Inhibitory effect of inhaled wood smoke on the discharge of pulmonary stretch receptors in rats

We investigated the inhibition of slowlyadapting pulmonary stretch receptors (PSRs) by inhaled wood smoke.Impulses were recorded from PSRs in 68 anesthetized, open-chest, andartificially ventilated rats. Eighty-one of one hundred five PSRs wereinhibited within one or two breaths when 6 ml of wood smoke weredelivered into the lungs. As a group(n = 105), PSR activity significantly decreased from a baseline of 19.0 ± 1.3 (SE) to a lowest level of12.9 ± 1.2 impulses/breath at the fourth or fifth breath after smoke delivery. This afferent inhibition usually persisted for 5-18 breaths. In contrast, smoke delivery did not affecttranspulmonary pressure. Delivery of gas-phase smoke or a hypercapnicgas mixture containing CO₂ at aconcentration (15%) matching that in the smoke produced a nearlyidentical inhibition in the same PSRs(n = 10). This afferent inhibition waslargely prevented by pretreatment with acetazolamide (an inhibitor ofcarbonic anhydrase; n = 10) but wasnot affected by pretreatment with the vehicle for acetazolamide (n = 8) or isoproterenol (abronchodilator; n = 10).These results suggest that 1) anincrease in H⁺ concentrationresulting from hydration of CO₂ inthe smoke may be responsible for the inhibitory effect of wood smoke onthe discharge of PSRs and 2) changesin lung mechanics are not the cause of this afferent inhibition.