Tachypnoeic response to amyl nitrite inhalation in the rabbit

Intratracheal inhalation of amyl nitrite, a non-specific smooth muscle relaxant, in the pentobarbitone/urethane anaesthetized rabbit caused reductions in tidal volume and both inspiratory and expiratory times, without a preceding apnoea, that were independent of the associated hypotension and of reflex influences from the carotid sinus region but dependent on supra-abdominal vagal integrity. In artificially ventilated, paralyzed rabbits amyl nitrite caused a pronounced sensitization of pulmonary stretch receptors (PSRs) during the inflation phase, typically with a reduction in the level of activity during the deflation phase. The time course of the change in the pattern of PSR activity paralleled that of the tachypnoeic response. The sensitization of a small sample of rapidly adapting 'irritant' receptors was of a significantly shorter duration. A unitary analysis of non-myelinated vagal afferents was not attempted. The sensitization of these vagal afferents cannot be attributed to the smooth muscle relaxant properties of amyl nitrite since other relaxants (sodium nitrite, sodium nitroprusside, phentolamine) did not possess this capacity, and such properties would be expected to diminish their activities.