MECHANISMS OF BRONCHOCONSTRICTION AFTER ALLERGEN INGESTION IN SENSITIZED GUINEA-PIGS

We examined whether oral administration of allergen induced bronchocon striction in sensitized guinea pigs and investigated the mechanisms of bronchoconstriction. The animals had been immunized intraperitoneally with a mixture of Ascaris suum extract and silica gel, and exposed to ozone. They were then challenged with an oral dose of A. suum extract (6 mg/kg), and respiratory resistance (Rrs) was measured up to 7 h. A fter oral administration of the allergen, an increase in Rrs was obser ved. The mean values at 1, 3,5 and 7 h after oral allergen challenge w ere 150 +/- 21, 149 +/- 11, 151 +/- 12 and 134 +/- 10% of the baseline value, respectively. When saline instead of the allergen was orally a dministered, almost no significant increase in Rrs was observed up to 7 h. Moreover, in nonsensitized guinea pigs, oral administration of al lergen produced no significant increase in Rrs for up to 7 h. When atr opine was administered as an aerosol, the increase in Rrs induced by a n oral allergen challenge was attenuated. Three of the five atropine-t reated guinea pigs showed temporary increases in Rrs immediately after the oral allergen challenge. The mean values of Rrs in the atropine-t reated animals challenged with oral allergen at 1, 3, 5 and 7 h were 1 06 +/- 3, 106 +/- 5, 115 +/- 5 and 102 +/- 4% of baseline value, respe ctively. In the animals which received oral allergen, the number of ne utrophils in bronchoalveolar lavage fluid (BALF) significantly increas ed 2.0-fold (p < 0.05), while no significant increase in the number of eosinophils, macrophages, or lymphocytes in BALF was observed. We con clude that oral allergen challenge can induce bronchoconstriction asso ciated with neutrophilia in BALF in sensitized guinea pigs, and that v agal reflex pathways play a role in bronchoconstriction.