Reperfusion of post-ischemic myocardium is accompanied by induction of hypertrophic and pro-apoptotic signaling pathways. The ODC/polyamine system might be involved in these processes. This study investigates the role of the ODC in regard to myocardial function, pro-hypertrophic and pro-apoptotic gene expression. Isolated, perfused hearts (n=48, normotensive wistar rats) were subjected to 45 min no-flow ischemia - 120 min reperfusion and divided into six groups: normoxie (Nx), ischemia (Isch), Nx+DFMO (DFMO=Difluoromethylornithine, Inhibitor of ODC), Isch+DFMO, Nx+DFMO+Put (Put=Putrescine, end- product of ODC) and Isch+DFMO+Put. Myocardial function was evaluated by continuous assessment of LVDP; the expression of pro-hypertrophic genes (ANF, ODC), anti-apoptotic genes (bcl-2, bcl-xl) and pro-apototic genes (bax) was detected by real time RT- PCR. There were no significant differences in the recovery of LVDP between DFMO and Put. The expression of ANF in the post-ischemic myocardium was increased; expression of other studied genes was unchanged or decreased. Inhibition of the ODC caused an increase of bcl-2 expression and diminished the expression of bax. Put intensified the expression of bcl-2 and bcl- xl and normalized the bax expression. Activation of the ODC in the post-ischemic myocardium leads to an pro-apoptotic process whereas inhibition of ODC abolished these effects.