A lung perfusion technique for the detection of antigenic intrapulmonary bronchoconstriction and its mediation.

A guinea pig intraluminal perfusion model was used to assess the effects of antigen challenge of airway reactivity and its pharmacologic modulation. Increases in airway perfusion pressure, following antigen provocation, could be reproduced 60 min later without significant modification of the response. We found no change in lung volume nor observed tissue edema following antigen provocation, and suggest that rises in perfusion pressure are due to decreases in airway caliber. Pharmacologically, the antihistamines, mepyramine and chlorpheniramine, and the antiallergic agent, disodium cromoglygate (DSCG), failed to inhibit antigenic bronchoconstriction. Indeed, mepyramine produced some potentiation of allergic bronchospasm. Compounds reported to inhibit 5-lipoxygenase (phenidone, benoxaprofen, and noradihydroguiaretic acid (NDGA)) or antagonize SRS-A (FPL 55712), produced inhibition of antigen-induced bronchoconstriction. The cyclooxygenase inhibitor, indomethacin, produced biphasic modulation of antigenic bronchoconstriction, potentiation at low doses, and inhibition at high concentrations. Overall, drug-induced modulation of allergic bronchoconstriction suggests that this model more closely resembles the antigenic reactions observed in the parenchymal strip preparation than in the trachea.