Ischemia/Reperfusion-induced Myocardial Damage: Role of Carbon Dioxide

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We investigated the acid-base characteristic alterations of blood cardioplegia (BCP) during aortic cross-clamping in hearts arrested with BCP and during in vitro simulated ischemia. In 40 patients undergoing cardiac surgery following an aortic cross clamp, hearts were infused with a hypothermic BCP intermittently and lastly with a normothermic BCP prior to aortic cross clamp release. We measured pH, pCO2, [HCO3-], and [Cl-] of the coronary sinus effluent in the final BCP. BCP was assessed under in-vitro gassing at with 95% N2 + 5% CO2 (n = 6), 50% N2 + 50% CO2 (n = 3), or 100% CO2 (n = 6). The coronary sinus effluent, compared with the pre-infused BCP, exhibited significantly lower pH and greater pCO2 with no change in the [HCO3-] level. In vitro, the 100% CO2 gassing groups exhibited a significant increase in [HCO3-] under high pCO2-induced acidification. Under anoxia and CO2 retention during aortic cross-clamping, BCP can be a bicarbonate donor to the myocardium.