Pharmacological reduction of infarct size : in search for a drug that mimics ischemic preconditioning

In the late 1960s, when the high mortality of myocardial infarction had caused a high level of public awareuess, the National Institutes of Health, USA, decided to fund projects directly related to the experimental treatment of infarcts, to develop animal models best suited to study infarct size after coronary occlusion, and to develop quantitative methods in animals and in man to measure infarcts. Many drugs, natural compounds, and physical methods were tested in the early phase of pragmatism and only a few forms of therapy met expectations when the measurements of infarct size became more precise. The most effective of these interventions, which is potentially able to reduce infarct size when applied within a certain window of time, is reperfusion. 1 In the initiated basic pathophysiological studies two major determinant factors of the progression of infarct size had been identified, the myocardial oxygen consumption during coronary occlusion and the amount of collateral blood flow. 2 But although drugs were found able to effectively reduce myocardial oxygen consumption, their infarct size reducing properties remained limited since they were depending on the reperfusion of the ischemic myocardium.

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