Antioxidant Effects of Euterpe Oleracea Mart. (Açai) on Myocardial Ischemia-Reperfusion Injury in Rats: Would it Represent a Good Way To Follow?

摘要

Abrupt occlusion of an epicardial coronary artery may result in acute myocardial infarction with elevation of the ST segment as the myocardium underwent an ischemic process. This promotes damage to the cardiomyocytes, mainly due to metabolic disturbances in the ATP generation with subsequent cell death and myocardial necrosis. Furthermore, reduced levels of intracellular ATP leads to an overload of cytosolic Ca and Na concentrations and heart function impairment. It would be expected that restoration of blood flow to the ischemic area in the myocardium to minimize the injury, but reperfusion may also induce additional damage to the cardiac cells, a phenomenon described as ischemia-reperfusion (I/R) injury which contributes to an increased infarct area and microvascular dysfunction, being sometimes lethal. Myocardial I/R injury involves several features that potentiate the final damage on the heart. Morphologically, I/R lesions presents contraction bands, karyolysis, disturbance of mitochondria, sarcolemma disruption, microvascular destruction, interstitial hemorrhage, and inflammation. Additionally, at reperfusion period an elevation in the production of reactive oxygen species (ROS) displays important roles for the I/R injury extent. The respiratory chain and NADPH oxidases of the NOX family are major sources of ROS that trigger the opening of mitochondrial permeability pore, causing irreversible damage to the cardiomyocytes. Usually, the rupture of atheroma and partial or complete obstruction of an epicardial coronary artery is followed by spontaneous or interventional reperfusion. However, reperfusion sometimes may not occur. Thus, we might realize that these burdens of factors augment the final infarct size and that it is complicated to recapitulate them by using animal models considering the vast anatomic and physiological differences from the human scenario. Nevertheless, most of the current knowledge about I/R-induced myocardial damage is derived from experimental studies in animals and rodent models of I/R injury can help to clarify potential pathophysiological mechanisms and identify new targets to treat this clinical condition. In this context, rat models of myocardial infarct and I/R injury have been instigating the pre-clinical research field to establish the therapeutic potential of natural agents in innumerous diseases. The antioxidant effect observed in some plant components might be useful for proposing their applicability to induce cardioprotection, and this characteristic could be, in part, proven by administrating natural products, for example, in rats with experimentally induced cardiac injury.