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Bronchial provocation with Ascaris allergen evoked bronchoconstriction in home-bred Macaca arctoides monkeys sensitized by experimental infection with embryonated Ascaris suum ova. Inhalation of Ascaris allergen by aerosol prior to infection produced no changes in lung function. In infected animals total lung resistance (RL) increased and dynamic lung compliance (Cdyn) decreased following Ascaris inhalation. The changes in lung function reached a peak, 2-5 min after allergen inhalation, lasted for approximately 30 min and were associated with increases in arterial plasma histamine levels and decreases in arterial Po2 levels. Reproducible changes in lung function were obtained when the monkeys were challenged at bi-weekly intervals and lung sensitivity to Ascaris was maintained for at least 6 months. Histamine produced similar changes in RL and Cdyn before and after infection. Ascaris-induced bronchoconstriction was reversed by the beta 2-stimulant, salbutamol, and was partially reversed by cholinergic blockade with atropine. The responses were not inhibited by antihistamines or sodium cromoglycate although a new anti-allergic agent, FPL 58668 (disodium salt), inhibited Ascaris-induced bronchoconstriction and the increase in plasma histamine levels seen after Ascaris inhalation. Ascaris-induced bronchoconstriction in experimentally infected monkeys provides an animal model demonstrating many of the characteristics of allergic asthma in man and does not require the use of wild-caught monkeys.
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