Cobalt chloride postconditioning as myoprotective therapy in cardiac ischemia-reperfusion

Since damage induced by ischemia-reperfusion (I/R) involves alterations in Ca²⁺ homeostasis and is reduced by ischemic postconditioning (IP) and that CoCl₂ can trigger changes resembling the response to a hypoxic event in normoxia and its blockade on Ca²⁺ current in heart muscle, our aim was to evaluate CoCl₂ 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were simultaneously analyzed in a model of I/R in which 0.23 mmol/L CoCl₂ was introduced upon reperfusion and kept or withdrawn after 20 min or introduced after 20 min of reperfusion. The presence of CoCl₂ did not affect diastolic pressure but increased post-ischemic contractile recovery, which peaked at 20 min and decreased at the end of reperfusion. This decrease was prevented when CoCl₂ was removed at 20 min of reperfusion. Total heat release increased throughout reperfusion, while economy increased between 15 and 25 min. No effect was observed when CoCl₂ was introduced at 20 min of reperfusion. In addition, both the area under the contracture curve evoked by 10 mmol/L caffeine-36 mmol/L Na⁺ and the contracture tension relaxation rate were higher with CoCl₂.Furthermore, CoCl₂ decreased the number of arrhythmias during reperfusion and the ventricular damaged area. The presence of CoCl₂ in reperfusion induces cardioprotection consistent with the improvement in cellular calcium handling. The use of CoCl₂ constitutes a potential cardioprotective tool of clinical relevance.