Protective effect of ACE inhibitors on ischemia-reperfusion-induced arrhythmias in rats: Is this effect related to the free radical scavenging action of these drugs?

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dc.authoridAcet, Ahmet/0000-0003-1131-1878
dc.authorwosidAcet, Ahmet/AAB-3273-2021
dc.contributor.authorBirincioglu, M
dc.contributor.authorAksoy, T
dc.contributor.authorOlmez, E
dc.contributor.authorAcet, A
dc.date.accessioned2024-08-04T20:11:57Z
dc.date.available2024-08-04T20:11:57Z
dc.date.issued1997
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThe antiarrhythmic effects of captopril, a sulphydryl-containing angiotensin converting enzyme (ACE) inhibitor, were compared with those of the non-sulphydryl-containing ACE inhibitor Lisinopril and the sulphydryl-containing agent glutathione in an in vivo rat model of coronary artery ligation. 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 lisinopril (0.1, 0.3 or 1 mg kg(-1)) caused marked decreases in mean arterial blood pressure (BP) and heart rate, whereas glutathione (5 mg kg(-1)) had no effect on them. The incidence of ventricular tachycardia (VT) on ischemia and reperfusion was significantly reduced by captopril and lisinopril. Captopril and 1 mg kg(-1) lisinopril also significantly decreased the number of VEB during occlusion and the duration of VT on reperfusion, respectively. These drugs also attenuated the incidence of reversible ventricular fibrillation (VF) and the number of ventricular ectopic beats (VEB) during reperfusion. However, glutathione only reduced the incidence of VT on reperfusion, significantly. These results suggest that, in this experimental model, ACE inhibitors limit the arrhythmias following ischemia-reperfusion and free radical scavenging action of these drugs does not have a major contributory role in their protective effect.en_US
dc.identifier.doi10.3109/10715769709065778
dc.identifier.endpage396en_US
dc.identifier.issn1071-5762
dc.identifier.issue4en_US
dc.identifier.pmid9416467en_US
dc.identifier.scopus2-s2.0-0031474585en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage389en_US
dc.identifier.urihttps://doi.org/10.3109/10715769709065778
dc.identifier.urihttps://hdl.handle.net/11616/93098
dc.identifier.volume27en_US
dc.identifier.wosWOS:A1997YK11600006en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherHarwood Acad Publ Gmbhen_US
dc.relation.ispartofFree Radical 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.subjectfree radicalsen_US
dc.subjectrat hearten_US
dc.titleProtective effect of ACE inhibitors on ischemia-reperfusion-induced arrhythmias in rats: Is this effect related to the free radical scavenging action of these drugs?en_US
dc.typeArticleen_US

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