This experimental study was planned to clarify whether diflouromethyl ornithine (DFMO), a suicidal inhibitor of ornithine decarboxylase, may reduce the injury of global ischemia after cardioplegic arrest in isolated rat hearts. In the first experimental group, the hearts were pretreated with DFMO-enriched Tyrode solution for five minutes before cardioplegic arrest. In the second experimental group, DFMO was added to the St. Thomas Hospital cardioplegic solution and in the last group it was applied in the first five minutes of reperfusion. In the first and second experimental groups, we did not see any advantage to adding DFMO. But in the last group, in which DFMO was applied in the reperfusion period, the hearts showed better contractility than the control group (8.8±1.1 g contractility/g heart weight versus 13.9±1.1, respectively, in the 10th minute of reperfusion). Creatinin kinase (124.5±13.2 IU/min-g heart versus 179.9±16.4 respectively) and lactate dehydrogenase (160.0±11.0 IU/min-g heart versus 193.3±11.8 respectively) levels were significantly lower in this group. The results of this experimental study show the importance of blockage of the ornithine decarboxylase in decreasing of myocardial injury after cardioplegic arrest. These preliminary results show that polyamines might play a role in reperfusion injury.