• Eulo Lupi Herrera, Jorge Gaspar, Héctor González Pacheco, Carlos Martínez Sánchez, Gustavo Pastelín Hernández, Pastor Luna Ortiz, and Edmundo Chávez Cosio.
• Del Instituto Nacional de Cardiologia "lgnacio Chávez", México, D.F.
• Arch Cardiol Mex. 2006 Oct 1;76 Suppl 4:S76-101.

AbstractAfter prolonged periods of ischemia and energy depletion, the ischemic myocardial cell can be jeopardized by specific causes within the reperfusion period. These causes can be viewed as unwanted aspects of the recovery process itself limiting its efficiency. Three potential initial causes of immediate reperfusion injury, aside from oxygen radicals, have been experimentally investigated in detail, and are briefly discussed: 1. re-energization; 2. rapid normalization of tissue pH; and 3. rapid normalization of tissue osmolality. These potential causes are not entirely independent. Understanding of the basic causes has opened novel perspectives for specific interference with these serious pathomechanisms. The experimental results obtained in the last years encourage the development of therapeutic approaches to reduce infarct size by specific measures applied during the early phase of reperfusion. In the clinical setting, reperfusion therapy for acute myocardial infarction (AMI) has shown to reduce mortality, yet it may also have deleterious effects, including myocardial necrosis and no-reflow. Almost two decades ago, great hope arose from the description of ischemic preconditioning. Unfortunately, ischemic preconditioning is not feasible in the clinical practice because the coronary artery is already occluded at the time of hospital admission of the AMI patient. Recently, in the dog model, a phenomenon called "postconditioning" has been described. It has been reported previouly that reperfusion injury can be significantly reduced by modifying the conditions and the composition of the initial reperfusate. Whereas preconditioning is triggered by brief episodes of ischemia-reperfusion performed just before a prolonged coronary artery occlusion, postconditioning is induced by a comparable sequence of reversible ischemia-reperfusion, but it is applied "just after the prolonged" ischemic insult. Protection afforded by postconditioning is as potent as that provided by preconditioning. Unlike preconditioning, the experimental design of postconditioning allows direct application in the clinical practice, especially during PTCA. It has been reported very recently, that postconditioning patients with ST segment elevation AMI, during coronary angioplasty protects the human heart in this clinical scenario. Obtaining such a beneficial effect by a simple manipulation of reperfusion is of major potential clinical interest. Now more than ever, mechanistic and pharmacological research in the field of reperfusion injury appears to be necessary and clinically relevant.

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