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

Abstract

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.

Responses of Tracheobronchial Receptors to Inhaled Furosemide in Anesthetized Rats

“…Differences in criteria for the AI or in experimental conditions might account for these differences. Although there has been controversy regarding the validity of the AI for defining RARs, the SARs identified in this study (AI р 25%) correspond well to those described by other investigators (8)(9)(10)(11)(12)(13).…”

“…There have been discrepancies (9)(10)(11)(12) in the definition of SARs and RARs in rats, depending on experimental conditions such as spontaneous versus artificial ventilation, and closed versus open chest. Criteria for their differentiation have included the AI, nerve fiber CV, responses to inflation or deflation, and responses to pharmacological agents (e.g., intravenous veratridine, intravenous histamine, and inhalation of diethyl ether).…”

CO2transduction in avian intrapulmonary chemoreceptors is critically dependent on transmembrane Na+/H+exchange

“…Low PCO 2 stimulates IPC firing, and high PCO 2 inhibits firing (9, 15, 16); thus the IPC response is backward compared with that of traditional respiratory chemoreceptors like the carotid bodies (18, 29), many presumptive central chemoreceptors (40), and snail pneumostome ganglia chemoreceptors (13,14). Many presumptive chemoreceptor neurons located in the mammalian medullary raphe, however, have also been shown to be inhibited by high PCO 2 (41, 54), as are reptilian IPC, mammalian pulmonary stretch receptors, and mammalian laryngeal CO 2 chemoreceptors (10,32,39,44). Thus the inverse CO 2 response (discharge rate inhibited by high CO 2 ) may be a common variant of respiratory chemosensitivity, just somewhat overlooked.…”