Methylprednisolone prevents propranolol-induced airway hyperreactivity in the Basenji-greyhound dog.

Abstract

To determine if corticosteroids would prevent beta-adrenergic-antagonist-induced increases in airway reactivity, we evaluated the ability of chronic methylprednisolone administration to prevent propranolol-induced airway hypereactivity to methacholine aerosol in the basenji-greyhound (BG) dog model of asthma. Initial studies included the measurement of lung resistance (RL) and dynamic compliance (Cdyn) with and without propranolol pretreatment in 5 BG and 5 mongrel dogs. A single dose of propranolol (2 mg/kg) did not significantly alter airway reactivity in the mongrels. The dose of methacholine needed to increase RL by 200% (ED200RL) was 0.20 +/- 0.05 mg/ml (mean +/- standard error of the mean [SEM]) in untreated and 0.18 +/- 0.04 mg/ml in propranolol-treated mongrels. In contrast, propranol significantly increased methacholine-reactivity in the BGs. The ED200RL for methacholine was 0.17 +/- 0.03 mg/ml in untreated and 0.05 +/- 0.02 mg/ml (P less than 0.05) in propranolol-treated BG dogs. Following the initial studies, the 5 BG dogs were given methylprednisolone (2 mg.kg-1.day-1) for 4 weeks, after which time propranolol no longer increased methylacholine reactivity in the BGs. The ED200RL was 0.16 +/- 0.03 mg/ml after 4 weeks of methylprednisolone and 0.22 +/- 0.06 mg/ml after propranolol administration in the BGs given 4 weeks of methylprednisolone treatment. The attenuation of propranolol-induced bronchoconstriction by corticosteroids may be a clinically useful intervention in asthmatic patients receiving beta-adrenergic antagonists in the perioperative period. However, further studies are needed to define the effective dose and duration of corticosteroid therapy that is needed.