Why the study?
Do radical scavengers or anoxic perfusion reduce creatine kinase release during the calcium paradox in the rat heart?
Do radical scavengers or anoxic perfusion reduce creatine kinase release during the calcium paradox in the rat heart?
This study finds no evidence that oxygen radicals are implicated in the release of creatine kinase during the calcium paradox in the rat heart.
Radical scavengers and anoxic perfusion do not limit CK release in Ca2+ paradox; leaves open alternative injury mechanisms in this rat model.
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.
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Daniels et al. (1994) studied this question.
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