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Oxidative stress augments chemoreflex sensitivity in rats exposed to chronic intermittent hypoxia

dc.contributor.authorMorgan B.J.
dc.contributor.authorBates M.L.
dc.contributor.authorRio R.D.
dc.contributor.authorWang Z.
dc.contributor.authorDopp J.M.
dc.date.accessioned2020-09-02T22:23:42Z
dc.date.available2020-09-02T22:23:42Z
dc.date.issued2016
dc.identifier10.1016/j.resp.2016.09.001
dc.identifier.citation234, , 47-59
dc.identifier.issn15699048
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5452
dc.descriptionChronic exposure to intermittent hypoxia (CIH) elicits plasticity of the carotid sinus and phrenic nerves via reactive oxygen species (ROS). To determine whether CIH-induced alterations in ventilation, metabolism, and heart rate are also dependent on ROS, we measured responses to acute hypoxia in conscious rats after 14 and 21 d of either CIH or normoxia (NORM), with or without concomitant administration of allopurinol (xanthine oxidase inhibitor), combined allopurinol plus losartan (angiotensin II type 1 receptor antagonist), or apocynin (NADPH oxidase inhibitor). Carotid body nitrotyrosine production was measured by immunohistochemistry. CIH produced an increase in the ventilatory response to acute hypoxia that was virtually eliminated by all three pharmacologic interventions. CIH caused a robust increase in carotid body nitrotyrosine production that was greatly attenuated by allopurinol plus losartan and by apocynin but unaffected by allopurinol. CIH caused a decrease in metabolic rate and a reduction in hypoxic bradycardia. Both of these effects were prevented by allopurinol, allopurinol plus losartan, and apocynin. © 2016 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectAntioxidant
dc.subjectChemoreceptor
dc.subjectIntermittent hypoxia
dc.subjectReactive oxygen species
dc.subject3 nitrotyrosine
dc.subjectallopurinol
dc.subjectapocynin
dc.subjectlosartan
dc.subjectreactive oxygen metabolite
dc.subject3-nitrotyrosine
dc.subjectacetophenone derivative
dc.subjectallopurinol
dc.subjectantiarrhythmic agent
dc.subjectantioxidant
dc.subjectapocynin
dc.subjectcarbon dioxide
dc.subjectcatecholamine
dc.subjectlosartan
dc.subjectreactive oxygen metabolite
dc.subjectscavenger
dc.subjecttyrosine
dc.subjectadult
dc.subjectamino acid synthesis
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectbreathing
dc.subjectcarotid body chemoreceptor
dc.subjectchemoreceptor reflex
dc.subjectchemosensitivity
dc.subjectchemosensitization
dc.subjectchronic intermittent hypoxia
dc.subjectcontrolled study
dc.subjectheart rate
dc.subjectimmunohistochemistry
dc.subjectlong term exposure
dc.subjectmale
dc.subjectmetabolic rate
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectrat
dc.subjectanalogs and derivatives
dc.subjectanalysis of variance
dc.subjectanimal
dc.subjectblood
dc.subjectbody weight
dc.subjectbreathing
dc.subjectcarotid sinus
dc.subjectchemoreceptor cell
dc.subjectdrug effects
dc.subjecthypoxia
dc.subjectmetabolism
dc.subjectoxidative stress
dc.subjectoxygen consumption
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectplethysmography
dc.subjectregression analysis
dc.subjectSprague Dawley rat
dc.subjecttidal volume
dc.subjecttime factor
dc.subjectAcetophenones
dc.subjectAllopurinol
dc.subjectAnalysis of Variance
dc.subjectAnimals
dc.subjectAnti-Arrhythmia Agents
dc.subjectAntioxidants
dc.subjectBody Weight
dc.subjectCarbon Dioxide
dc.subjectCarotid Sinus
dc.subjectCatecholamines
dc.subjectChemoreceptor Cells
dc.subjectFree Radical Scavengers
dc.subjectHeart Rate
dc.subjectHypoxia
dc.subjectLosartan
dc.subjectMale
dc.subjectOxidative Stress
dc.subjectOxygen Consumption
dc.subjectPlethysmography
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectReactive Oxygen Species
dc.subjectRegression Analysis
dc.subjectRespiration
dc.subjectTidal Volume
dc.subjectTime Factors
dc.subjectTyrosine
dc.titleOxidative stress augments chemoreflex sensitivity in rats exposed to chronic intermittent hypoxia
dc.typeArticle


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