title: The administration of oxytocin during early reperfusion, dose-dependently protects the isolated male rat heart against ischemia/reperfusion injury.
abstract: In our previous study, the administration of oxytocin (OT) could precondition the heart against ischemia/reperfusion injury. In this study, to investigate the cardiac postconditioning effect of oxytocin, isolated rat hearts were mounted on a Langendorff perfusion apparatus. In all groups, the hearts underwent 30 min of regional ischemia followed by 120 min of reperfusion. In the ischemia/reperfusion (IR) group, ischemia and reperfusion was induced. In the ischemic postconditioning (Ipost) group, hearts underwent 6 cycles of 10s reperfusion and 10s ischemia at the beginning of reperfusion. In the other groups (III-IX), OT was perfused 5 min before the onset of reperfusion and continued for 25 min with following doses (Molar): 10(-12), 5 × 10(-12), 8 × 10(-12), 10(-11), 2 × 10(-11), 5 × 10(-11), and 10(-10). The infarct size and coronary effluent levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and malondialdehyde (MDA) were calculated at the end of reperfusion. The infarct size decreased considerably in Ipost group compared to IR group (P<0.05). Also, the infusion of oxytocin by doses of 8 × 10(-12)M, 10(-11)M and 2 × 10(-11)M dose-dependently reduced infarct size (P<0.05) significantly compared to the IR group. LDH level in coronary effluent was markedly decreased in Ipost group and treatment with oxytocin by doses of 8 × 10(-12)M, 10(-11)M, 2 × 10(-11)M and 5 × 10(-11)M (P<0.05) compared to IR group. Ipost, OT 2 × 10(-11)and 10(-11)M significantly decreased CK-MB level (P<0.05). Ipost, OT 8 × 10(-12), 10(-11) and 2 × 10(-11)M significantly decreased MDA level as compared to IR group. Our study shows that oxytocin dose-dependently exerts cardiac postconditioning.
authors.affiliation: Department of physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: Masood Aali
authors.initials: MA
authors.lastname: Anvari
authors.forename: Alireza
authors.initials: A
authors.lastname: Imani
authors.forename: Mahdieh
authors.initials: M
authors.lastname: Faghihi
authors.forename: Seyed Morteza
authors.initials: SM
authors.lastname: Karimian
authors.forename: Maryam
authors.initials: M
authors.lastname: Moghimian
authors.forename: Maryam
authors.initials: M
authors.lastname: Khansari
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D066298:In Vitro Techniques; D057775:Ischemic Postconditioning / Q000379:methods*; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000009:adverse effects*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D010121:Oxytocin / Q000008:administration & dosage* / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D012306:Risk; D013997:Time Factors
chemical_list: D010121:Oxytocin