Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins
Postconditioning is a simple and safe strategy for cardioprotection and infarct size limitation. Our previous study showed that oxytocin (OT) exerts postconditioning effect on ischemic/reperfused isolated rat heart. The aim of this study was to investigate the involvement of OT receptor, mitochondri...
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| Format: | Article |
| Language: | English |
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Tehran University of Medical Sciences
2015-10-01
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| Series: | Acta Medica Iranica |
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| Online Access: | https://acta.tums.ac.ir/index.php/acta/article/view/4275 |
| _version_ | 1818529163332550656 |
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| author | Alireza Imani Maryam Khansari Yaser Azizi Kamran Rakhshan Mahdieh Faghihi |
| author_facet | Alireza Imani Maryam Khansari Yaser Azizi Kamran Rakhshan Mahdieh Faghihi |
| author_sort | Alireza Imani |
| collection | DOAJ |
| description | Postconditioning is a simple and safe strategy for cardioprotection and infarct size limitation. Our previous study showed that oxytocin (OT) exerts postconditioning effect on ischemic/reperfused isolated rat heart. The aim of this study was to investigate the involvement of OT receptor, mitochondrial ATP-sensitive potassium channel (mKATP), nitric oxide (NO) and cyclooxygenase (COX) pathways in OT postconditioning. Isolated rat hearts were divided into10 groups and underwent 30 min of regional ischemia followed by 120 min of reperfusion (n =6). In I/R (ischemia/reperfusion) group, ischemia and reperfusion were induced without any treatment. In OT group, oxytocin was perfused 5 min prior to beginning of reperfusion for 25 min. In groups 3-6, atosiban (oxytocin receptor blocker), L-NAME (N-Nitro-L-Arginine Methyl Ester, non-specific nitric oxide synthase inhibitor), 5-HD (5-hydroxydecanoate, mKATP inhibitor) and indomethacin (cyclooxygenase inhibitor) were infused prior to oxytocin administration. In others, he mentioned inhibitors were perfused prior to ischemia without oxytocin infusion. Infarct size, ventricular hemodynamic, coronary effluent, malondialdehyde (MDA) and lactate dehydrogenase (LDH) were measured at the end of reperfusion. OT perfusion significantly reduced infarct size, MDA and LDH in comparison with IR group. Atosiban, 5HD, L-NAME and indomethacin abolished the postconditioning effect of OT. Perfusion of the inhibitors alone prior to ischemia had no effect on infarct size, hemodynamic parameters, coronaryeffluent and biochemical markers as compared with I/R group. In conclusion, this study indicates that postconditioning effects of OT are mediated by activation of mKATP and production of NO and Prostaglandins (PGs). |
| first_indexed | 2024-12-11T17:03:24Z |
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| issn | 0044-6025 1735-9694 |
| language | English |
| last_indexed | 2024-12-11T17:03:24Z |
| publishDate | 2015-10-01 |
| publisher | Tehran University of Medical Sciences |
| record_format | Article |
| series | Acta Medica Iranica |
| spelling | doaj.art-976069cd73724037a68a589df2f9a0052022-12-22T00:57:46ZengTehran University of Medical SciencesActa Medica Iranica0044-60251735-96942015-10-015384251Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and ProstaglandinsAlireza Imani0Maryam Khansari1Yaser Azizi2Kamran Rakhshan3Mahdieh Faghihi41Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.1Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.1Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.1Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.Postconditioning is a simple and safe strategy for cardioprotection and infarct size limitation. Our previous study showed that oxytocin (OT) exerts postconditioning effect on ischemic/reperfused isolated rat heart. The aim of this study was to investigate the involvement of OT receptor, mitochondrial ATP-sensitive potassium channel (mKATP), nitric oxide (NO) and cyclooxygenase (COX) pathways in OT postconditioning. Isolated rat hearts were divided into10 groups and underwent 30 min of regional ischemia followed by 120 min of reperfusion (n =6). In I/R (ischemia/reperfusion) group, ischemia and reperfusion were induced without any treatment. In OT group, oxytocin was perfused 5 min prior to beginning of reperfusion for 25 min. In groups 3-6, atosiban (oxytocin receptor blocker), L-NAME (N-Nitro-L-Arginine Methyl Ester, non-specific nitric oxide synthase inhibitor), 5-HD (5-hydroxydecanoate, mKATP inhibitor) and indomethacin (cyclooxygenase inhibitor) were infused prior to oxytocin administration. In others, he mentioned inhibitors were perfused prior to ischemia without oxytocin infusion. Infarct size, ventricular hemodynamic, coronary effluent, malondialdehyde (MDA) and lactate dehydrogenase (LDH) were measured at the end of reperfusion. OT perfusion significantly reduced infarct size, MDA and LDH in comparison with IR group. Atosiban, 5HD, L-NAME and indomethacin abolished the postconditioning effect of OT. Perfusion of the inhibitors alone prior to ischemia had no effect on infarct size, hemodynamic parameters, coronaryeffluent and biochemical markers as compared with I/R group. In conclusion, this study indicates that postconditioning effects of OT are mediated by activation of mKATP and production of NO and Prostaglandins (PGs).https://acta.tums.ac.ir/index.php/acta/article/view/4275OxytocinPostconditioningmKATPNOCyclooxygenaseIsolated heart |
| spellingShingle | Alireza Imani Maryam Khansari Yaser Azizi Kamran Rakhshan Mahdieh Faghihi Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins Acta Medica Iranica Oxytocin Postconditioning mKATP NO Cyclooxygenase Isolated heart |
| title | Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins |
| title_full | Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins |
| title_fullStr | Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins |
| title_full_unstemmed | Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins |
| title_short | Stimulation of Oxytocin Receptor during Early Reperfusion Period Protects the Heart against Ischemia/Reperfusion Injury: the Role of Mitochondrial ATPSensitive Potassium Channel, Nitric Oxide, and Prostaglandins |
| title_sort | stimulation of oxytocin receptor during early reperfusion period protects the heart against ischemia reperfusion injury the role of mitochondrial atpsensitive potassium channel nitric oxide and prostaglandins |
| topic | Oxytocin Postconditioning mKATP NO Cyclooxygenase Isolated heart |
| url | https://acta.tums.ac.ir/index.php/acta/article/view/4275 |
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