Platelet aggregation in atopic and normal patients

Abstract Platelet aggregation was used as a model to evaluate the proposed beta blockade in subjects with allergic rhinitis and asthma. Studies using epinephrine, adenosine diphosphate (ADP), and streptococcal M protein as aggregating agents showed that there was no significant difference in platelet aggregation between atopics and controls. Furthermore, aggregation induced by all three agents was inhibited by propranolol and phentolamine, as well as by caffeine and dibutyryl cyclic adenosine monophosphate (AMP). This inhibition was evidenced with platelets from both atopics and controls. The results suggest that with platelet aggregation the atopic population taken as a whole does not differ from the normal population. Although certain atopic subjects exhibit unique aggregation patterns, pharmacologic manipulation of this system fails to document that these unique patterns are due to beta blockade.