EFFECT OF PHARMACOLOGIC AGENTS ON ANTIGEN-INDUCED DECREASES IN SPECIFIC LUNG CONDUCTANCE IN SHEEP

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Abstract
The primary mediators responsible for the decrease in specific lung conductance (SGL) after airway challenge with Ascaris suum antigen in allergic sheep were studied. On different occasions, separated by 10-14 days, pulmonary resistance and thoracic gas volume were measured in 5 sheep with A. suum hypersensitivity before and for 2 h after a standard inhalation challenge with this antigen. Initially and at the end of the study, inhalation challenge decreased mean SGL to 38 and 44% of baseline, respectively. Pretreatment by i.v. injection of the H1 receptor antagonist, chloropheniramine (2 mg/kg), completely prevented the antigen-induced decrease in SGL. Similar results were obtained with inhalation of the mediator release blocking agent, disodium cromoglycate (1 mg/kg), prior to antigen challenge. The decrease in SGL after inhalation challenge was not modified by pretreatment with the H2 receptor antagonist, metiamide (3 mg/kg), the anticholinergic agent, atropine (0.2 mg/kg), the prostaglandin synthetase inhibitor, indomethacin (2 mg/kg) by i.v. injection, or with inhalation of FPL-55712 [7-(3-(4-acetyl-3-hydroxy-2-propylphenoxy)-2-hydroxypropoxy)-4-oxo-8-propyl-4H-1-benzopyran-2-carboxylic acid monosodium salt] (1% solution), an antagonist of slow-reacting substance of anaphylaxis (SRS.A). During allergic bronchoconstriction in sheep, the decrease in SGL is probably mediated by histamine via H1 receptors. Other liberated or activated mediators including SRS.A do not decrease SGL, and cholinergic reflex mechanisms are apparently not involved in this response.