The purpose of this investigation was to determine the primary mediators responsible for the decrease in specific lung conductance (SG(L)) after airway challenge with Ascaris suum antigen in allergic sheep. On different occasions, separated by 10 to 14 days, pulmonary resistance and thoracic gas volume were measured in 5 sheep with Ascaris 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 SG to 38 and 44% of baseline, respectively. Pretreatment by intravenous injection of the H1 receptor antagonist chlorpheniramine (2 mg/kg) completely prevented the antigen-induced decrease in SG(L). Similar results were obtained with inhalation of the mediator release blocking agent, disodium cromoglycate (1 mg/kg), prior to antigen challenge. The decrease in (SG(L)) 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 intravenous injection, or with inhalation of FPL-55712 (1% solution), an antagonist of slow-reacting substance of anaphylaxis (SRS-A). We concluded that during allergic bronchoconstriction in sheep (1) the decrease in (SG(L)) is mediated by histamine via H1 receptors, (2) other liberated or activated mediators including SRS-A do not decrease SG(L), and (3) cholinergic reflex mechanisms are not involved in this response.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Review of Respiratory Disease|
|State||Published - Dec 1 1981|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine