Effect of aerosolized histamine on occlusion pressure and ventilation in humans.

To define further the mechanism by which inspiratory neural activity is increased in asthma, we studied the effect of aerosolized histamine on occlusion pressure (P100) and ventilation in conscious humans while end-tidal CO2 partial pressure was maintained at a constant, slightly hypercapnic level. The dose of histamine we employed varied from subject to subject but was such that it produced a 70% reduction in specific airway conductance in each subject. In 9 of the 13 subjects tested, inhaled histamine significantly increased P100. This increase was not due to changes in functional residual capacity, which was not affected by aerosolized histamine. Inhalation of isoproterenol abolished the effects of histamine on specific airway conductance and P100. Anesthesia of the airways by lidocaine eliminated the effect of histamine on P100 but did not alter the magnitude of the change in specific airway conductance produced by histamine. We conclude that the increase in occlusion pressure seen after the inhalation of histamine in humans depends on both contraction of bronchial smooth muscle and stimulation of airway receptors.