5‐Hydroxytryptamine mediates the post‐embolic increase in respiratory rate in anaesthetized rabbits

Armstrong, DJ; Kay, IS

doi:10.1113/expphysiol.1990.sp003424

Cited by 6 publications

(6 citation statements)

References 12 publications

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“…Following systemic allergen or endotoxin exposure, platelets accumulate in the lungs of mice and release serotonin which is thought to contribute to the pathophysiology of anaphylactic shock (Yoshida et al 2002). Experimental pulmonary embolism in rabbits leads to serotonin release (presumably from platelets) that in turn stimulates 5-HT3 receptors on intrapulmonary vagal C-fibres causing reflex tachypnoea (Armstrong & Kay, 1990). Intrapulmonary entrapment of activated platelets leads to reflex-mediated circulatory collapse in part due to 5-HT3 receptor-mediated afferent nerve activation (Kay & Armstrong, 1991).…”

Section: Role Of Endogenous Serotoninmentioning

confidence: 99%

Activation of mouse bronchopulmonary C‐fibres by serotonin and allergen‐ovalbumin challenge

Potenzieri¹,

Meeker²,

Undem³

2012

The Journal of Physiology

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Key points• Mast cell-derived serotonin is a principal mediator of allergic reactions in rodents. Serotonin can also be released from platelets during various pathological conditions. • Vagal C-fibres innervating the respiratory tract can be subdivided into nodose (placodal) C-fibres or jugular (neural crest) C-fibres). Activation of vagal placodal and/or neural crest vagal C-fibres probably contributes to the dyspnoea, cough and reflex parasympathetic drive commonly associated with serotonin.• Serotonin used different receptor subtypes to evoke strong action potential discharge in placodal (5-HT3 receptors) versus neural crest (non-5-HT3 receptors)-derived vagal C-fibres in the mouse lung.• Mast cell derived serotonin may activate neural crest C-fibres, but did not stimulate placodal C-fibres.• The effect of extracellular serotonin on vagal afferent activation therefore depends on its cellular source and the C-fibre phenotype.Abstract The effect of serotonin on capsaicin-sensitive vagal C-fibre afferent nerves was evaluated in an ex vivo vagally innervated mouse lung preparation. Action potentials arising from receptive fields in the lungs were recorded with an extracellular electrode positioned in the nodose/jugular ganglion. Among the 62 capsaicin-sensitive C-fibres studied (conduction velocity ∼0.5 m s −1 ), 71% were of the nodose phenotype and 29% of the jugular phenotype. The nodose C-fibres responded strongly to serotonin and this effect was blocked with the 5-HT3-receptor antagonist ondansetron. Using single cell RT-PCR, we noted that the vast majority of nodose neurons retrogradely labelled from the lung, expressed 5-HT3 receptor mRNA. The jugular C-fibres also responded strongly to serotonin with action potential discharge, but this effect was not inhibited by ondansetron. Lung-specific jugular neurons did not express 5-HT3 receptor mRNA but frequently expressed 5-HT1 or 5-HT4 receptor mRNA. Mast cells are the major source of serotonin in healthy murine airways. Ovalbumin-induced mast cell activation in actively sensitized lungs caused action potential discharge in jugular but not nodose C-fibres. The data show that vagal C-fibres in the respiratory tract of the mouse are strongly activated by serotonin. Depending on the C-fibre subtype both 5-HT3 and non-5-HT3 mechanisms are involved.

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Section: Role Of Endogenous Serotoninmentioning

confidence: 99%

Activation of mouse bronchopulmonary C‐fibres by serotonin and allergen‐ovalbumin challenge

Potenzieri¹,

Meeker²,

Undem³

2012

The Journal of Physiology

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“…Although not specifically identified as the mediator(s) involved in this electrophysiological study (3), many mediators such as cyclooxygenase metabolites, oxygen radicals, histamine, and serotonin could be released as a consequence of platelet aggregation (18). In their studies, Armstrong and co-workers (1,4) showed that the reflex tachypneic response to glass-bead microembolization in rabbits was totally prevented by platelet depletion and partially attenuated by pretreatment with a serotoninreceptor antagonist. The tachypneic response to microembolization in rabbits has been shown to be a reflex elicited by the stimulation of pulmonary C fibers (12).…”

mentioning

confidence: 97%

“…These results suggest that 1) cyclooxygenase products are necessary for the stimulation of PCs by PAE, whereas changes in lung mechanics are not, and 2) the functional importance of cyclooxygenase products may be mediated in part through the formation of z OH. lung vagal sensory receptors; microembolism; reflex tachypnea; ibuprofen; dimethylthiourea; cyclooxygenase system; hydroxyl radical PULMONARY MICROEMBOLISM is known to cause reflex tachypnea (1,4,12). Vagal lung C-fiber afferents are believed to play an important role in eliciting this respiratory response (1,4,12).…”

mentioning

confidence: 99%

“…lung vagal sensory receptors; microembolism; reflex tachypnea; ibuprofen; dimethylthiourea; cyclooxygenase system; hydroxyl radical PULMONARY MICROEMBOLISM is known to cause reflex tachypnea (1,4,12). Vagal lung C-fiber afferents are believed to play an important role in eliciting this respiratory response (1,4,12). Indeed, previous electrophysiological studies have demonstrated stimulation of vagal lung C-fiber nerve endings by emboli such as starch particles, plastic spheres, or glass beads (2,3,21).…”

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confidence: 99%

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Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs

Chen¹,

Lee

Kou

1997

Journal of Applied Physiology

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We investigated the involvement of the cyclooxygenase metabolites and hydroxyl radical (.OH) in the stimulation of vagal pulmonary C fibers (PCs) by pulmonary air embolism (PAE). Impulses were recorded from PCs in 51 anesthetized, open-chest, and artificially ventilated dogs. Fifty of 59 PCs were stimulated by infusion of air into the right atrium (0.2 ml.kg-1.min-1 for 10 min). As a group (n = 59), PC activity increased from a baseline of 0.4 +/- 0.1 to a peak of 1.7 +/- 0.2 impulses/s during the period from 1 min before to 2 min after the termination of PAE induction. In PCs initially stimulated by PAE induction, PAE was repeated after the intervening treatment (iv) with saline (n = 9), ibuprofen (a cyclooxygenase inhibitor; n = 11), or dimethylthiourea (a .OH scavenger; n = 12). The responses of PCs to PAE were not altered by saline vehicle but were abolished by ibuprofen and significantly attenuated by dimethylthiourea. Although hyperinflation of the lungs reversed the PAE-induced bronchomotor responses, it did not reverse the stimulation of PCs (n = 8). These results suggest that 1) cyclooxygenase products are necessary for the stimulation of PCs by PAE, whereas changes in lung mechanics are not, and 2) the functional importance of cyclooxygenase products may be mediated in part through the formation of .OH.

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“…15,28 The brain regions with a high density of 5-HT3 receptors are the area postrema, olfactory bulb and amygdala. 29 Ondansetron is a drug that is well absorbed from the gastrointestinal tract and rapidly penetrates the brain barriers.…”

Section: Discussionmentioning

confidence: 99%

Effects of ondansetron on respiratory pattern and sensation of experimentally induced dyspnea

et al. 2002

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CONTEXT: Dyspnea remains a therapeutic challenge, especially in chronic respiratory conditions. Recent studies have shown that the induction of unpleasant dyspnea sensations activates areas in the insular cortex. OBJECTIVE: This study was designed to investigate the potential effects of ondansetron, a potent anti-serotonin agent, on induced dyspnea sensation. TYPE OF STUDY: A randomized double blind study. SETTING: Pulmonary Function Laboratory of Hospital das Clínicas de Ribeirão Preto. PARTICIPANTS: Ten healthy male volunteers (mean age ± standard error = 23.1 ± 0.41 years) without respiratory diseases and showing normal spirometric tests. INTERVENTIONS: Uncomfortable breathing was induced in the volunteers on two different days, via the use of inspiratory resistors (loads of 0, 7, 14 and 21 cm H2O/l/sec) and breathholding, two hours after taking 8 mg of ondansetron (Ond) or placebo (Plac). MAIN MEASUREMENTS: Respiratory discomfort during breathing under loading was evaluated on a 100-mm visual analog scale. The maximum length of time of voluntary apnea was measured in seconds. RESULTS: The mean maximum voluntary apnea time did not differ between the ondansetron and placebo days (Plac = 96 ± 6.6 sec vs. Ond = 100 ± 7.9 sec). Ondansetron did not influence the dyspnea sensation induced by different inspiratory loads (0 cm H2O/l/sec: Ond = 1.4 mm ± 0.44 vs. Plac = 2.1 ± 0.85 mm; 7 cm H2O/l/sec: Ond = 16.6 ± 2.74 mm vs. Plac = 13.7 ± 2.06 mm; 14 cm H2O/l/sec; Ond = 30.5 ± 4.50 mm vs. Plac = 27.1 ± 3.44 mm; 21 cm H2O/l/sec: Ond = 50.3 ± 6.72 mm vs. Plac = 49.4 ± 6.72 mm). Ondansetron led to significant decreases in tidal volume under basal conditions and when breathing under the highest inspiratory loading (0 cm H2O/l/sec: Ond = 0.83 ± 0.26 l vs. Plac = 1.0 ± 0.28 l; 21 cm H2O/l/sec: Ond = 0.86 ± 0.23 l vs. Plac = 1.1 ± 0.22 l) CONCLUSION: The present results suggest that 5-HT3 receptors do not play an important role in the mediation of dyspnea sensations.

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5‐Hydroxytryptamine mediates the post‐embolic increase in respiratory rate in anaesthetized rabbits

Cited by 6 publications

References 12 publications

Activation of mouse bronchopulmonary C‐fibres by serotonin and allergen‐ovalbumin challenge

Activation of mouse bronchopulmonary C‐fibres by serotonin and allergen‐ovalbumin challenge

Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs

Effects of ondansetron on respiratory pattern and sensation of experimentally induced dyspnea

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