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Secondary Burn Progression Mitigated by an Adenosine 2A Receptor Agonist.
Haywood, Nathan; Byler, Matthew R; Zhang, Aimee; Rotar, Evan P; Money, Dustin; Gradecki, Sarah E; Ta, Huy Q; Salmon, Morgan; Kron, Irving L; Laubach, Victor E; Mehaffey, J Hunter; Roeser, Mark E.
Afiliación
  • Haywood N; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Byler MR; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Zhang A; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Rotar EP; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Money D; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Gradecki SE; Department of Pathology, University of Virginia School of Medicine, Charlottesville, USA.
  • Ta HQ; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Salmon M; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Kron IL; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Laubach VE; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Mehaffey JH; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
  • Roeser ME; Department of Surgery, University of Virginia School of Medicine, Charlottesville, USA.
J Burn Care Res ; 43(1): 133-140, 2022 01 05.
Article en En | MEDLINE | ID: mdl-33769530
Current burn therapy is largely supportive with limited therapies to curb secondary burn progression. Adenosine 2A receptor (A2AR) agonists have anti-inflammatory effects with decreased inflammatory cell infiltrate and release of proinflammatory mediators. Using a porcine comb burn model, we examined whether A2AR agonists could mitigate burn progression. Eight full-thickness comb burns (four prongs with three spaces per comb) per pig were generated with the following specifications: temperature 115°C, 3-kg force, and 30-second application time. In a randomized fashion, animals (four per group) were then treated with A2AR agonist (ATL-1223, 3 ng/kg/min, intravenous infusion over 6 hours) or vehicle control. Necrotic interspace development was the primary outcome and additional histologic assessments were conducted. Analysis of unburned interspaces (72 per group) revealed that ATL-1223 treatment decreased the rate of necrotic interspace development over the first 4 days following injury (p < .05). Treatment significantly decreased dermal neutrophil infiltration at 48 hours following burn (14.63 ± 4.30 vs 29.71 ± 10.76 neutrophils/high-power field, p = .029). Additionally, ATL-1223 treatment was associated with fewer interspaces with evidence of microvascular thrombi through postburn day 4 (18.8% vs 56.3%, p = .002). Two weeks following insult, the depth of injury at distinct burn sites (adjacent to interspaces) was significantly reduced by ATL-1223 treatment (2.91 ± 0.47 vs 3.28 ± 0.58 mm, p = .038). This work demonstrates the ability of an A2AR agonist to mitigate burn progression through dampening local inflammatory processes. Extended dosing strategies may yield additional benefit and improve cosmetic outcome in those with severe injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Quemaduras / Agonistas del Receptor de Adenosina A2 Límite: Animals Idioma: En Revista: J Burn Care Res Asunto de la revista: TRAUMATOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Quemaduras / Agonistas del Receptor de Adenosina A2 Límite: Animals Idioma: En Revista: J Burn Care Res Asunto de la revista: TRAUMATOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido