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Lipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats

dc.contributor.authorFernández R.
dc.contributor.authorCortés P.
dc.contributor.authordel Rio R.
dc.contributor.authorAcuña-Castillo C.
dc.contributor.authorReyes E.P.
dc.contributor.authorReyes E.P.
dc.date.accessioned2020-09-02T22:17:28Z
dc.date.available2020-09-02T22:17:28Z
dc.date.issued2015
dc.identifier10.1007/978-3-319-18440-1_18
dc.identifier.citation860, , 161-166
dc.identifier.issn00652598
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4446
dc.descriptionThe acute kidney injury (AKI) observed during sepsis is due to an uncontrolled release of inflammatory mediators. Septic patients develop electrolytic disturbances and one of the most important is ionized hypocalcemia. AKI adversely affects the function of other organs and hypocalcemia is associated with cardiovascular and respiratory dysfunctions. Since carotid body chemoreceptors modulate the systemic inflammatory response during sepsis syndromes, we used pentobarbitone-anesthetized male Sprague-Dawley rats in control condition (SHAM surgery) and after bilateral carotid neurotomy (carotid chemo/baro-denervated, BCN). We evaluate serum creatinine (CRE), serum neutrophil gelatinase-associated lipocaline (NGAL), ionized calcium (iCa) and cardiac Troponin I (cTnI) 90 min after the IP administration of 15 mg/kg lipopolysaccharide (LPS) or saline. In the SHAM group, LPS failed to induce significant changes CRE, NGAL, or iCa, and increased cTnI. Conversely, in the BCN group LPS increased CRE and NGAL, decreased iCa, and enhanced the increase of cTnI. Our results suggest that carotid chemo/baro-receptors might contribute to the regulation of both renal function and calcemia during sepsis. In addition, results imply that the carotid chemo-baroreceptors serve as an immunosensory organ. © Springer International Publishing Switzerland 2015.
dc.language.isoen
dc.publisherSpringer New York LLC
dc.subjectAcute kidney injury
dc.subjectCardiac Troponin I
dc.subjectCarotid body
dc.subjectIonized hypocalcemia
dc.subjectSepsis
dc.subjectcalcium
dc.subjectcreatinine
dc.subjectlipopolysaccharide
dc.subjectneutrophil gelatinase associated lipocalin
dc.subjecttroponin I
dc.subjectacute phase protein
dc.subjectcreatinine
dc.subjectlipocalin
dc.subjectlipopolysaccharide
dc.subjectneutrophil gelatinase-associated lipocalin protein, rat
dc.subjectoncoprotein
dc.subjectacute kidney failure
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectcarotid body chemoreceptor
dc.subjectcontrolled study
dc.subjectcreatinine blood level
dc.subjectdenervation
dc.subjectelectrocardiogram
dc.subjecthypocalcemia
dc.subjectionized hypocalcemia
dc.subjectmale
dc.subjectnonhuman
dc.subjectpressoreceptor
dc.subjectpriority journal
dc.subjectprotein blood level
dc.subjectrat
dc.subjectsepsis
dc.subjectAcute Kidney Injury
dc.subjectanimal
dc.subjectblood
dc.subjectcarotid body
dc.subjectelectrocardiography
dc.subjecthypocalcemia
dc.subjectphysiology
dc.subjectSprague Dawley rat
dc.subjectRattus
dc.subjectAcute Kidney Injury
dc.subjectAcute-Phase Proteins
dc.subjectAnimals
dc.subjectCarotid Body
dc.subjectCreatinine
dc.subjectDenervation
dc.subjectElectrocardiography
dc.subjectHypocalcemia
dc.subjectLipocalins
dc.subjectLipopolysaccharides
dc.subjectMale
dc.subjectPressoreceptors
dc.subjectProto-Oncogene Proteins
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.titleLipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats
dc.typeArticle


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