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

Ozdemir R., Parlakpinar H., Polat A., ÇOLAK C., ERMİŞ N., Acet A.

TOXICOLOGY, vol.219, pp.142-149, 2006 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 219
  • Publication Date: 2006
  • Doi Number: 10.1016/j.tox.2005.11.022
  • Journal Name: TOXICOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.142-149
  • Keywords: ETA receptor antagonist (BQ-123), endothelin, NO, reactive oxygen radicals, rat, ISCHEMIA-REPERFUSION INJURY, NITRIC-OXIDE, DYSFUNCTION, MELATONIN, BLOOD, MODEL, RATS
  • Bezmialem Vakıf University Affiliated: Yes


Objective: 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.