Abstract
Bronchial vasodilation in dogs is mediated largely by vagal pathways. To examine the relative contribution of cholinergic and noncholinergic parasympathetic pathways and of sensory axon reflexes to vagal bronchial vasodilation, we electrically stimulated the peripheral vagus nerve in 10 chloralose-anesthetized dogs and measured bronchial artery flow. Moderate-intensity electrical stimulation (which did not activate C-fiber axons) caused a rapid voltage- and frequency-dependent vasodilation. After atropine, vasodilation was slower in onset and reduced at all voltages and frequencies: bronchial vascular conductance increased by 9.0 1.5 (SE) ml min1 100 mmHg1 during stimulation before atropine and 5.5 1.4 ml min1 100 mmHg1 after ( P < 0.02). High-intensity stimulation (sufficient to recruit C fibers) was not studied before atropine because of the resulting cardiac arrest. After atropine, high-intensity stimulation increased conductance by 12.0 2.5 ml min1 100 mmHg1. Subsequent blockade of ganglionic transmission, with arterial blood pressure maintained by a pressure reservoir, abolished the response to moderate-intensity stimulation and reduced the increase to high-intensity stimulation by 82 5% ( P < 0.01). In 13 other dogs, we measured vasoactive intestinal peptide-like immunoreactivity in venous blood draining from the bronchial veins. High-intensity vagal stimulation increased vasoactive intestinal peptide concentration from 5.7 1.8 to 18.4 4.1 fmol/ml ( P = 0.001). The results suggest that in dogs cholinergic and noncholinergic parasympathetic pathways play the major role in vagal bronchial vasodilation.