Mechanism of action of oxytocin as cardioprotection in rat model of myocardial infarction

Oxytocin (OT) is well known for its role in reproduction. However, evidence has emerged suggesting a role in cardiovascular system but less is known about the role of this hormone in the injured heart. We elucidate oxytocin cardioprotective effects against myocardial infarction (MI). Male rats were divided into six groups: control without surgery, sham without occlusion, MI, OT pretreated then MI, combined OT and LNAME (NO synthase inhibitor) then MI and combined OT and indomethacin (cyclooxygenase blocker) then MI. Twenty-four hours post-MI induction, hemodynamics parameters, inflammation markers, oxidative stress markers, apoptotic gene expression, brain naturitic peptide (BNP), and histopathological assessment were carried out. When compared to MI model group, OT significantly reduced LVEDP and increased LVSP and ± dP/dt.Also, it significantly decreased serum levels of BNP, TNF-α, IL-6, and TBARS with an increase in the activities of SOD and GPx. Furthermore, BAX and p53 mRNA were decreased. Interestingly, no significant improvement in any of the markers was detectable when we administrated OT with L-NAME. While the same results observed when we treated the rat with OT and indomethacin. We conclude that OT protected against the sequelae of myocardial infarction. These findings provide new insight into therapeutic strategies for myocardial infarction.