Beagles, sensitized to ragweed allergen at birth, were subjected to inhalation of the ragweed extract into the lower respiratory tract inducing a systemic anaphylactic response that manifested in bronchoconstriction, alteration of a breathing pattern, increase in bronchial mucociliary clearance, and temporary cardiovascular depression. The researchers believed that, in these dogs, exclusive exposure of the upper respiratory tract to the same ragweed allergen would precipitate the development of allergic rhinitis that was responsive to treatment with a-adrenergic agonists.
To test this hypothesis, they evaluated the degree of nasal congestion induced by ragweed and histamine in cohorts of ragweed-sensitized, sham-sensitized, and nonsensitized dogs. Nasal congestion was assessed by the measurement of the resistance to conducting air, i.e., nasal airway resistance (RNA) and the relative cross-sectional areas and the volume of nasal passages.
Three series of experiments were conducted on subgroups selected from 14 adult beagle dogs of both sexes, weighing 9.514.5 kg. Five dogs were neonatally sensitized to ragweed, three were their sham-sensitized littermates, and six dogs were nonsensitized. Newborn dogs were sensitized with intraperitoneal injections containing ragweed extract in a saline mix and aluminum hydroxide within 24 hours of birth. Injections were repeated weekly for six weeks and biweekly until 16 weeks of age. In the sham-sensitized animals, only the aluminum hydroxide in saline was injected. Five-milliliter samples of venous blood were drawn from each dog beginning at four months of age and thereafter four times per year to measure serum ragweed-specific IgE levels.