Caffeic acid phenethyl ester (CAPE) supplemented St. Thomas’ hospital cardioplegic solution improves the antioxidant defense system of rat myocardium during ischemia-reperfusion injury

Cardioplegic arrest remains the method of choice for myocardial protection in cardiac surgery. Caffeic acid phenethyl ester (CAPE) prevents lipid peroxidation induced by ischemia-reperfusion injury and has a potent antioxidant property. We investigated the advantages of CAPE supplemented cardioplegic solution (St. Thomas’ Hospital cardioplegic solution No.: 2) on the antioxidant defense system of myocardium against ischemia-reperfusion injury. Isolated rat hearts were mounted on a nonrecirculating type of Langendorff apparatus. The hearts were arrested for 60 min with cardioplegic solution given at 20-min intervals and then reperfused for 15 min. The hearts were divided into three groups. Cold saline (0.9%, 4 °C) in group 1, St. Thomas’ Hospital solution in group 2 and CAPE added St. Thomas’ Hospital solution in group 3 were used as the cardioplegic solution. Krebs–Henseleit buffer solution was used for reperfusion. The tissues were examined biochemically for oxidative stress. Significant differences among the three groups existed in tissue myeloperoxidase (MPO), catalase (CAT), Na +–K + ATPase activity and in the concentrations of malonydealdehyde (MDA) and 3-nitrotyrosine (3-NT). Group 2 showed significant changes in MPO ( P = 0.04), Na +–K + ATPase enzyme activity ( P = 0.02) and the levels of MDA ( P = 0.004) and 3-NT ( P = 0.01) in comparison with group 1. Group 3 efficiently reduced MDA levels ( P = 0.004) and also led to significant decrease in levels of MPO ( P = 0.006), 3-NT ( P = 0.01) and Na +–K + ATPase activity ( P = 0.01) and increase in the level of CAT ( P = 0.004) in comparison with group 1. Significant changes were also found in the levels of MDA ( P = 0.03), MPO ( P = 0.04) and CAT ( P = 0.009) in comparison between groups 2 and 3. We demonstrated that the administration of CAPE into cardioplegic solutions improves the antioxidant defense system of rat heart during the ischemia-reperfusion injury.