The role of prostaglandin synthesis stimulation in the protective effect of captopril on ischaemia-reperfusion arrhythmias in rats in vivo

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dc.authoridAcet, Ahmet/0000-0003-1131-1878
dc.authorwosidAcet, Ahmet/AAB-3273-2021
dc.contributor.authorBirincioglu, M
dc.contributor.authorOlmez, E
dc.contributor.authorAksoy, TA
dc.contributor.authorAcet, A
dc.date.accessioned2024-08-04T20:11:54Z
dc.date.available2024-08-04T20:11:54Z
dc.date.issued1997
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAttenuation of ischaemia-reperfusion induced arrhythmias by several angiotensin converting enzyme (ACE) inhibitors, such as captopril, has been demonstrated. The role of prostaglandin synthesis stimulation in this protective effect of ACE inhibition was evaluated in an in vivo rat model. To produce arrhythmia, the left main coronary artery was occluded for 7 min, followed by 7 min of reperfusion. Captopril (3 mg kg(-1)) and a prostaglandin synthesis inhibitor, indomethacin (2 mg kg(-1)) alone or together were administered by intravenous (i.v.) injection 10 min before occlusion. Captopril reduced the incidence of ventricular tachycardia (VT) and the number of ventricular ectopic beats (VEE) on ischaemia and reperfusion as well as the incidence of reversible ventricular fibrillation (VF) on reperfusion. These protective effects of captopril against ischaemia-reperfusion-induced arrhythmias were prevented by indomethacin. Captopril also caused a sustained decrease of preocclusion values in the arterial blood pressure (BP) and heart rate (HR), whereas in the presence of indomethacin, captopril had no significant effect on either HR or arterial BP values except the heart rate value just before occlusion. Indomethacin alone did not affect either the severity of arrhythmias or the haemodynamic parameters. These results suggest that, in this experimental model, the protective effects of ACE inhibitors on the arrhythmias following ischaemia-reperfusion are mediated by the stimulation of prostaglandin synthesis and the haemodynamic effects of these drugs may have a contributory role in their protective effect. (C) 1997 The Italian Pharmacological Society.en_US
dc.identifier.doi10.1006/phrs.1997.0232
dc.identifier.endpage304en_US
dc.identifier.issn1043-6618
dc.identifier.issue4en_US
dc.identifier.pmid9425619en_US
dc.identifier.scopus2-s2.0-0031258108en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage299en_US
dc.identifier.urihttps://doi.org/10.1006/phrs.1997.0232
dc.identifier.urihttps://hdl.handle.net/11616/93085
dc.identifier.volume36en_US
dc.identifier.wosWOS:A1997YK19800007en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAcademic Press Ltden_US
dc.relation.ispartofPharmacological Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectACE inhibitionen_US
dc.subjectreperfusion arrhythmiasen_US
dc.subjectprostaglandin synthesisen_US
dc.titleThe role of prostaglandin synthesis stimulation in the protective effect of captopril on ischaemia-reperfusion arrhythmias in rats in vivoen_US
dc.typeArticleen_US

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