Aims: 

Previous studies demonstrated the contribution of reactive oxygen species (ROS) produced by monoaminooxidases (MAO) to myocardial injury caused by post-ischaemic reperfusion and the protective effects afforded by irreversible MAO inhibitors. The present study was aimed at characterizing the effects of a reversible MAO-A inhibitor, moclobemid (Mocl), in the in vivo rat model of regional ischaemia.

Methods: 

Anesthetized rats subjected to 30 min ischaemia by coronary ligation and 2 h reperfusion were randomized to receive: (i) no additional interventions (Ctrl), (ii) acute administration of 4 mg/kg Mocl IV 15 minutes before ischaemia (MoclAc) and (iii) chronic administration of 4 mg/kg IP, daily for 3 weeks (MoclChr). Occurrence of arrhythmias (ventricular premature beats, VPBs; ventricular tachycardia, VT and ventricular fibrillation, VF) was assessed along with of infarct size measurement by means of triphenyltetrazolium chloride staining.

Results: 

Myocardial injury expressed as the percent of infarct to risk area ratio (I/R%) was significantly reduced by both acute and chronic Mocl treatment (1.43 ± 0.9%, 6.37 ± 2.6% and 32.19 ± 1.6% in MoclAc, MoclChr and Ctrl groups, respectively; mean ± SEM; p < 0.05). In addition, no arrhythmias were observed in MoclAc group (arrhythmia score 0), whereas < 30 VPBs (arrhythmia score 1) appeared during ischaemia in MoclChr group as compared to arrhythmia scores of 2 (>30 VPBs) and 3 (< three episodes of VF/VT) seen in controls.

Conclusion: 

Both acute and chronic administration of Mocl elicited remarkable cardioprotection detected as reduction of infarct size and arrhythmogenicity caused by regional ischaemia-reperfusion in rat hearts.