It was reported that N,N,N'N'-tetrakis-[2-pyridylmethyl]-ethylenediamine (TPEN), a transition metal chelator, confers cardioprotection against myocardial ischemic injury. In this study, we investigated the effect of TPEN targeting reperfusion period in isolated rat hearts.

Langendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. Hearts were randomly assigned to either control (n = 9) or 10 µM of TPEN (n = 8) groups. TPEN was perfused for a period of 5 min before and 30 min after reperfusion.

The ratio of infarct area/ischemic area (AN/AR) was significantly reduced in TPEN treated hearts (6.9 ± 1.7%, P < 0.001) compared to control hearts (29.5 ± 3.2%). Recovery of left ventricular developed pressure (LVDP), rate-pressure product (RPP), +dP/dt_max, and -dP/dt_min in the control group after reperfusion were 53.8 ± 6.2%, 51.0 ± 6.3%, 51.9 ± 5.7%, and 51.4 ± 5.7%, respectively, of the baseline levels. In the TPEN group, LVDP, RPP, +dP/dt_max, and -dP/dt_min returned to 58.5 ± 4.6%, 54.8 ± 6.4%, 61.7 ± 4.9%, and 53.4 ± 3.9%, respectively, of the baseline levels. There were no significant differences in the cardiodynamic variables between the two groups (P > 0.05).

Pharmacological postconditioning with TPEN reduces myocardial infarction however, TPEN does not modify post-ischemic systolic dysfunction in isolated rat hearts.