Stimulation of pulmonary rapidly adapting receptors by inhaled wood smoke in rats.
1. The stimulation of pulmonary rapidly adapting receptors (RARs) by wood smoke was investigated. Impulses from seventy RARs were recorded in fifty-nine anaesthetized, open-chest and artificially ventilated rats; responses to delivery of 6 ml of wood smoke into the lungs were studied in sixty-one receptors whereas responses to histamine (10 or 100 microg kg-1, i.v.) were studied in the other nine. 2. Delivery of wood smoke stimulated fifty-two of the sixty-one RARs studied. When stimulated, an intense burst of discharge was evoked within 1 or 2 s of smoke delivery. This increased activity quickly peaked in 1-3 s (Delta = 15.8 +/- 1.6 impulses s-1; n = 61; mean +/- s.e.m.), then declined and yet remained at a level higher than the baseline activity. The mean duration of the stimulation was 25.1 +/- 2.7 s. In contrast, smoke delivery did not affect tracheal pressure. 3. Peak responses of RARs to wood smoke were partially reduced by removal of smoke particulates and were largely attenuated by pretreatment with dimethylthiourea (DMTU, a hydroxyl radical scavenger), indomethacin (Indo, a cyclo-oxygenase inhibitor), or both DMTU and Indo (DMTU + Indo). Conversely, the peak responses of RARs were not significantly affected by pretreatment with isoprenaline (a bronchodilator) or vehicle for these chemicals. Additionally, pretreatment with DMTU, Indo, or DMTU + Indo did not significantly alter the RAR sensitivity to mechanical stimulation (constant-pressure lung inflation; 20 cmH2O). 4. Of the nine RARs tested, six were stimulated by histamine and their sensitivity to this chemical irritant was not altered by pretreatment with DMTU + Indo. 5. The results suggest that both the particulates and gas phases are responsible for, and both the hydroxyl radical and cyclo-oxygenase products are involved in, the stimulation of RARs by wood smoke. Furthermore, changes in lung mechanics following smoke delivery are not the cause of this afferent stimulation.
Lai
C J
CJ
Institute of Physiology, School of Medicine and Life Science, National Yang-Ming University, Taipei, Taiwan 11221, Republic of China.
Kou
Y R
YR
D000818:Animals; D001993:Bronchodilator Agents / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D005260:Female; D016166:Free Radical Scavengers / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008168:Lung / Q000502:physiology*; D008297:Male; D008465:Mechanoreceptors / Q000187:drug effects*; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012906:Smoke; D013268:Stimulation, Chemical; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology
D001993:Bronchodilator Agents; D016861:Cyclooxygenase Inhibitors; D016166:Free Radical Scavengers; D012906:Smoke; D006632:Histamine; C038983:1,3-dimethylthiourea; D013890:Thiourea; D007545:Isoproterenol; D007213:Indomethacin