Since damage induced by ischemia-reperfusion (I/R) involves alterations in Ca homeostasis and is reduced by ischemic postconditioning (IP) and that CoCl can trigger changes resembling the response to a hypoxic event in normoxia and its blockade on Ca current in heart muscle, our aim was to evaluate CoCl as an IP therapeutic tool. Mechanic and energetic parameters of isolated and arterially perfused male Wistar rat heart ventricles were simultaneously analyzed in a model of I/R in which 0.23 mmol/L CoCl was introduced upon reperfusion and kept or withdrawn after 20 min or introduced after 20 min of reperfusion.
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