Cardiovascular autonomic dysfunction in non-obese diabetic mice

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorMORAES, Oscar A.
dc.contributor.authorCOLUCCI, Juliana A.
dc.contributor.authorSOUZA, Leandro E.
dc.contributor.authorSCAPINI, Katia B.
dc.contributor.authorMORAES-SILVA, Ivana C.
dc.contributor.authorMOSTARDA, Cristiano
dc.contributor.authorANGELIS, Katia De
dc.contributor.authorCASARINI, Dulce E.
dc.contributor.authorIRIGOYEN, Maria Claudia
dc.date.accessioned2014-01-28T22:33:00Z
dc.date.available2014-01-28T22:33:00Z
dc.date.issued2013
dc.description.abstractIt is known that diabetes is associated with autonomic dysfunction; however, data about autonomic function in non-obese diabetic mice (NOD) remain scarce. We evaluated the autonomic profile of NOD mice. Female mice, 24-28 week old, were divided in two groups: NOD (n = 6) and control (n = 6, Swiss mice). NOD mice with glycemia >= 300 mg/dl were used. Heart rate variability (HRV) and arterial pressure variability (APV) in time and frequency domains, symbolic analysis of heart rate (HR) and baroreflex sensitivity were evaluated. HR and arterial pressure (AP) were similar between the groups; however, HRV (total variance of RR interval: NOD = 21.07 +/- 3.75 vs. C = 42.02 +/- 6.54 ms(2)) and the vagal modulation index RMSSD were lower in NOD group (4.01 +/- 032 vs. 8.28 +/- 0.97 ms). Moreover, the absolute and normalized low-frequency (LF) components were also enhanced in NOD (normalized = 61.0 +/- 4.0%) as compared to control mice (normalized = 20.0 +/- 4.0%). Both the absolute and normalized high-frequency (HF) components were lower in NOD (normalized = 39.0 +/- 4.0%) when compared to the control group (normalized = 80.0 +/- 4.0). In the symbolic analysis the 0V pattern, an indication of sympathetic activity, was higher in NOD and 2LV pattern, an indication of parasympathetic activity, was lower in the NOD than in the control group. Both bradycardic and tachycardic responses were decreased in NOD (3.01 +/- 0.72 vs. 4.54 +/- 0.36 bpm/mm Hg and 2.49 +/- 031 vs. C = 3.43 +/- 033 bpm/mm Hg) when compared to the control group. Correlation analysis showed negative correlations between vagal indexes (RMSSD, %HF and 2LV) and glycemic levels. In conclusion, NOD mice develop severe diabetes correlated with autonomic dysfunction.
dc.description.indexMEDLINE
dc.identifier.citationAUTONOMIC NEUROSCIENCE-BASIC & CLINICAL, v.177, n.2, p.143-147, 2013
dc.identifier.doi10.1016/j.autneu.2013.03.011
dc.identifier.issn1566-0702
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/4539
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofAutonomic Neuroscience-Basic & Clinical
dc.rightsrestrictedAccess
dc.rights.holderCopyright ELSEVIER SCIENCE BV
dc.subjectDiabetes mellitus
dc.subjectAutonomic nervous system
dc.subjectBaroreflex
dc.subjectMice
dc.subjectInbred NOD
dc.subject.otherheart-rate-variability
dc.subject.otherrenin-angiotensin system
dc.subject.othernod mice
dc.subject.otherbaroreflex sensitivity
dc.subject.otherarterial-pressure
dc.subject.otherreflex control
dc.subject.otherrats
dc.subject.otherneuropathy
dc.subject.othermodulation
dc.subject.othermodel
dc.subject.wosNeurosciences
dc.titleCardiovascular autonomic dysfunction in non-obese diabetic mice
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalMORAES, Oscar A.:Univ Sao Paulo FMUSP, Sch Med, Heart Inst InCor, Hypertens Unit, BR-05403000 Sao Paulo, Brazil; Nove de Julho Univ, Sao Paulo, Brazil
hcfmusp.author.externalCOLUCCI, Juliana A.:Univ Fed Sao Paulo, Dept Med, Div Nephrol, Sao Paulo, Brazil
hcfmusp.author.externalMORAES-SILVA, Ivana C.:Univ Sao Paulo FMUSP, Sch Med, Heart Inst InCor, Hypertens Unit, BR-05403000 Sao Paulo, Brazil
hcfmusp.author.externalANGELIS, Katia De:Nove de Julho Univ, Sao Paulo, Brazil
hcfmusp.author.externalCASARINI, Dulce E.:Univ Fed Sao Paulo, Dept Med, Div Nephrol, Sao Paulo, Brazil
hcfmusp.citation.scopus7
hcfmusp.contributor.author-fmusphcLEANDRO EZIQUIEL DE SOUZA
hcfmusp.contributor.author-fmusphcKATIA BILHAR SCAPINI
hcfmusp.contributor.author-fmusphcCRISTIANO TEIXEIRA MOSTARDA
hcfmusp.contributor.author-fmusphcMARIA CLAUDIA COSTA IRIGOYEN
hcfmusp.description.beginpage143
hcfmusp.description.endpage147
hcfmusp.description.issue2
hcfmusp.description.volume177
hcfmusp.origemWOS
hcfmusp.origem.pubmed23622812
hcfmusp.origem.scopus2-s2.0-84883773139
hcfmusp.origem.wosWOS:000325665700011
hcfmusp.publisher.cityAMSTERDAM
hcfmusp.publisher.countryNETHERLANDS
hcfmusp.relation.referenceAbd El Dayem SM, 2011, ANADOLU KARDIYOL DER, V11, P224, DOI 10.5152/akd.2011.061
hcfmusp.relation.referenceBillman GE, 2009, AM J PHYSIOL-HEART C, V297, pH1171, DOI 10.1152/ajpheart.00534.2009
hcfmusp.relation.referenceCHANG KSK, 1986, J MOL CELL CARDIOL, V18, P617, DOI 10.1016/S0022-2828(86)80969-5
hcfmusp.relation.referenceColucci JA, 2011, J RENIN-ANGIO-ALDO S, V12, P15, DOI 10.1177/1470320310375456
hcfmusp.relation.referenceDall'Ago P, 2002, BRAZ J MED BIOL RES, V35, P843, DOI 10.1590/S0100-879X2002000700013
hcfmusp.relation.referenceDe Angelis K, 2012, AM J PHYSIOL-REG I, V302, pR950, DOI 10.1152/ajpregu.00450.2011
hcfmusp.relation.referenceDe Angelis K, 2004, J APPL PHYSIOL, V96, P2174, DOI 10.1152/japplphysiol.00870.2003
hcfmusp.relation.referenceFazan R, 1999, J HYPERTENS, V17, P489, DOI 10.1097/00004872-199917040-00006
hcfmusp.relation.referenceFlecknell P.A., 1992, LAB ANIM, V26, P241
hcfmusp.relation.referenceFu WX, 2012, NAT IMMUNOL, V13, P361, DOI 10.1038/ni.2233
hcfmusp.relation.referenceGross V, 2008, AUTON NEUROSCI-BASIC, V138, P108, DOI 10.1016/j.autneu.2007.11.006
hcfmusp.relation.referenceGuzzetti S, 2005, CIRCULATION, V112, P465, DOI 10.1161/CIRCULATIONAHA.104.518449
hcfmusp.relation.referenceHeeren MV, 2009, MATURITAS, V62, P200, DOI 10.1016/j.maturitas.2008.12.011
hcfmusp.relation.referenceHong LZ, 2012, PHYSIOL RES, V61, P443
hcfmusp.relation.referenceJorge L, 2012, EXP DIABETES RES, DOI 10.1155/2012/108680
hcfmusp.relation.referenceKodama S, 2003, SCIENCE, V302, P1223, DOI 10.1126/science.1088949
hcfmusp.relation.referenceLa Rovere MT, 1998, LANCET, V351, P478
hcfmusp.relation.referenceMAEDA CY, 1995, HYPERTENSION, V26, P1100
hcfmusp.relation.referenceMakino S, 1980, Jikken Dobutsu, V29, P1
hcfmusp.relation.referenceCamm AJ, 1996, EUR HEART J, V17, P354
hcfmusp.relation.referenceMarco Giovana Seno Di, 2008, Int J Biochem Cell Biol, V40, P747, DOI 10.1016/j.biocel.2007.10.016
hcfmusp.relation.referenceMaser RE, 2003, DIABETES CARE, V26, P1895, DOI 10.2337/diacare.26.6.1895
hcfmusp.relation.referenceMostarda C, 2009, AUTON NEUROSCI-BASIC, V145, P11, DOI 10.1016/j.autneu.2008.10.010
hcfmusp.relation.referencePorta A, 2007, AM J PHYSIOL-HEART C, V293, pH702, DOI 10.1152/ajpheart.00006.2007
hcfmusp.relation.referenceSchaan BD, 1997, BRAZ J MED BIOL RES, V30, P1081
hcfmusp.relation.referenceSchmidt RE, 2003, AM J PATHOL, V163, P2077, DOI 10.1016/S0002-9440(10)63565-1
hcfmusp.relation.referenceSchmidt RE, 2002, INT REV NEUROBIOL, V50, P257
hcfmusp.relation.referenceSchumer M.P., 1998, DIABETES SPECTRUM, V11, P227
hcfmusp.relation.referenceSoares PPDA, 2004, AUTON NEUROSCI-BASIC, V113, P24, DOI 10.1016/j.autneu.2004.05.002
hcfmusp.relation.referenceVinik AI, 2007, CIRCULATION, V115, P387, DOI 10.1161/CIRCULATIONAHA.106.634949
hcfmusp.relation.referenceWEGNER JA, 1987, MED SCI SPORT EXER, V19, P497
hcfmusp.relation.referenceWichi R, 2007, CARDIOVASC DIABETOL, V6, DOI 10.1186/1475-2840-6-14
hcfmusp.relation.referenceZamo FS, 2010, CLINICS, V65, P85, DOI 10.1590/S1807-59322010000100013
hcfmusp.relation.referenceZimmet PZ, 1997, J DIABETES COMPLICAT, V11, P60, DOI 10.1016/S1056-8727(96)00090-6
hcfmusp.scopus.lastupdate2024-05-10
relation.isAuthorOfPublicationb273c648-931c-4157-aac9-771a86fa08dc
relation.isAuthorOfPublicatione8906456-b5ea-43c3-a7cf-4cdc353e7ab0
relation.isAuthorOfPublicationf9789375-7c13-4bac-ac71-2638b9902219
relation.isAuthorOfPublication124821b6-302b-4392-8a9a-b693916724e1
relation.isAuthorOfPublication.latestForDiscovery124821b6-302b-4392-8a9a-b693916724e1
Arquivos
Pacote Original
Agora exibindo 1 - 1 de 1
Nenhuma Miniatura disponível
Nome:
art_SOUZA_Cardiovascular_autonomic_dysfunction_in_non_obese_diabetic_mice_2013.PDF
Tamanho:
311.39 KB
Formato:
Adobe Portable Document Format
Descrição:
publishedVersion (English)