BACKGROUND: The aim of the present study is to assess the role of endogenous oxytocin (OT) in cardioprotective effects of ischemic preconditioning (IPC) in anesthetized rat. MATERIALS AND METHODS: Animals were divided into five groups: 1) ischemia-reperfusion (IR); (n=6), hearts were subjected to 25 min regional ischemia and 60 min reperfusion, 2) OT; (n=6), oxytocin was administered (0.03 μg/kg i.p) 10 min prior to ischemia, 3) IPC; (n=7), IPC was induced via a 5 min regional ischemia followed by 5 min of reperfusion before IR, 4) IPC+ATO (Atosiban); (n=6), atosiban (1.5 μg/kg i.p) was used as OT receptor selective antagonist in the beginning of IPC and 5) IR+ATO; (n=6), atosiban was injected 10 min prior to ischemia-reperfusion. RESULTS: In our experiment, Infarct size was decreased significantly in OT and IPC groups compared to IR (23 ± 1.5% and 19 ± 0.6% vs. 45 ± 2.9% in IR group, P<0.05). Administration of atosiban in IPC+ATO group increased infarct size to 39 ± 0.9% in comparison with OT and IPC groups (P<0.05). The use of OT and IPC prior to ischemia significantly declined ventricular arrhythmias severity in compared to IR group (1.2 ± 0.4 and 1 ± 0.5 respectively, vs. 4 ± 0.4 in IR group, P<0.05). Blockade of OT receptor by atosiban abolished the cardiopreconditioning effects of IPC. CONCLUSION: This study shows that, in part, the cardioprotective effects of IPC can be induced by endogenous OT.
BACKGROUND: The aim of the present study is to assess the role of endogenous oxytocin (OT) in cardioprotective effects of ischemic preconditioning (IPC) in anesthetized rat. MATERIALS AND METHODS: Animals were divided into five groups: 1) ischemia-reperfusion (IR); (n=6), hearts were subjected to 25 min regional ischemia and 60 min reperfusion, 2) OT; (n=6), oxytocin was administered (0.03 μg/kg i.p) 10 min prior to ischemia, 3) IPC; (n=7), IPC was induced via a 5 min regional ischemia followed by 5 min of reperfusion before IR, 4) IPC+ATO (Atosiban); (n=6), atosiban (1.5 μg/kg i.p) was used as OT receptor selective antagonist in the beginning of IPC and 5) IR+ATO; (n=6), atosiban was injected 10 min prior to ischemia-reperfusion. RESULTS: In our experiment, Infarct size was decreased significantly in OT and IPC groups compared to IR (23 ± 1.5% and 19 ± 0.6% vs. 45 ± 2.9% in IR group, P<0.05). Administration of atosiban in IPC+ATO group increased infarct size to 39 ± 0.9% in comparison with OT and IPC groups (P<0.05). The use of OT and IPC prior to ischemia significantly declined ventricular arrhythmias severity in compared to IR group (1.2 ± 0.4 and 1 ± 0.5 respectively, vs. 4 ± 0.4 in IR group, P<0.05). Blockade of OT receptor by atosiban abolished the cardiopreconditioning effects of IPC. CONCLUSION: This study shows that, in part, the cardioprotective effects of IPC can be induced by endogenous OT.
Authors: Tamara Merz; Britta Lukaschewski; Daniela Wigger; Aileen Rupprecht; Martin Wepler; Michael Gröger; Clair Hartmann; Matthew Whiteman; Csaba Szabo; Rui Wang; Christiane Waller; Peter Radermacher; Oscar McCook Journal: Intensive Care Med Exp Date: 2018-10-19