Selective endothelin a (ETA) receptor antagonist (BQ-123) reduces both myocardial infarct size and oxidant injury

Basit Öğe Kaydı
dc.authoridParlakpınar, Hakan/0000-0001-9497-3468
dc.authoridParlakpinar, Hakan/0000-0001-9497-3468
dc.authoridAcet, Ahmet/0000-0003-1131-1878
dc.authoridÇOLAK, CEMİL/0000-0001-5406-098X
dc.authoridPolat, Alaadin/0000-0002-6920-3856
dc.authorwosidErmis, Necip/A-5184-2018
dc.authorwosidParlakpınar, Hakan/T-6517-2018
dc.authorwosidParlakpinar, Hakan/V-6637-2019
dc.authorwosidAcet, Ahmet/AAB-3273-2021
dc.authorwosidErmis, Necip/HJP-7061-2023
dc.authorwosidÖZDEMIR, RENK/I-9560-2013
dc.authorwosidÇOLAK, CEMİL/ABI-3261-2020
dc.contributor.authorOzdemir, R
dc.contributor.authorParlakpinar, H
dc.contributor.authorPolat, A
dc.contributor.authorColak, C
dc.contributor.authorErmis, N
dc.contributor.authorAcet, A
dc.date.accessioned2024-08-04T20:15:12Z
dc.date.available2024-08-04T20:15:12Z
dc.date.issued2006
dc.departmentİnönü Üniversitesien_US
dc.description.abstractObjective: Endothelins (ET) can be considered stress-responsive regulators working in paracrine and autocrine fashion. It has been suggested that elevated levels of ET may be responsible for the low coronary re-flow phenomena. Ischemia-reperfusion (I/R) was shown to stimulate ET release in rat heart; however, the mechanism(s) of this effect has not been clarified. Therefore, this study was focused to investigate the effect of BQ-123, selective ETA receptor antagonist, on three aspects of myocardial ischemia-reperfusion (MI/R) injury: hemodynamic parameters, infarct size and oxidant-antioxidant status in the absence and presence of ET-1 in an vivo rat model. Methods and results: To produce MI/R, a branch of the descending left coronary artery was occluded for 30 min followed by 2 h reperfusion. ECG changes, blood pressure (BP), and heart rate (HR) were measured before occlusion and continued both occlusion and reperfusion. Forty rats were randomly assigned to five groups equally: (1) sham-operated rats without coronary ligation, (2) I/R group, (3) I/R + BQ-123-treated group (10 mu g/kg/min i.v.), (4) I/R + ET-treated group (25 ng/kg/min i.v.), (5) I/R + ET + BQ-123-treated group. The results are expressed as mean +/- S.E.M. In the ET-1 plus I/R group, the ratio between the infarcted area and area at risk 56 +/- 1% was significantly higher than I/R group (49 +/- 1%). In the BQ-123 group with or without exogenous ET-1 treatment in I/R group, this ratio was significantly lower at 40 +/- 2 and 37 +/- 1%, respectively. As compared to sham group, I/R increased lipid peroxidation whereas decreased nitric oxide (NO), glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) contents. This decreased antioxidant enzymatic defense could result in aggravated oxidative damage in I/R group rat hearts. ET-1 administration group showed severe oxidative damage. BQ-123 administrations to I/R group with or without ET-1 caused significantly decrease in lipid peroxidation and increased in SOD, CAT activities and NO generation and GSH content when compared with I/R group alone. Conclusions: The most important finding of the present study is that the ET blockade reduced I/R-induced myocardial injury. The mechanism of this reduction was speculated to be a resistance to ischemic injury in the subcellular levels of the myocardium conferred by a reduction of vascular constriction and improvement of imbalance in the antioxidant status. (c) 2005 Elsevier Ireland Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.tox.2005.11.022
dc.identifier.endpage149en_US
dc.identifier.issn0300-483X
dc.identifier.issn1879-3185
dc.identifier.issue1-3en_US
dc.identifier.pmid16406210en_US
dc.identifier.scopus2-s2.0-31044447786en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage142en_US
dc.identifier.urihttps://doi.org/10.1016/j.tox.2005.11.022
dc.identifier.urihttps://hdl.handle.net/11616/94234
dc.identifier.volume219en_US
dc.identifier.wosWOS:000235299700015en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Ireland Ltden_US
dc.relation.ispartofToxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectETA receptor antagonist (BQ-123)en_US
dc.subjectendothelinen_US
dc.subjectNOen_US
dc.subjectreactive oxygen radicalsen_US
dc.subjectraten_US
dc.titleSelective endothelin a (ETA) receptor antagonist (BQ-123) reduces both myocardial infarct size and oxidant injuryen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu