ArticleExperimental physiology2011
Arachidonic acid products in airway nociceptor activation during acute lung injury.
Article in Experimental physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Mechanisms Involved in the Stimulatory and Inhibitory Effects of 5-Hydroxytryptamine on Vagal Mechanosensitive Afferents in Rat Lung.Frontiers in physiology · 2022Article
- Sustained sensitizing effects of tumor necrosis factor alpha on sensory nerves in lung and airways.Pulmonary pharmacology & therapeutics · 2017Review
- Immediate and delayed potentiating effects of tumor necrosis factor-α on TRPV1 sensitivity of rat vagal pulmonary sensory neurons.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Cough and expiration reflexes elicited by inhaled irritant gases are intensified in ovalbumin-sensitized mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Hypersensitivity of Vagal Pulmonary Afferents Induced by Tumor Necrosis Factor Alpha in Mice.Frontiers in physiology · 2017Article
- Article
- Activation of opioid μ-receptors, but not δ- or κ-receptors, switches pulmonary C-fiber-mediated rapid shallow breathing into an apnea in anesthetized rats.Respiratory physiology & neurobiology · 2012Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We have reported that airway nociceptors [C fibre receptors (CFRs) and high-threshold Aδ fibre receptors (HTARs)] are activated during oleic acid (OA)-induced acute lung injury. In the present studies, we tested the hypothesis that this nociceptor activation is mediated by arachidonic acid products. In anaesthetized, open-chest, mechanically ventilated rabbits, we examined the response of the nociceptors to intravenous injection of OA before and after blocking the cyclo-oxygenase pathways with indomethacin. Pretreatment with indomethacin (20 mg kg(-1)) decreased the background activities of both CFRs (from 0.48 ± 0.12 to 0.25 ± 0.08 impulses/s, n = 7, P < 0.05) and HTARs (from 0.54 ± 0.14 to 0.23 ± 0.08 impulses/s, n = 10, P < 0.01). It also blocked the response of the nociceptors to OA. Likewise, pretreatment with thromboxane synthase inhibitor (ketoconazole) also blocked the nociceptor response to OA. In addition, local microinjection or intravenous injection of a thromboxane mimetic stimulated CFRs and HTARs. The present results clearly indicate that arachidonic acid metabolites mediate airway nociceptor activation during OA-induced acute lung injury and suggest that thromboxane may be a key mediator.
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