Assessment of the pulmonary origin of bronchoconstrictor vagal tone

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Abstract
In anesthetized, spontaneously breathing cats the sensory component of the vagal nerves were sectioned at the level of nodose ganglion. 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. By studying the cardiac and bronchomotor effects induced by electrical stimulation of the supranodose portion of the vagal nerve, the integrity of the efferent vagal component was tested. Unilateral right sensory vagotomy was followed by a 29% reduction in total pulmonary resistance. Section of the contralateral sensory vagal component (sensory bivagotomy) produced a weak supplementary effect (total decrease of total pulmonary resistance: 31%). No additive bronchomotor effect could be observed after the bilateral section of efferent vagal fibers (total bivagotomy). In intact cats blockade of the 2 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. Injection [i.v.] of phenyl diguanide, immediately after the blockade of the C vagal fibers by procaine, did not modify bronchomotor tone. The C pulmonary afferents, which are activated by phenyl diguanide, are mainly involved in this mechanism. The pulmonary irritant receptors seem to play a minor role. The i.v. administration of histamine under the same conditions provides evidence that the corresponding neurons (small sized myelinated fibers) are potent during the procaine application. It appears that bronchoconstrictor vagal tone has an exclusive peripheral origin and pulmonary endings, in particular those connected with non-medullated fibers, are probably involved in this mechanism.