Bronchial, alveolar, and vascular-induced anaphylaxis and irritant-inducedcardiovascular and pulmonary responses

We examine the respiratory, bronchomotor, cardiac, and vascular responses t o histamine and ragweed allergen delivered to the bronchi or alveoli compar tments and the potential role of sensory nerves and reflexes mediating the histamine-induced responses. The masses of aerosols deposited in the bronch i and alveoli were quantitated using radioaerosol techniques. Activation of sensory nerves and/or histamine-induced mediator release were characterize d by depositing nedocromil sodium aerosol prior to histamine challenge. The histamine-induced responses due to vagosympathetic transmission were deter mined by performing bilateral vagotomy. Both histamine and ragweed increase d respiratory rate, ventilation, and bronchomotor tone whether deposited in the bronchial or alveolar regions. However, these responses were not elici ted when histamine was administered intravenously. Precipitous allergen-ind uced decreases in heart rate and systolic and diastolic pressure were maxim al 72 sec following ragweed deposition in alveolar regions of the lungs. In creases in respiratory rate were mediated via the vagus whether delivered t o the bronchi, alveoli, or vasculature. Histamine-induced increases in resp iratory rate and bronchomotor tone were attenuated by nedocromil. When hist amine was delivered to the alveolar regions, increases in lung resistance a ppeared to be mediated primarily via the vagus and when delivered to the br onchial airways primarily by its action on smooth muscle or local reflexes. Histamine-induced hypotension and bradycardia appear to be mediated by the direct action of histamine on the cardiovascular system rather than throug h a vagally mediated reflex.