ASSESSMENT OF THE PULMONARY ORIGIN OF BRONCHOCONSTRICTOR VAGAL TONE

1. In anaesthetized spontaneously breathing cats, the sensory component of the vagal nerves was sectioned at the level of nodose ganglion, using a method described previously (Mei, 1966; Mei & Dussardier, 1966). 2. The strength of the Hering—Breuer reflex (inhibitory ratio, i.e. T1/T0) provided a test for effectiveness of section of vagal afferents, particularly respiratory afferents. On the other hand, by studying the cardiac and bronchomotor effects induced by electrical stimulation of the supranodose portion of the vagal nerve, it was possible to test the integrity of the efferent vagal component. 3. Unilateral right sensory vagotomy was followed by a 29% reduction in total pulmonary resistance. 4. Section of the contralateral sensory vagal component (sensory bivagotomy), produced a weak supplementary effect (total decrease of total pulmonary resistance: 31%). 5. No additive bronchomotor effect could be observed after the bilateral section of efferent vagal fibres (total bivagotomy). 6. In intact cats, blockade of the two vagal nerves by procaine induced a decrease in pulmonary resistance similar to those produced by the sensory bivagotomy (23%). This bronchodilatator effect was concomitant with a complete disappearance of the C wave of the compound vagal potential. 7. Intravenous injection of phenyl diguanide, immediately after the blockade of the C vagal fibres by procaine did not modify bronchomotor tone. This result confirms that the C pulmonary afferents, which are activated by phenyl diguanide, are mainly involved in this mechanism. 8. The pulmonary irritant receptors seem to play a minor role. In fact, the I.V. administration of histamine under the same conditions, provides evidence that the corresponding neurones (small sized myelinated fibres) are potent during the procaine application. 9. From these results, it appears that bronchoconstrictor vagal tone has an exclusive peripheral origin and that pulmonary endings, in particular those connected with non‐medullated fibres, are probably involved in this mechanism. © 1979 The Physiological Society