Abstract

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 V T, 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°C and below, input in all three types of fiber was significantly reduced, attenuation being least marked in C fibers. Between 12°C and 7°C, attenuation of RAR input was significantly less than that of PSRs. At 7°C, virtually none of the hyperinflation-evoked increase in PSR activity and only 10% of that in RAPs passed the cooling platform - indeed RAR input was less than during normal ventilation at 37°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°C is almost certainly triggered by C fibers.

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