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Updated: Jun 22, 2026

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
Published on: April 7, 2021
Protective effects of adenosine A2A receptor agonist in ventilator-induced lung injury in rats
Chin-Ming Chen1, Oscar Penuelas, Kieran Quinn
1Department of Intensive Care Medicine and Internal Medicine, Chi Mei Medical Center, Tainan, Taiwan.
Objectives:
Mechanical 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.
Hypothesis:
The administration of A2A receptors agonist ameliorates VILI.
Methods:
Rats 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.
Results:
The 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.
Conclusions:
The selective A2A receptor agonist may have a place as a novel therapeutic approach in reducing VILI.

