• Chin-Ming Chen, Oscar Penuelas, Kieran Quinn, Kuo-Chen Cheng, Chien-Feng Li, Haibo Zhang, and Arthur S Slutsky.
• Department of Intensive Care Medicine and Internal Medicine, Chi Mei Medical Center, Tainan, Taiwan.
• Crit. Care Med. 2009 Jul 1; 37 (7): 2235-41.

ObjectivesMechanical ventilation is associated with overwhelming inflammatory responses that are associated with ventilator-induced lung injury (VILI) in patients with acute respiratory distress syndrome. The activation of adenosine A2A receptors has been reported to attenuate inflammatory cascades.HypothesisThe administration of A2A receptors agonist ameliorates VILI.MethodsRats were subjected to hemorrhagic shock and resuscitation as a first hit to induce systemic inflammation. The animals randomly received the selective A2A receptor agonist CGS-21680 or a vehicle control in a blinded fashion at the onset of resuscitation phase. They were then randomized to receive mechanical ventilation as a second hit with a high tidal volume of 20 mL/kg and zero positive end-expiratory pressure, or a low tidal volume of 6 mL/kg with positive end-expiratory pressure of 5 cm H2O.ResultsThe administration of CGS-21680 attenuated lung injury as evidenced by a decrease in respiratory elastance, lung edema, lung injury scores, neutrophil recruitment in the lung, and production of inflammatory cytokines, compared with the vehicle-treated animals.ConclusionsThe selective A2A receptor agonist may have a place as a novel therapeutic approach in reducing VILI.

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