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dc.contributor.authorNardocci G.
dc.contributor.authorMartin A.
dc.contributor.authorAbarzúa S.
dc.contributor.authorRodríguez J.
dc.contributor.authorSimon F.
dc.contributor.authorReyes E.P.
dc.contributor.authorAcuña-Castillo C.
dc.contributor.authorNavarro C.
dc.contributor.authorCortes P.P.
dc.contributor.authorFernández R.
dc.date.accessioned2020-09-02T22:24:14Z
dc.date.available2020-09-02T22:24:14Z
dc.date.issued2015
dc.identifier10.1016/j.jneuroim.2014.12.002
dc.identifier.citation278, , 44-52
dc.identifier.issn01655728
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5547
dc.descriptionSepsis progresses to multiple organ dysfunction (MOD) due to the uncontrolled release of inflammatory mediators. Carotid chemo/baro-receptors could play a protective role during sepsis. In anesthetized male rats, we measured cardiorespiratory variables and plasma TNF-α, glucocorticoids, epinephrine, and MOD marker levels 90. min after lipopolysaccharide (LPS) administration in control (SHAM surgery) and bilateral carotid chemo/baro-denervated (BCN) rats. BCN prior to LPS blunted the tachypneic response and enhanced tachycardia and hypotension. BCN-LPS rats also showed blunted plasma glucocorticoid responses, boosted epinephrine and TNF-α responses, and earlier MOD onset with a lower survival time compared with SHAM-LPS rats. Consequently, the complete absence of carotid chemo/baro-sensory function modified the neural, endocrine and inflammatory responses to sepsis. Thus, carotid chemo/baro-receptors play a protective role in sepsis. © 2014 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier
dc.subjectBilateral carotid/sinus neurotomy
dc.subjectCarotid body
dc.subjectEpinephrine
dc.subjectGlucocorticoids
dc.subjectMultiple organ dysfunction
dc.subjectSepsis
dc.subjectTissue damage
dc.subjectTNF-α
dc.subjectadrenalin
dc.subjectcortisone
dc.subjectglucocorticoid
dc.subjecthydrocortisone
dc.subjectlipopolysaccharide
dc.subjecttumor necrosis factor alpha
dc.subjectadrenalin
dc.subjectglucocorticoid
dc.subjectlipopolysaccharide
dc.subjecttumor necrosis factor alpha
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectbilateral carotid sinus neurotomy
dc.subjectbreathing rate
dc.subjectcardiovascular response
dc.subjectcorticosterone blood level
dc.subjectdeath
dc.subjectdisease severity
dc.subjectheart rate
dc.subjecthypotension
dc.subjectmale
dc.subjectmultiple organ failure
dc.subjectnonhuman
dc.subjectprotein blood level
dc.subjectrat
dc.subjectrisk factor
dc.subjectsepsis
dc.subjectsurgical technique
dc.subjectsurvival time
dc.subjectsystolic blood pressure
dc.subjecttachycardia
dc.subjecttachypnea
dc.subjecttidal volume
dc.subjecttissue injury
dc.subjecttreatment response
dc.subjectanimal
dc.subjectblood
dc.subjectbreathing
dc.subjectcarotid body
dc.subjectchemically induced
dc.subjectcomplication
dc.subjectdenervation
dc.subjectdrug effects
dc.subjectmetabolism
dc.subjectmultiple organ failure
dc.subjectnonparametric test
dc.subjectphysiology
dc.subjectpressoreceptor
dc.subjectprocedures
dc.subjectsepsis
dc.subjectSprague Dawley rat
dc.subjectsurvival
dc.subjecttoxicity
dc.subjectAnimals
dc.subjectCarotid Body
dc.subjectDenervation
dc.subjectEpinephrine
dc.subjectGlucocorticoids
dc.subjectHeart Rate
dc.subjectLipopolysaccharides
dc.subjectMale
dc.subjectMultiple Organ Failure
dc.subjectPressoreceptors
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectRespiration
dc.subjectSepsis
dc.subjectStatistics, Nonparametric
dc.subjectSurvival Analysis
dc.subjectTidal Volume
dc.subjectTumor Necrosis Factor-alpha
dc.titleSepsis progression to multiple organ dysfunction in carotid chemo/baro-denervated rats treated with lipopolysaccharide
dc.typeArticle


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