Does ischemic preconditioning increase flap survival by ADORA2B receptor activation?
CLINICAL HEMORHEOLOGY AND MICROCIRCULATION, vol.75, no.2, pp.151-162, 2020 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 75 Issue: 2
- Publication Date: 2020
- Doi Number: 10.3233/ch-190730
- Journal Name: CLINICAL HEMORHEOLOGY AND MICROCIRCULATION
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
- Page Numbers: pp.151-162
- Keywords: Adenosine, ADORA 2B, ischemia, reperfusion, flap survival, ACUTE KIDNEY INJURY, ECTO-5'-NUCLEOTIDASE CD73, ADENOSINE RECEPTORS, SIGNALING PROTECTS, BLOOD-FLOW, RECONSTRUCTION, POLYDEOXYRIBONUCLEOTIDE
- Akdeniz University Affiliated: Yes
Abstract
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.