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- Amoroso, Matteo, 1984, et al.
(författare)
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The effect of hemodilution on free flap survival: A systematic review of clinical andexperimental studies.
- 2020
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Ingår i: Clinical hemorheology and microcirculation. - 1875-8622. ; 75:4, s. 457-466
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Forskningsöversikt (refereegranskat)abstract
- Acute normovolemic hemodilution (ANH) has been proposed as a microsurgical technique to improve blood flow in free flaps.Here, we present the first systematic review of clinical and experimental studies on the effect of ANH.We performed a systematic literature search of PubMed, Medline, the Cochrane Library, Google Scholar, and ClinicalTrials.gov using search strategies and a review process in agreement with the PRISMA statement and the Cochrane Handbook for systematic reviews of interventions. PICO criteria were defined before bibliometric processing of the retrieved articles, which were analyzed with the SYRCLE RoB tool for risk of bias and the GRADE scale for level of evidence.We retrieved 74 articles from the literature search, and after processing according to PICO criteria, only four articles remained, all of which were experimental. The rating for risk of bias was uncertain according to SYRCLE RoB results, and the level of evidence was low according to GRADE evaluation.There is no clinical evidence for the effect of ANH on microcirculation in free flaps, and experimental studies provide weak evidence supporting the use of hemodilution in reconstructive microsurgery.
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- Ulker, Pinar, et al.
(författare)
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LDOES ischemic preconditioning increase flap survival by ADORA2B receptor activation?
- 2020
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Ingår i: Clinical hemorheology and microcirculation. - 1875-8622. ; 75:2, s. 151-162
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Tidskriftsartikel (refereegranskat)abstract
- 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.To investigate the role of adenosine and ADORA2BR activation in IPC-mediated tissue protection in an epigastric flap model.Animals were divided into five main groups, all of which were then divided into two subgroups depending on whether or not they were exposed to IPC before the I/R procedure, which consisted of 6 hours of ischemia and 6 days of reperfusion. No drugs were administered in Group 1 (the control group). Animals in Group 2 were pretreated with CD73-inhibitor before IPC application or the ischemic period. Animals in Group 3 were pretreated with adenosine. Animals in Group 4 were pretreated with an ADORA2BR antagonist, and those in Group 5 with an ADORA2BR agonist. After 6 days of reperfusion, tissue survival was evaluated via histological and macroscopic analysis.IPC application significantly enhanced CD73 expressions and adenosine concentrations (p<0.01). Flap survivals were increased by IPC in Group 1 (p<0.05). However, CD73 inhibition blocked this increase (Group 2). In Group 3, adenosine improved flap survival even in the absence of IPC (p<0.01). While an ADORA2BR antagonist attenuated the tissue-protective effect of IPC (p<0.01), the ADORA2BR agonist improved flap survival by mimicking IPC in groups 4 and 5.These results provide pharmacological evidence for a contribution of CD73 enzyme-dependent adenosine generation and signaling through ADORA2BR to IPC-mediated tissue protection. They also suggest for the first time that ADORA2BR agonists may be used as a potential preventive therapy against I/R injury in flap surgeries.
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