GRANULOCYTE RESPONSE INVITRO TO ISOPROTERENOL, HISTAMINE, AND PROSTAGLANDIN-E1 DURING TREATMENT WITH BETA-ADRENERGIC AEROSOLS IN ASTHMA

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Abstract
Isoproterenol (ISO) inhibition of in vitro granulocyte (PMN) zymosan-induced lysosomal enzyme .beta.-glucuronidase release is decreased in asthma. To determine whether the regular administration of .beta.-adrenergic sympathomimetics in the treatment of asthma affected this abnormality, the PMN response to ISO was measured serially in a group of 11 asthmatics who received aerosols of ISO (600 .mu.g/day) or albuterol (680 .mu.g/day) for 12 wk. The maximal bronchodilator response to .beta.-adrenergic aerosols was unchanged during the study period. ISO (1.0-100 .mu.M) inhibition of PMN lysomal enzyme release was significantly impaired after the patients received either aerosol sympathomimetic for 4 wk, and the change in PMN response to ISO was evident at this time. Impairment in PMN response to ISO was significantly decreased in its ability to stimulate formation of cyclic AMP. The impaired ISO response persisted during the next 8 wk. Histamine inhibition of lysosomal enzyme release from granulocytes was impaired 4 wk after use of .beta.-adrenergic aerolysosomal enzyme release from granulocytes was impaired 4 wk after use of .beta.-adrenergic aerosols. No significant change in the PMN response to prostaglandin E1 was found. Decreased PMN response to .beta.-adrenergic agonists in asthma is accentuated by the use of adrenergic aerosols, but the drugs are only 1 factor that contributes to defective .beta.-adrenergic function in asthma.

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