Reciprocal action of pulmonary vagal afferents on tracheal smooth muscle tension in dogs.

Tracheal smooth muscle usually relaxes when the lungs are transiently inflated, an effect attributed to inhibitory input from pulmonary stretch receptors (PSRs). Relaxation is often followed by contraction, however, and occasionally contraction is the sole response. We attempted to identify the afferents responsible for this reflex contraction. In anesthetized, artificially ventilated dogs with open chest we recorded transverse tension in an upper tracheal segment innervated only by the superior laryngeal nerves and periodically hyperinflated the lungs as the cervical vagus nerves were cooled. Hyperinflation usually evoked tracheal relaxation when vagal temperature was 37 degrees C, but contraction became more frequent as temperature decreased and was the sole response below 8 degrees C. We hypothesise that above 6 degrees C contraction was triggered by rapidly adapting receptors and lung C fibers, whereas below 6 degrees C only C fibers were involved. Contraction, which appeared to represent the bronchomotor counterpart of Head's paradoxical reflex, was abolished below 2 degrees C. Cooling alone without periodic hyperinflation increased baseline tracheal tension to a maximum at 7-8 degrees C; further cooling often decreased tension, sometimes to control levels. Cutting the pulmonary vagal branches abolished these effects. Our results indicate that PSRs and C fibers act reciprocally, one causing bronchodilation, the other bronchoconstriction, and that background activity in C fibers may contribute to bronchomotor tone, an effect unmasked by selectively blocking A fibers.