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Capsaicin-induced bronchial vasodilation in dogs: central and peripheral neural mechanisms.

In 21 anesthetized dogs, we placed a flow probe around the right bronchial artery and examined changes in bronchial blood flow and bronchial vascular conductance when pulmonary C-fibers were stimulated by right atrial injection of capsaicin. When vagus nerves were intact, capsaicin evoked a pulmonary depressor chemoreflex and increased bronchial blood flow by 125% and bronchial vascular conductance by 175%; flow in an adjacent intercostal artery did not increase. Injection of color-coded microspheres revealed that blood flow to mucosa of lower trachea and to a peripheral bronchus doubled, whereas flow to posterior tracheal wall increased little. Cooling (to -1 degree C) or cutting cervical vagi (in 17 dogs) abolished the pulmonary chemoreflex and abolished all bronchial vascular effects in nine dogs but 33% of the vasodilation persisted in eight. In five of six dogs, this persisting vasodilation was potentiated by phosphoramidon (a neutral endopeptidase inhibitor that retards breakdown of neuropeptides released by C-fibers). Atropine reduced the capsaicin-induced bronchial vasodilation by approximately 30%. We conclude that the bronchial vasodilation was largely due to a centrally mediated vagal reflex and that a neuropeptide-dependent axon-reflex component was also present in about one-half the dogs.