Subnormal inhibition of active E rosette formation by isoproterenol in bronchial asthma

Three different groups of patients were studied: group A was on active attacks of asthma with bronchodilator therapy; group B was also on active attacks of asthma but free of any treatment; and group C was of remissive asthma due to hyposensitization, and free of any other treatment. Active E rosette forming populations of all the three groups showed much less reduction by beta-adrenergic agonist isoproterenol as comparing to normal controls, but had equal degrees of inhibition by cAMP and theophilline to normal subjects. Dysfunction of beta-adrenergic receptors in bronchial asthma, as presented in this study, was in accordance with Szentivanyi's theory of beta-adrenergic blockage. Therapy with sympathomimetic bronchodilators might have desensitizing effect on beta-adrenergic receptors. Symptom-relieving hyposensitization could'nt restore the beta-receptor functions in asthmatic patients. The significance of beta-receptor dysfunction in bronchial asthma was discussed.