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In a model of hypertriglyceridemia and hypertension in rats (HTG), induced by adding refined sugar to the animals' drinking water, we investigated the response to an acute stress, such as ischemia and reperfusion. In addition, we examined the contribution of calcium overload and free radical release to the injury caused by the post-ischemic reperfusion in a pathological state compared with the normal state.Ischemia was induced in the whole anaesthetized animal, by occlusion of the left coronary artery for 4 min, followed by reperfusion for 6 min. To prevent either calcium overload or lipid oxidative processes during reperfusion, either Ketorolac (KET), a calcium ionophore-like drug, or α-Phenyl-N-ter-butyl nitrone (PBN), a spin-trapping agent, was administered beforehand.Ketorolac failed to protect the HTG animals from heart damage, as seen by the incidence of reperfusion dysrhythmias, release of lactate dehydrogenase and creatine kinase to the plasma, and non-recovery of the sinus rhythm. On the other hand, PBN was able to prevent these harmful events in the HTG heart by diminishing lipoperoxidation.The results suggest that, in HTG animals, the oxidative processes make a major contribution to the reperfusion injury and that the sole protection from calcium overload provided by KET is not sufficient to avoid damage compared with control rats.