The influence of procaine and isoprenaline on the lung deflation reflex during the histamine-induced bronchial asthma attack.

The histamine-induced respiratory reflex response arising from the lung deflation (irritant) receptors was influenced by both procaine and isoprenaline, but in an essentially different manner. Procaine administered via the pulmonary circulation prevented or interrupted the asthmatic tachypnoea associated with stimulation of the lung deflation receptors. The effect was less consistently obtained when the drug was given by way of the bronchial circulation or as an aerosol. It is concluded that the lung deflation receptors in the guinea-pig are located in sites easily accessible by way of the pulmonary circulation, i.e., in the peripheral airways. Isoprenaline, irrespective of the way of administration, counteracted the asthmatic increase in bronchial resistance which underlies the stimulation of the lung deflation receptors. A respiratory response, however, characterized by increased respiratory rate, still occurred when the drug was administered either before or after histamine inhalation. The tachypnoic response to isoprenaline is probably of central origin.