ABSTRACT
It is now more than a decade since Cushley and coworkers frrst administered aerosolized adenosine to a group of six allergic and seven nonallergic asthmatic subjects. Whereas there was no discernible effect on airway caliber in normal individuals, the asthmatics experienced concentration-related bronchoconstriction at concentrations greater than 6.7 x w-2 mg/ml. Responsiveness to adenosine was similar in the two asthmatic groups, and time-course studies using single doses of adenosine calculated to produce a 35% to 40% decrease in sGaw showed that bronchoconstriction reached maximum at 5 min and was followed by slow recovery over the next 45-60 min (1). Since these observations were made, considerable effect has been directed at elucidating the mechanism of this effect, using it to explore the mechanism of other observations in asthmatic subjects, and determining whether or not adenosine has a role as a mediator in asthma.
