Does ischemic preconditioning increase flap survival by ADORA2B receptor activation?

ÜLKER P., ÖZKAN Ö., Amoroso M., AYDIN ASLAN M., Bassorgun I., Ubur M. C., ...Daha Fazla

CLINICAL HEMORHEOLOGY AND MICROCIRCULATION, cilt.75, sa.2, ss.151-162, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 75 Sayı: 2
  • Basım Tarihi: 2020
  • Doi Numarası: 10.3233/ch-190730
  • Dergi Adı: CLINICAL HEMORHEOLOGY AND MICROCIRCULATION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.151-162
  • Anahtar Kelimeler: Adenosine, ADORA 2B, ischemia, reperfusion, flap survival, ACUTE KIDNEY INJURY, ECTO-5'-NUCLEOTIDASE CD73, ADENOSINE RECEPTORS, SIGNALING PROTECTS, BLOOD-FLOW, RECONSTRUCTION, POLYDEOXYRIBONUCLEOTIDE
  • Akdeniz Üniversitesi Adresli: Evet

Özet

BACKGROUND: Ischemic preconditioning (IPC) is defined as raising tolerance to subsequent ischemic stress by exposing tissues to sub-lethal ischemia. Although many candidates have been suggested, recent studies have clearly demonstrated that adenosine-mediated ADORA2B receptor (ADORA2BR) activation is the main mechanism involved in IPC. While the tissue-protective role of this mechanism has been demonstrated in different ischemia/reperfusion (I/R) models, its role in flap surgery-derived I/R damage has not to date been investigated.