Ischemic Preconditioning: Only a Laboratory Finding?

pp 571-578

Abstract

In1986, Murry et al. defined ischemic precondition-ing UP) as a rapid adaptive response to repetitive brief ischemic insults which slow the rate of cell death during a subsequent prolonged ischemia. Since then preconditioning have been achieved in multiple species and with multiple protocols.

There is no question that IP limits infarct size and that probably its benefits may be extended on other deleterious effects associated with ischemic/reperfusion such as prolonged post ischemic dysfunction (myocardial stunning), reperfusion induced arrhythmias and loss of vasodilator reserve of coronary vessels. Preconditioning is not explained by an increase of collateral perfusion and it is not a consequence of myocardial stunning. A metabolic mechanism is proposed as an explanation. Activation of adenosine receptors (Al), presumable by adenosine released during the brief ischemia, is the most attractive hypothesis to explain the reduction in infarction size.Another hypothesis proposed is the opening of ATP sensitive K channels. Authors agree that acute protection is not due to the synthesis of cardio protective proteins but that these proteins induced by brief ischemia may afford a second window of protection.No universal explanation has been provided including all protective effects and all animal species studied.The clinical relevance of IP remains to be elucidated but there is some evidence that IP protection might occur in humans. Coronary angioplasty, preinfarction angina and coronary artery by-pass surgery have been proposed as clinical models to study this phenomenon.