Abstract
Rat hearts were depleted of Ca 2+ (<10 −9M) for 10 min, followed by 15 min of Ca 2+-repletion. The calcium paradox injury occurs during Ca 2+-repletion, after a period of calcium depletion. The calcium paradox injury was assessed by percent recovery (hemodynamics, [Ca 2+] i, and energy levels) during Ca 2+-repletion. A decrease in Na + concentration during Ca 2+-depletion did not allow for recovery during Ca 2+-repletion, however 2.5% and 5% ethanol during Ca 2+-depletion allowed for an approximate 50% recovery during Ca 2+-repletion. A combination of ethanol (2.5% or 5%) with a low extracellular Na + concentration (88 mM) allowed for complete recovery. Ethanol prevented a depletion of diastolic [Ca 2+] i during Ca 2+-depletion, and allowed for a return of normal diastolic [Ca 2+] i during Ca 2+-repletion. Ethanol modulates the activity of the Na + Ca 2+ exchanger and protects against the Ca 2+-paradox injury.
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