Abstract:Experiments were conducted with chloralose-urethan anesthetized rats to assess the effects of 1) bilateral stimulation of the cervical vagus nerves and 2) parasympathomimetic and sympathomimetic agents. Transpulmonary pressure (Ptp) was used as an index of airway smooth muscle tone, and peak inspiratory Ptp (Ptppeak) values were used for a comparison of responses. In untreated animals, vagal stimulation elicited an increase in Ptppeak of 155%. Cooling of the vagus nerves to 15 degrees C abolished the response … Show more
“…A solution of these chemicals at a volume of 0.7 ml was slowly injected into the vein over a period of 20 s. The doses of DMTU and indomethacin have been used previously in the studies of respiratory responses to inhaled wood smoke (Kou et al 1997) and cigarette smoke (Hong, Rodger & Lee, 1995), respectively. The dose of isoprenaline is higher than that required to block the bronchoconstriction evoked by vagal stimulation in rats (Haselton, Reynolds & Schultz, 1995). In a second group of nine receptors from six rats, afferent responses of each receptor to bolus intravenous injection of histamine (10 or 100 μg kg −1 ) were studied.…”
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 μg kg−1, i.v.) were studied in the other nine.
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 (Δ= 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.
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).
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.
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.
“…A solution of these chemicals at a volume of 0.7 ml was slowly injected into the vein over a period of 20 s. The doses of DMTU and indomethacin have been used previously in the studies of respiratory responses to inhaled wood smoke (Kou et al 1997) and cigarette smoke (Hong, Rodger & Lee, 1995), respectively. The dose of isoprenaline is higher than that required to block the bronchoconstriction evoked by vagal stimulation in rats (Haselton, Reynolds & Schultz, 1995). In a second group of nine receptors from six rats, afferent responses of each receptor to bolus intravenous injection of histamine (10 or 100 μg kg −1 ) were studied.…”
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 μg kg−1, i.v.) were studied in the other nine.
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 (Δ= 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.
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).
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.
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.
“…The stock solution of acetazolamide (20 mg/kg) or isoproterenol (0.1 mg/kg) required for each animal was further diluted in saline to a final volume of 0.7 ml and was slowly injected into the vein over a period of 20 s. The dose of acetazolamide has been reported to inhibit 99.99% of carbonic anhydrase (20). The dose of isoproterenol has been shown to block the bronchoconstriction evoked by vagal stimulation in rats (11).…”
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.
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