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The effects of lidocaine and hexamethonium on prostaglandin F 2 ‐alpha‐ and histamine‐induced bronchoconstriction in sulfur dioxide‐treated beagle dogs
Author(s) -
Malo P. E.,
Griffin R. L.
Publication year - 1983
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430030107
Subject(s) - hexamethonium , bronchoconstriction , beagle , bronchospasm , lidocaine , anesthesia , chemistry , histamine , prostaglandin , pharmacology , endocrinology , atropine , medicine , asthma , airway
The effects of local deposition of the topical anesthetic lidocaine and of ganglionic blockade by hexamethonium were investigated in pharmacologic bronchoconstriction with sulfer dioxide (SO 2 )‐induced hyperreactive beagle dogs. Control bronchopulmonary provocations, i.e., increases in pulmonary resistance (R L ) and decreases in dynamic lung compliance (C DYN ), were accomplished by aerosols of prostaglandin F 2 ‐alpha (PGF 2α ) and histamine (HIST) after a six‐month chronic inhalation study using 500 ppm SO 2 . Pretreatment with a lidocaine aerosol (2.0%; 30 breaths) failed to produce any inhibition of bronchospasm induced by aerosols of PGF 2α or HIST. An IV infusion of hexamethonium (10.0 mg/kg) significantly inhibited PGF 2α ‐induced percent changes in both R L (226.4 ± 45.2% vs. 134.7 ± 28.7%) and C DYN (52.6 ± 10.8% vs. 35.9 ± 8.8%) but failed to produce significant inhibition against HIST‐induced bronchospasm. These results suggest that the bronchial hyperreactivity attributed to SO 2 exposure in our model is probably due in fact to an increased sensitivity of the afferent portion of the cholinergic pathway due to lidocaine's failure to provide inhibition at this site. No change occurs at the ganglia based on the similar action of hexamethonium in this study as to previously published work.