Adenosine 2A Receptor Agonism Improves Survival in Extracorporeal Cardiopulmonary Resuscitation.

Autor: Wisniewski AM; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Chancellor WZ; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Young A; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Money D; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Beller JP; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Charlton J; Department of Pediatrics, University of Virginia Health System, Charlottesville, Virginia., Lunardi N; Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia., Yang Z; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Laubach VE; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Mehaffey JH; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Kron IL; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia., Roeser ME; Department of Surgery, University of Virginia Health System, Charlottesville, Virginia. Electronic address: mr8e@virginia.edu.
Jazyk: angličtina
Zdroj: The Journal of surgical research [J Surg Res] 2024 Sep; Vol. 301, pp. 404-412. Date of Electronic Publication: 2024 Jul 18.
DOI: 10.1016/j.jss.2024.06.033
Abstrakt: Introduction: Despite resuscitation advances including extracorporeal cardiopulmonary resuscitation (ECPR), freedom from neurologic and myocardial insult after cardiac arrest remains unlikely. We hypothesized that adenosine 2A receptor (A2AR) agonism, which attenuates reperfusion injury, would improve outcomes in a porcine model of ECPR.
Methods: Adult swine underwent 20 min of circulatory arrest followed by defibrillation and 6 h of ECPR. Animals were randomized to receive saline vehicle or A2AR agonist (ATL1223 or Regadenoson) infusion during extracorporeal membrane oxygenation. Animals were weaned off extracorporeal membrane oxygenation and monitored for 24 h. Clinical and biochemical end points were compared.
Results: The administration of A2AR agonists increased survival (P = 0.01) after cardiac arrest compared to vehicle. Markers of neurologic damage including S100 calcium binding protein B and glial fibrillary acidic protein were significantly lower with A2AR agonist treatment.
Conclusions: In a model of cardiac arrest treated with ECPR, A2AR agonism increased survival at 24 h and reduced neurologic damage suggesting A2AR activation may be a promising therapeutic target after cardiac arrest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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