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Bronchial vasodilator pathways in the vagus nerve of dogs

Pisarri, T. E ; Zimmerman, M. P ; Adrian, T. E ; Coleridge, J. C. G ; Coleridge, H. M

Journal of applied physiology (1985), 1999-01, Vol.86 (1), p.105-113 [Periódico revisado por pares]

Bethesda, MD: Am Physiological Soc

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Título:
Bronchial vasodilator pathways in the vagus nerve of dogs
Autor: Pisarri, T. E ; Zimmerman, M. P ; Adrian, T. E ; Coleridge, J. C. G ; Coleridge, H. M
Assuntos: Air breathing ; Animals ; Autonomic Pathways - physiology ; Biological and medical sciences ; Blood vessels ; Bronchi - blood supply ; Bronchi - innervation ; Bronchi - physiology ; Dogs ; Electric Stimulation ; Fundamental and applied biological sciences. Psychology ; Male ; Nervous system ; Parasympathetic Nervous System - physiology ; Peptides ; Radioimmunoassay ; Regional Blood Flow - physiology ; Respiratory system ; Respiratory system: anatomy, metabolism, gas exchange, ventilatory mechanics, respiratory hemodynamics ; Stimulation, Chemical ; Vagus Nerve - physiology ; Vasoactive Intestinal Peptide - metabolism ; Vasoactive Intestinal Peptide - physiology ; Vasodilation - physiology ; Vertebrates: respiratory system
É parte de: Journal of applied physiology (1985), 1999-01, Vol.86 (1), p.105-113
Notas: ObjectType-Article-2
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Descrição: 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
Editor: Bethesda, MD: Am Physiological Soc
Idioma: Inglês

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Bronchial vasodilator pathways in the vagus nerve of dogs

Pisarri, T. E ; Zimmerman, M. P ; Adrian, T. E ; Coleridge, J. C. G ; Coleridge, H. M

Bethesda, MD: Am Physiological Soc

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