Background/Aims: We investigated whether the degree of hypothermia determines the impairment in cardiac muscle function upon rewarming and whether the sarcoplasmic reticulum Ca2+ release channel, RyR2, contributes to hypothermia-induced changes in myoplasmic [Ca2+].Methods: Tension measurements using rat papillary muscle and calcium transients (Fluorescent Ca2+ indicator Fura 2-AM) in rat ventricular myocytes were compared during deep (10°C-16°C) and moderate hypothermic (28°C) myocardial temperatures. In a second experiment, myocytes were pretreated with dantrolene, an RyR2 antagonist; calcium transients were determined at control temperatures (32°C), 16°C, and upon rewarming (32°C).Results: Papillary muscle contractility and myocyte calcium transients were significantly reduced during and after rewarming from 16°C. At 28°C, papillary muscle isometric tension was potentiated and calcium transients were unaffected. After rewarming from 28°C, excitation-contraction coupling was maintained as isometric tension returned to 90% of control values. After rewarming from 16°C, myocytes pretreated with dantrolene had return of calcium transients to 89% of control values while myocytes not treated with dantrolene recovered to only 50% of their control values.Conclusion: We conclude that deep hypothermia, as opposed to moderate hypothermia of the myocardium, disrupts excitation-contraction coupling at cellular and tissue levels. Our finding of preserved calcium transients in dantrolene-pretreated myocytes exposed to deep hypothermia suggests a potential role for the RyR2 channel in post-hypothermia reductions in cardiac function.

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© 2002 S. Karger AG, Basel
2002
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