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

OZDEMIR R., PARLAKPINAR H., POLAT A., Colak C., ERMIS N., ACET A.

TOXICOLOGY, cilt.219, ss.142-149, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 219
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1016/j.tox.2005.11.022
  • Dergi Adı: TOXICOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.142-149
  • Anahtar Kelimeler: ETA receptor antagonist (BQ-123), endothelin, NO, reactive oxygen radicals, rat, ISCHEMIA-REPERFUSION INJURY, NITRIC-OXIDE, DYSFUNCTION, MELATONIN, BLOOD, MODEL, RATS
  • İnönü Üniversitesi Adresli: Evet

Özet

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.