Tissue damage and hypoxia stimulates adenosine formation in extracellular space by degradation of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) through the action of nucleotidases such as CD39 and CD73. Rapid degradation of adenosine intracellularly occurs by adenosine kinase and adenosine deaminase, after being taken up through sodium-independent nucleoside transporters (equilibrative nucleoside transporter (ENT)). As ticagrelor inhibits the ENT membrane, adenosine accumulates in the extracellular space, leading to adenosine-mediated effects, such as stimulation of lung neuroreceptors, probably through binding to adenosine membrane receptors (A1, A2A, A2B, and A3), and later to interaction with adenylyl cyclase and formation of cyclic adenosine monophosphate (cAMP). Theophylline blockade of adenosine receptors probably explains inhibition of adenosine-mediated effects.⁴