bay-60-6583 and Wounds-and-Injuries

Inflammation is responsible for secondary organ failure after trauma and hemorrhagic shock (T/HS). Adenosine, acting through four G protein-coupled cell surface receptors, A1, A2A, A2B, and A3, exerts a number of tissue protective and anti-inflammatory effects. The goal of the present study was to test the effect of A2B adenosine receptor stimulation on T/HS-induced organ injury and inflammation in rats. Rats after T/HS were resuscitated with Ringer's lactate containing the A2B receptor agonist BAY 60-6583 or its vehicle. We found that BAY 60-6583 decreased T/HS-induced lung permeability and plasma creatine kinase levels but failed to affect T/HS-induced lung neutrophil infiltration and IκBα expression and plasma alanine aminotransferase levels. Thus, we conclude that stimulation of A2B receptors protects against T/HS-induced lung and muscle injury.

Topics: Acute Lung Injury; Aminopyridines; Animals; Blotting, Western; Disease Models, Animal; Inflammation; Male; Purinergic P1 Receptor Agonists; Rats; Rats, Sprague-Dawley; Receptor, Adenosine A2B; Shock, Hemorrhagic; Wounds and Injuries