[The biochemical and cellular bases of myocardial ischemia-reperfusion damage]

In recent years evidence has accumulated indicating a possible myocardial injury secondary to reperfusion. However, it is not exactly known whether injury, at the time of reperfusion, merely represents an acceleration of the damage resulting from ischemia, or whether there is a specific additional injury caused by reperfusion itself. Some pathological events have been associated to reperfusion such as reperfusion arrhythmias, stunning myocardium and vascular damage with no reflow. In this review we discuss the hypotheses that explain the cellular events involved in reperfusion damage: calcium overload, free radical damage and others; also we describe both the experimental models commonly used and drugs assayed in recent years to lower the intensity of this phenomenon.