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J Appl Physiol 84: 1138-1143, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 4, 1138-1143, April 1998

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

C. J. Lai and Y. R. Kou

Institute of Physiology, School of Medicine and Life Science, National Yang-Ming University, Shih-Pai, Taipei, Taiwan 11221, Republic of China

We investigated the inhibition of slowly adapting pulmonary stretch receptors (PSRs) by inhaled wood smoke. Impulses were recorded from PSRs in 68 anesthetized, open-chest, and artificially ventilated rats. Eighty-one of one hundred five PSRs were inhibited within one or two breaths when 6 ml of wood smoke were delivered 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 of 12.9 ± 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 affect transpulmonary pressure. Delivery of gas-phase smoke or a hypercapnic gas mixture containing CO2 at a concentration (15%) matching that in the smoke produced a nearly identical inhibition in the same PSRs (n = 10). This afferent inhibition was largely prevented by pretreatment with acetazolamide (an inhibitor of carbonic anhydrase; n = 10) but was not affected by pretreatment with the vehicle for acetazolamide (n = 8) or isoproterenol (a bronchodilator; n = 10). These results suggest that 1) an increase in H+ concentration resulting from hydration of CO2 in the smoke may be responsible for the inhibitory effect of wood smoke on the discharge of PSRs and 2) changes in lung mechanics are not the cause of this afferent inhibition.

airway irritation; vagal sensory receptors; carbon dioxide; hydrogen ion; carbonic anhydrase


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