Abstract
The role of the vagal reflex in bronchoconstriction induced by histamine, acetylcholine, serotonin, and PGF2α was investigated in anesthetized dogs using a complete vagal blockade by cooling. We devised a thermode for vagal cooling. 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-Rössler 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°C. When the vagus nerves were cooled to 0°C, the ventilation overflow decreased. On the other hand, when the nerves were rewarmed, the ventilation overflow increased again. Bronchoconstriction was produced by close intraarterial injection of histamine, acetylcholine, serotonin, or PGF2α at a dosage of 10 μg 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 PGF2α was 0.0001%. Inhalations for 10 min were also inhibited by vagal cooling. These findings indicate that the thermode devised in this study is useful for vagal cooling and that vagally mediated bronchoconstriction is a relatively major component of bronchoconstriction induced by chemical mediators.
