MECHANISM OF RAPID, SHALLOW BREATHING AFTER INHALING HISTAMINE AEROSOL IN EXERCISING DOGS

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Abstract
In 4 unsedated, exercising dogs, the effects of inhaled histamine aerosol were studied on minute volume of ventilation, respiratory frequency, tidal volume, total pulmonary resistance and dynamic pulmonary compliance. Inhalation (5 breaths) of 1-2% histamine aerosols increased minute ventilation (mean, 50%; P < 0.001) by increasing respiratory frequency (mean 166%; P < 0.001), despite decreasing tidal volume (mean, 42%; P < 0.0001). Total pulmonary resistance increased (mean, 200%; P < 0.001), and dynamic pulmonary compliance decreased (mean, 51%; P < 0.001). Breathing supplemental O2 did not affect the ventilatory response to histamine. Adding external resistive loads to a dog''s airway did not simulate the pattern of rapid, shallow breathing produced by histamine. Inhalation of terbutaline prevented the changes in total pulmonary resistance and dynamic pulmonary compliance but did not alter the ventilatory response to histamine. When conduction in the cervical vagus nerves (which were implanted chronically in skin loops) was blocked by cooling, the ventilatory response to histamine was abolished. Histamine stimulated breathing by stimulation of receptors whose afferent pathways are in the vagus nerves; the effective stimulus is not bronchoconstriction but is presumably due to direct stimulation of airway receptors.

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