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Following isovolemic hemodilution (AIH), lowering blood viscosity induces acceleration of erythrocyte velocity resulting in improved tissue oxygen delivery. Using a rat model of myocardial infarct, we tested the hypothesis that AIH would attenuate myocardial damage due to transient coronary occlusion.Prospective, randomized, and controlled animal study.Animal research laboratory in a university hospital.Male Sprague-Dawley rats.All rats were subjected to 30 mins of left coronary artery occlusion followed by 48 hrs of reperfusion. Before the ischemic period, the anesthetized rats were randomly allocated to undergo either 15 mins of waiting (controls) or AIH to achieve a hematocrit of 30% (AIH-CO) by stepwise blood withdrawal and isovolemic compensation with 6% hydroxyethylstarch 200–0.5.Hemodynamic variables were comparable in the two groups, except for higher indexes of stroke volume in the AIH-CO group. During coronary occlusion and the reperfusion period, AIH resulted in a lower incidence of fatal ventricular tachyarrhythmia (17% vs. 50% in control group, p < .05) and higher survival at 48 hrs of postreperfusion (83% vs. 42%, p < .05).Preischemic hemodilution significantly attenuated myocardial damage as shown by lower release of cardiac troponin I and reduction in myocardial infarct size as measured by tetrazolin staining. Histologic examination revealed no difference regarding peri-ischemic infiltration with neutrophil granulocytes.Our data provide the first experimental demonstration that preischemic moderate AIH confers cardioprotection and improves survival in a rat model of myocardial infarct.