ROLE OF VAGUS NERVES IN BRONCHOCONSTRICTION INDUCED BY CHEMICAL MEDIATORS

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Abstract
The role of the vagal reflex in bronchoconstriction induced by histamine, acetylcholine, serotonin and PG[prostaglandin]F2.alpha. was investigated in anesthetized dogs using a complete vagal blockade by cooling. A thermode for vagal cooling was devised. The vagal cooling was performed by circulating cold water through the thermode attached to fit snugly around the bilateral cervical vagus nerves. Airway musculature response was measured as a change in ventilation overflow with a modification of the Konzett-Rossler method. Drugs were injected close intraarterially into the right bronchial artery and inhaled into the airway. Afferent impulses of the vagus nerve were abolished by cooling at 0.degree. C. When the vagus nerves were cooled to 0.degree. C, the ventilation overflow decreased. When the nerves were rewarmed, the ventilation overflow increased again. Bronchoconstriction was produced by close intraarterial injection of histamine, acetylcholine, serotinin or PGF2.alpha. at a dosage of 10 .mu.g each. The bronchoconstrictions produced by these agents were inhibited by vagal cooling. The bronchoconstrictions induced by histamine, acetylcholine and serotonin were all 0.00125%, and that by PGF2.alpha. was 0.0001%. Inhalations for 10 min were also inhibited by vagal cooling. Evidently this thermode is useful for vagal cooling and vagally mediated bronchoconstriction is a relatively major component of bronchoconstriction induced by chemical mediators.

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