Innervation of airway smooth muscle. Efferent mechanisms

Andersson, Rolf G. G.; Grundström, N.

doi:10.1016/0163-7258(87)90055-6

Cited by 54 publications

(33 citation statements)

References 154 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NANCe responses of the guinea-pig isolated bronchus to EFS are believed to reflect the antidromic activation of a subset of intramural sensory neurones (Andersson & Grundstrom, 1987). The ability of capsaicin to abolish NANCe responses (Andersson & Grundstrom, 1983;Lundberg et al, 1983; Present Study, Figure lb), suggests that the transmitter(s) in this pathway is a sensory neuropeptide (Buck & Burks, 1986), although its identity remains to be established.…”

Section: Discussionmentioning

confidence: 97%

Effects of BRL 38227 on neurally‐mediated responses in the guinea‐pig isolated bronchus

Good

Clapham

Hamilton

1992

British J Pharmacology

View full text Add to dashboard Cite

1 In guinea-pig isolated bronchus treated with indomethacin (2.8 gM), electrical field stimulation (EFS; 10 Hz, 0.5 ms, 60-70 V, for 10 s) evoked a tetrodotoxin (3 JM)-sensitive, biphasic contraction comprising a rapid, atropine (1 tLM)-sensitive cholinergic response succeeded by a slowly developing, capsaicin (10lM)-sensitive, non-adrenergic, non-cholinergic excitatory (NANCe) response.2 BRL 38227 (0.3-3 AM), salmeterol (0.003-3 pM) and ketotifen (1.0-300 AM) each produced concentration-dependent inhibition of both NANCe and cholinergic responses to EFS in guinea-pig isolated bronchus. 3 Substance P (SP; 1 ,M) and neurokinin A (NKA; 0.07 Mm) produced contractions equivalent in magnitude to the NANCe response to EFS, which were inhibited by salmeterol (1 pM), but not by BRL 38227 (3 Mm) or ketotifen (100 AM). 4 Acetylcholine (ACh; 6 AM) was equi-effective with the electrical activation of cholinergic neurones. BRL 38227 (3 AM) slightly inhibited responses to ACh (6 pM). Salmeterol (1 pM) and ketotifen (100 MM) markedly inhibited responses to ACh (6 Mm). 5 In bronchial rings pre-contracted with ACh (100 pM), BRL 38227 (0.1-30 pM), salmeterol (0.001-3tMM) and ketotifen (0.1-100 MM) each produced concentration-dependent relaxation. Unlike ketotifen, BRL 38227 and salmeterol only partially (18.8 ± 2.1% and 51.8 ± 3.9% respectively) reversed the ACh-induced contraction. 6 The (+ )-analogue of BRL 38227, BRL 38226 (0.3-100 MM), was without effect on responses to EFS and had no effect on the inhibition caused by BRL 38227. The K+-channel

show abstract

Section: Discussionmentioning

confidence: 97%

Effects of BRL 38227 on neurally‐mediated responses in the guinea‐pig isolated bronchus

Good

Clapham

Hamilton

1992

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…In many species, including humans, the density of b-adrenoceptors in the lungs is higher than in any other tissue 36 and blocking these receptors with drugs, such as propranolol, worsens airway obstruction in people with asthma. [39][40][41][42] In animal studies, propranolol has been shown to inhibit the benefit of VNS in reducing bronchoconstriction.…”

Section: Discussionmentioning

confidence: 99%

“…This norepinephrine may potentially bind to b 2 -adrenoceptors on airway smooth muscle to induce bronchodilation or to modulate cholinergic neurotransmissions in human airways via prejunctional inhibitory a 2 -adrenoceptors. 36 Alternatively, stimulation may activate iNANC nerves and release of nitric oxide to relax pulmonary smooth muscle. 37,38 Another possibility is that afferent VNS triggered catecholamine release from the adrenal medulla.…”

Section: Discussionmentioning

confidence: 99%

Feasibility of Percutaneous Vagus Nerve Stimulation for the Treatment of Acute Asthma Exacerbations

Miner

Lewis

Mosnaim

et al. 2012

Academic Emergency Medicine

View full text Add to dashboard Cite

Objectives: This study assessed the feasibility of an investigational vagus nerve stimulation (VNS) device for treating acute asthma exacerbations in patients not responding to at least 1 hour of initial standard care therapy.Methods: This was a prospective, nonrandomized study of patients treated in the ED for moderate to severe acute asthma (forced expiratory volume in 1 second [FEV 1 ] 25% to 70% of predicted). Treatment entailed percutaneous placement of an electrode near the right carotid sheath and 60 minutes of VNS and continued standard care. VNS voltage was adjusted to perceived improvement, muscle twitching, or adverse events (AEs). All AEs, vital signs, FEV 1 , perceived work of breathing (WOB), and final disposition were recorded.Results: Twenty-five subjects were enrolled. There were no serious AEs and no significant changes in vital signs. No subject required terminating VNS. One patient had minor bleeding from the procedure, and one had a hematoma and withdrew prior to VNS. AEs related to VNS were temporary and included cough (1 of 24), swallowing difficulty (2 of 24), voice change (2 of 24), and muscle twitching (14 of 24). These resolved when VNS ended. The FEV 1 improved at 15 minutes (median = 15.8%, 95% confidence interval [CI] = 9.3% to 22.4%), 30 minutes (median = 21.3%, 95% CI = 8.1% to 36.5%), and 60 minutes (median = 27.5%, 95% CI = 11.3% to 43.5%). WOB improved at 15 minutes (median = 53.9%, 95% CI = 33.7% to 73.9%), 30 minutes (median = 69.1%, 95% CI = 56.4% to 81.8%), and 60 minutes (median = 81.0%, 95% CI = 68.5% to 93.5%).Conclusions: Percutaneous VNS did not result in serious AEs and was associated with improvements in FEV 1 and perceived dyspnea. Percutaneous VNS appears to be feasible for use in the treatment of moderate to severe acute asthma in patients unresponsive to initial standard care treatment.

show abstract

“…[2][3][4] In guinea pig trachea, airway smooth-muscle relaxation is controlled by both adrenergic and non-adrenergic non-cholinergic pathways. 5 Mediators involved in these pathways include epinephrine and norepinephrine, as well as nitric oxide and vasoactive intestinal peptide, respectively. 6 In a previous work 2 we reported that O 3 induced an impairment of prejunctional adrenergic relaxation without affecting the post-junctional guinea pig tracheal responses to isoproterenol (ISO) and sodium nitroprusside (NP), a well-known nitric oxide donor.…”

Section: Introductionmentioning

confidence: 99%

Ozone induces impairment of adrenergic relaxation in thoracic guinea pig tracheas

Sommer

Vargas

Campos

et al. 2001

J of Applied Toxicology

View full text Add to dashboard Cite

The effect of ozone on airway relaxation mechanisms has been seldom studied. We exposed guinea pigs to ozone (0.3, 0.6 or 1.2 ppm for 4 h) and studied the in vitro tracheal responses to isoproterenol and nitroprusside, looking for differences between cervical and thoracic regions. We found that ozone did not alter responses to nitroprusside, whereas it produced a concentration-dependent decrease in the responses to isoproterenol in thoracic but not cervical tracheas. Thus, in isolated organ studies care should be taken to avoid mixing cervical and thoracic tracheal regions, at least when adrenergic responses are to be evaluated.

show abstract

Innervation of airway smooth muscle. Efferent mechanisms

Cited by 54 publications

References 154 publications

Effects of BRL 38227 on neurally‐mediated responses in the guinea‐pig isolated bronchus

Effects of BRL 38227 on neurally‐mediated responses in the guinea‐pig isolated bronchus

Feasibility of Percutaneous Vagus Nerve Stimulation for the Treatment of Acute Asthma Exacerbations

Ozone induces impairment of adrenergic relaxation in thoracic guinea pig tracheas

Contact Info

Product

Resources

About