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Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart

BACKGROUND: Remote preconditioning is a phenomenon in which brief episodes of ischemia and reperfusion to remote organs protect the target organ against sustained ischemia/reperfusion (I/R)-induced injury. Protective effects of remote aortic preconditioning (RAPC) are well established in the heart,...

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Autores principales: Taliyan, Rajeev, Singh, Manjeet, Sharma, Pyare Lal, Yadav, Harlokesh Narayan, Sidhu, Kulwinder Singh
Formato: Texto
Lenguaje:English
Publicado: Medknow Publications 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982203/
https://www.ncbi.nlm.nih.gov/pubmed/21187869
http://dx.doi.org/10.4103/0975-3583.70917
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author Taliyan, Rajeev
Singh, Manjeet
Sharma, Pyare Lal
Yadav, Harlokesh Narayan
Sidhu, Kulwinder Singh
author_facet Taliyan, Rajeev
Singh, Manjeet
Sharma, Pyare Lal
Yadav, Harlokesh Narayan
Sidhu, Kulwinder Singh
author_sort Taliyan, Rajeev
collection PubMed
description BACKGROUND: Remote preconditioning is a phenomenon in which brief episodes of ischemia and reperfusion to remote organs protect the target organ against sustained ischemia/reperfusion (I/R)-induced injury. Protective effects of remote aortic preconditioning (RAPC) are well established in the heart, but their mechanisms still remain to be elucidated. OBJECTIVE: This study has been designed to investigate the possible involvement of α-1-adrenergic receptor (AR) and K(ATP) channels in cardio-protective effect of RAPC in isolated rat heart. MATERIALS AND METHODS: Four episodes of ischemia and reperfusion, each comprising of 5 min occlusion and 5 min reperfusion, were used to produce RAPC. Isolated perfused rat heart was subjected to global ischemia for 30 min followed by reperfusion for 120 min. Coronary effluent was analyzed for LDH and CK-MB release to assess the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. RESULTS: Phenylephrine (20 μ/kg i.p.), as α-1-AR agonist, was noted to produce RAPC-like cardio-protection. However, administration of glibenclamide concomitantly or prior to phenylephrine abolished cardioprotection. Moreover, prazocin (1 mg/kg. i.p), as α-1-AR antagonist and glibenclamide (1 mg/kg i.p), a K(ATP) channel blocker, abolished the cardioprotective effect of RAPC. CONCLUSION: These data provide the evidence that α-1-AR activation involved in cardioprotective effect of RAPC-mediated trough opening of K(ATP) channels.
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spelling pubmed-29822032010-12-23 Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart Taliyan, Rajeev Singh, Manjeet Sharma, Pyare Lal Yadav, Harlokesh Narayan Sidhu, Kulwinder Singh J Cardiovasc Dis Res Original Paper BACKGROUND: Remote preconditioning is a phenomenon in which brief episodes of ischemia and reperfusion to remote organs protect the target organ against sustained ischemia/reperfusion (I/R)-induced injury. Protective effects of remote aortic preconditioning (RAPC) are well established in the heart, but their mechanisms still remain to be elucidated. OBJECTIVE: This study has been designed to investigate the possible involvement of α-1-adrenergic receptor (AR) and K(ATP) channels in cardio-protective effect of RAPC in isolated rat heart. MATERIALS AND METHODS: Four episodes of ischemia and reperfusion, each comprising of 5 min occlusion and 5 min reperfusion, were used to produce RAPC. Isolated perfused rat heart was subjected to global ischemia for 30 min followed by reperfusion for 120 min. Coronary effluent was analyzed for LDH and CK-MB release to assess the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. RESULTS: Phenylephrine (20 μ/kg i.p.), as α-1-AR agonist, was noted to produce RAPC-like cardio-protection. However, administration of glibenclamide concomitantly or prior to phenylephrine abolished cardioprotection. Moreover, prazocin (1 mg/kg. i.p), as α-1-AR antagonist and glibenclamide (1 mg/kg i.p), a K(ATP) channel blocker, abolished the cardioprotective effect of RAPC. CONCLUSION: These data provide the evidence that α-1-AR activation involved in cardioprotective effect of RAPC-mediated trough opening of K(ATP) channels. Medknow Publications 2010 /pmc/articles/PMC2982203/ /pubmed/21187869 http://dx.doi.org/10.4103/0975-3583.70917 Text en © Journal of Cardiovascular Disease Research http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Paper
Taliyan, Rajeev
Singh, Manjeet
Sharma, Pyare Lal
Yadav, Harlokesh Narayan
Sidhu, Kulwinder Singh
Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
title Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
title_full Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
title_fullStr Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
title_full_unstemmed Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
title_short Possible involvement of α1-adrenergic receptor and K(ATP) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
title_sort possible involvement of α1-adrenergic receptor and k(atp) channels in cardioprotective effect of remote aortic preconditioning in isolated rat heart
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982203/
https://www.ncbi.nlm.nih.gov/pubmed/21187869
http://dx.doi.org/10.4103/0975-3583.70917
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