Does ischemic preconditioning increase flap survival by ADORA2B receptor activation?
CLINICAL HEMORHEOLOGY AND MICROCIRCULATION, cilt.75, sa.2, ss.151-162, 2020 (SCI-Expanded, Scopus)
- 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.