Attenuation of pulmonary afferent input by vagal cooling in dogs.

In open chest, artificially ventilated, anesthetized dogs, we examined the effect of vagal cooling on the pulmonary afferent input evoked by hyperinflating the lungs to 3 VT, recording the activity of slowly adapting pulmonary stretch receptors (PSRs), rapidly adapting receptors (RARs) and pulmonary C fibers rostral to the cooling platform. At 15 degrees C and below, input in all three types of fiber was significantly reduced, attenuation being least marked in C fibers. Between 12 degrees C and 7 degrees C, attenuation of RAR input was significantly less than that of PSRs. At 7 degrees C, virtually none of the hyperinflation-evoked increase in PSR activity and only 10% of that in RARs passed the cooling platform--indeed RAR input was less than during normal ventilation at 37 degrees C; by contrast, 40% of the hyperinflation-evoked increase in C fiber activity was still transmitted. Cooling had similar effects on C fiber input evoked by capsaicin. If reflexes are attenuated in proportion to the attenuation of afferent input, our results suggest that a hyperinflation-evoked reflex that survives vagal cooling below 6 degrees C is almost certainly triggered by C fibers.