Linked Life Data

17950047

Source:http://linkedlifedata.com/resource/pubmed/id/17950047

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-2-4
pubmed:abstractText
Pulmonary C-fibers are stimulated by irritant air pollutants producing apnea, bronchospasm, and decrease in HR. Chemoreflex responses resulting from C-fiber activation are sometimes mediated by TRPV1 and release of substance P. While acrolein has been shown to stimulate C-fibers, the persistence of acrolein effects and the role of C-fibers in these responses are unknown. These experiments were designed to determine the effects of whole-body acrolein exposure and pulmonary chemoreflex response post-acrolein. Rats were exposed to either air or 3 ppm acrolein for 3 h while ventilatory function and HR were measured; 1-day later response to capsaicin challenge was measured in anesthetized rats. Rats experienced apnea and decrease in HR upon exposure to acrolein, which was not affected by either TRPV1 antagonist or NK(1)R antagonist pretreatment. Twenty-four hours later, capsaicin caused apnea and bronchoconstriction in control rats, which was potentiated in rats exposed to acrolein. Pretreatment with TRPV1 antagonist or NK(1)R antagonist prevented potentiation of apneic response and bronchoconstriction 24h post-exposure. These data suggest that although potentiation of pulmonary chemoreflex response 24h post-acrolein is mediated by TRPV1 and release of substance P, cardiopulmonary inhibition during whole-body acrolein exposure is mediated through other mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1569-9048
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
160-71
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17950047-Acrolein, pubmed-meshheading:17950047-Air Pollutants, pubmed-meshheading:17950047-Animals, pubmed-meshheading:17950047-Capsaicin, pubmed-meshheading:17950047-Chemoreceptor Cells, pubmed-meshheading:17950047-Drug Synergism, pubmed-meshheading:17950047-Irritants, pubmed-meshheading:17950047-Male, pubmed-meshheading:17950047-Nerve Fibers, Unmyelinated, pubmed-meshheading:17950047-Pulmonary Ventilation, pubmed-meshheading:17950047-Rats, pubmed-meshheading:17950047-Rats, Sprague-Dawley, pubmed-meshheading:17950047-Receptors, Neurokinin-1, pubmed-meshheading:17950047-Reflex, pubmed-meshheading:17950047-Respiration, pubmed-meshheading:17950047-Respiratory Mechanics, pubmed-meshheading:17950047-Respiratory System, pubmed-meshheading:17950047-Sensory System Agents, pubmed-meshheading:17950047-Substance P, pubmed-meshheading:17950047-TRPV Cation Channels
pubmed:year
2008
pubmed:articleTitle
Potentiation of pulmonary reflex response to capsaicin 24h following whole-body acrolein exposure is mediated by TRPV1.
pubmed:affiliation
Curriculum in Toxicology, University of North Carolina, Chapel Hill, NC 27599-7270, United States. hazari.mehdi@epa.gov
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural