title: Role of central oxytocin in stress-induced cardioprotection in ischemic-reperfused heart model.
abstract: OBJECTIVE
  There is growing evidence that stress contributes to cardiovascular disease and triggers the release of oxytocin. Moreover previous studies confirmed oxytocin mimics the protection associated with ischemic preconditioning. The present study was aimed to assess the possible cardioprotective effects of the centrally released oxytocin in response to stress and intracerebroventricular (i.c.v.) administration of exogenous oxytocin in ischemic-reperfused isolated rat heart.
  
  
  METHODS
  Rats were divided in two main groups and all of them were subjected to i.c.v. infusion of vehicle or drugs: unstressed rats [control: vehicle, oxytocin (OT; 100 ng/5 μl), atosiban (ATO; 4.3 μg/5 μl) as oxytocin antagonist, ATO+OT] and stressed rats [St: stress, OT+St, ATO+St]. After anesthesia, hearts were isolated and subjected to 30 min regional ischemia and 60 min reperfusion (IR). Acute stress protocol included swimming for 10 min before anesthesia. Myocardial function, infarct size, coronary flow, ventricular arrhythmia, and biochemical parameters such as creatine kinase and lactate dehydrogenase were measured. Ischemia-induced ventricular arrhythmias were counted during the occlusion period.
  
  
  RESULTS
  The plasma levels of oxytocin and corticosterone were significantly elevated by stress. Unexpectedly hearts of stressed rats showed a marked depression of IR injury compared to control group. I.c.v. infusion of oxytocin mimicked the cardioprotective effects of stress, yet did not elevate plasma oxytocin level. The protective effects of both stress and i.c.v. oxytocin were blocked by i.c.v. oxytocin antagonist.
  
  
  CONCLUSIONS
  These findings suggest that i.c.v. infusion of exogenous oxytocin and centrally released endogenous oxytocin in response to stress could play a role in induction of a preconditioning effect in ischemic-reperfused rat heart via brain receptors.
authors.affiliation: Department of Physiology, School of Medicine, Gonabad University of Medical Science, Gonabad, Islamic Republic of Iran.
authors.forename: Maryam
authors.initials: M
authors.lastname: Moghimian
authors.forename: Mahdieh
authors.initials: M
authors.lastname: Faghihi
authors.forename: Seyed Morteza
authors.initials: SM
authors.lastname: Karimian
authors.forename: AliReza
authors.initials: A
authors.lastname: Imani
authors.forename: Fariba
authors.initials: F
authors.lastname: Houshmand
authors.forename: Yaser
authors.initials: Y
authors.lastname: Azizi
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D002316:Cardiotonic Agents / Q000008:administration & dosage*; D004195:Disease Models, Animal; D066298:In Vitro Techniques; D007276:Injections, Intraventricular; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D010121:Oxytocin / Q000008:administration & dosage* / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D018045:Receptors, Oxytocin / Q000378:metabolism; D013312:Stress, Physiological / Q000502:physiology*; D013315:Stress, Psychological / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D002316:Cardiotonic Agents; D018045:Receptors, Oxytocin; D010121:Oxytocin