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1 Department of Biomedical Sciences, Creighton University School of Medicine, Omaha, Nebraska 68178-0405; and 2 Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130
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 · min
1 · 100 mmHg
1 during stimulation
before atropine and 5.5 ± 1.4 ml · min
1 · 100 mmHg
1 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 · min
1 · 100 mmHg
1. 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.
cholinergic vasodilation; axon reflex; bronchial artery; vasoactive intestinal peptide
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