Daniels S, Duncan C J
Zoology Department, School of Life Sciences, Liverpool University, England.
J Cardiovasc Pharmacol. 1994 Jan;23(1):51-6. doi: 10.1097/00005344-199401000-00007.
No reduction in creatine kinase (CK) release during standard Ca2+ paradox in the Langendorff-perfused rat heart was afforded by anoxic perfusion, nor by addition of the radical scavengers superoxide dismutase (150,000 U/L), catalase (150,000 U/L), mannitol (15 or 50 mM), dimethylthiourea (DMTU, 10 mM), the antioxidant vitamin E (0.25 or 0.75 mM), or the iron chelator desferrioxamine (0.8 mM). Even under mild Ca(2+)-paradox conditions, achieved by (a) reducing the duration of the Ca(2+)-free period, (b) increasing [Ca2+]0 during the "Ca(2+)-free" period, or (c) reperfusing with 0.1 mM Ca2+, no protection was achieved by mannitol, DMTU, or desferrioxamine. Perfusion with N2 did not cause a reduction in CK release caused by caffeine or dinitrophenol or Ca2+ paradox. We conclude that no evidence supports the hypothesis that oxygen radicals are implicated in release of CK in Ca2+ paradox.
在Langendorff灌流的大鼠心脏中，缺氧灌注以及添加自由基清除剂超氧化物歧化酶（150,000 U/L）、过氧化氢酶（150,000 U/L）、甘露醇（15或50 mM）、二甲基硫脲（DMTU，10 mM）、抗氧化剂维生素E（0.25或0.75 mM）或铁螯合剂去铁胺（0.8 mM），均不能减少标准钙悖论期间肌酸激酶（CK）的释放。即使在通过以下方式实现的轻度钙悖论条件下：（a）缩短无钙期的持续时间，（b）在“无钙”期增加[Ca2+]0，或（c）用0.1 mM Ca2+再灌注，甘露醇、DMTU或去铁胺也无法提供保护。用N2灌注不会导致由咖啡因、二硝基苯酚或钙悖论引起的CK释放减少。我们得出结论，没有证据支持氧自由基与钙悖论中CK释放有关的假设。
