,细胞存活率明显上升(P <0 0 1) ,肌浆网钙ATP酶活性提高(P <0 0 1)而5 HD合并缺氧预适应组较缺氧预适应组LDH释放增多(P <0 0 5 ) ,细胞存活率下降显著(P <0 0 1) ,肌浆网钙ATP酶活性下降(P <0 0 1)。结论肌浆网钙ATP酶与mitoKATP开放均参与了缺氧预适应早期相的保护作用,且2者之间的作用具有相关性。

EFFECTS AND MECHANISMS OF mitoKATP AND SR Ca2+-ATPase ON CARDIOMYOCYTES PROTECTION OF HYPOXIA PRECONDITIONING

Objectivest To investigate the role of Ca~2+ -adenosine triphosphatase (ATPase) of sarcoplasmic reticulumin(SR) in the protection of hypoxia preconditioning on myocardiocytes and its correlation to the opening of mitochondrial ATP-sensitive K+ channel(mitoKATP). Methods The primary cultured neonatal rat cardiomyocytes were divided randomly into four groups: ①normal control; ②hypoxia/reoxygenation(H/R) group; ③hypoxia preconditioning(HPC) group; ④5-HD(inhibitor of mitoKATP)+hypoxia preconditioning group. The LDH release, cell viability and activity of Ca~2+ -ATPase of sarcoplasmic reticulum in each groups were measured. Results Compared with H/R group, The LDH release in HPC group decreased remarkably(P<0.01), myocytes viability in HPC group increased (P<0.01) and the activity of Ca~2+ -ATPase of SR increased significantly. However, in 5-HD with HPC group, Compared with HPC group, the LDH release increased (P<0.05). myocytes viability and the activity of Ca~2+ -ATPase of SR decreased (P<0.01). Conclusion The Ca~2+ -ATPase of SR and mitoKATP may be involved in the protection mechanism of early hypoxia preconditioning, and there may be relativity in the two facts.