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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorTHEOBALDO, Mariana Cardillo-
dc.contributor.authorLLIMONA, Flavia-
dc.contributor.authorPETRONI, Ricardo Costa-
dc.contributor.authorRIOS, Ester Correia Sarmento-
dc.contributor.authorVELASCO, Irineu Tadeu-
dc.contributor.authorSORIANO, Francisco Garcia-
dc.identifier.citationPLOS ONE, v.8, n.9, article ID e74369, 9p, 2013-
dc.description.abstractThe effects of hypertonic saline solution (HSS) have been shown in several animal models of ischemia and shock. Literature has shown potential benefits of HSS modulating inflammatory response after sepsis in an animal model. We studied the HSS effects in sepsis through cecal ligation and puncture (CLP) in Balb-C mice. Groups studied: 1-CLP without treatment (CLP-C); 2-CLP treated with normal saline solution NaCl 0.9% - 34 ml/Kg (CLP-S); 3-CLP treated with HSS NaCl 7.5% - 4 ml/Kg (CLPH); and 4-group (Basal) without no CLP or treatment. Volume infusion was always applied 30 min after CLP. Lung and peritoneal lavage were harvested after 6h and 24h of CLP to analyze cytokines amount, oxide nitric, lipid peroxidation and neutrophil infiltration. Neutrophil infiltration, ICAM-1, CXCR-2, and CXCL-1 in lung were reduced by HSS (CLP-H) compared to CLP-C or CLP-S. Neutrophil in peritoneal lavage was increased in 24h with HSS (CLP-H) compared to CLP and CLP-S. Peritoneal CXCR-2 was increased in CLP-C and CLP-S but presented a lower increase with HSS (CLP-H) after 6 hours. GRK-2 presented difference among the groups at 24 h, showing a profile similar to neutrophil infiltration. Pro-inflammatory cytokines (TNF-alpha and IL-6) were reduced by HSS treatment; CLP-S increased TNF-alpha IL-10 was increased in lung tissue by the HSS treatment. The oxidative stress (TBARS and nitric oxide biochemistry markers) was reduced with HSS. Animal survival was 33.3% in CLP-C group, 46.6% in CLP-S group and 60% in the CLP-H group after the sixth day. The HSS protects the animal against sepsis. Our results suggest that the volume replacement modulate pro and anti-inflammatory mediators of an inflammatory response, but HSS presented a more effective and potent effect.-
dc.description.sponsorshipFAPESP [2009/15530-0]-
dc.relation.ispartofPlos One-
dc.subject.othersevere hemorrhagic-shock-
dc.subject.otherseptic shock-
dc.titleHypertonic Saline Solution Drives Neutrophil from Bystander Organ to Infectious Site in Polymicrobial Sepsis: A Cecal Ligation and Puncture Model-
dc.rights.holderCopyright PUBLIC LIBRARY SCIENCE-
dc.subject.wosMultidisciplinary Sciences-
dc.type.categoryoriginal article-
hcfmusp.publisher.citySAN FRANCISCO-
hcfmusp.relation.referenceAbraham E, 1999, INTENS CARE MED, V25, P556, DOI 10.1007/s001340050903-
hcfmusp.relation.referenceALBELDA SM, 1994, FASEB J, V8, P504-
hcfmusp.relation.referenceAlberti C, 2002, INTENS CARE MED, V28, P108, DOI 10.1007/s00134-001-1143-z-
hcfmusp.relation.referenceAlves JC, 2008, SHOCK, V30, P3, DOI 10.1097/SHK.0b013e3181818466-
hcfmusp.relation.referenceAngus DC, 2001, CRIT CARE MED, V29, P1303, DOI 10.1097/00003246-200107000-00002-
hcfmusp.relation.referenceBONE RC, 1992, CHEST, V101, P1644, DOI 10.1378/chest.101.6.1644-
hcfmusp.relation.referenceCohen J, 2002, NATURE, V420, P885, DOI 10.1038/nature01326-
hcfmusp.relation.referenceConde KA, 2013, PLOS ONE, V6-
hcfmusp.relation.referenceCraciun FL, 2010, J IMMUNOL, V185, P6930, DOI 10.4049/jimmunol.1002300-
hcfmusp.relation.referenceDal-Pizzol F, 2006, AM J RESP CRIT CARE, V173, P84, DOI 10.1164/rccm.200507-1118OC-
hcfmusp.relation.referenceda Silva FP, 2009, FRONT BIOSCI, V14, P4464, DOI 10.2741/3542-
hcfmusp.relation.referenceDinarello CA, 1997, CHEST, V112, p321S, DOI 10.1378/chest.112.6_Supplement.321S-
hcfmusp.relation.referenceFrazier WJ, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0050071-
hcfmusp.relation.referenceFriedman G, 1998, CRIT CARE MED, V26, P2078, DOI 10.1097/00003246-199812000-00045-
hcfmusp.relation.referenceGLAUSER MP, 1994, CLIN INFECT DIS, V18, pS205-
hcfmusp.relation.referenceHENSON PM, 1987, J CLIN INVEST, V79, P669, DOI 10.1172/JCI112869-
hcfmusp.relation.referenceHOLZHEIMER RG, 1991, INFECTION, V19, P447, DOI 10.1007/BF01726463-
hcfmusp.relation.referenceLeendertse M, 2009, INFECT IMMUN, V77, P485, DOI 10.1128/IAI.00863-08-
hcfmusp.relation.referenceMajcherczyk PA, 1999, J BIOL CHEM, V274, P12537, DOI 10.1074/jbc.274.18.12537-
hcfmusp.relation.referenceMalbrain MLNG, 2005, CURR OPIN CRIT CARE, V11, P156, DOI 10.1097/01.ccx.0000155355.86241.1b-
hcfmusp.relation.referenceMelo ES, 2010, MOL IMMUNOL, V47, P2587, DOI 10.1016/j.molimm.2010.06.011-
hcfmusp.relation.referenceMercerJones MA, 1997, SHOCK, V8, P193, DOI 10.1097/00024382-199709000-00007-
hcfmusp.relation.referenceMorath S, 2001, J EXP MED, V193, P393, DOI 10.1084/jem.193.3.393-
hcfmusp.relation.referenceNduka OO, 2009, CRIT CARE CLIN, V25, P677, DOI 10.1016/j.ccc.2009.08.002-
hcfmusp.relation.referenceNoppens RR, 2012, CRIT CARE MED, V40, P2149, DOI 10.1097/CCM.0b013e31824e6750-
hcfmusp.relation.referenceOliveira RP, 2002, CRIT CARE, V6, P418-
hcfmusp.relation.referencePetroni RC, 2012, SHOCK, V37, P524, DOI 10.1097/SHK.0b013e31824c7665-
hcfmusp.relation.referenceRemick DG, 1998, CRIT CARE MED, V26, P895, DOI 10.1097/00003246-199805000-00025-
hcfmusp.relation.referenceRios ECS, 2011, CLINICS, V66, P469, DOI 10.1590/S1807-59322011000300019-
hcfmusp.relation.referenceRittirsch D, 2007, J LEUKOCYTE BIOL, V81, P137, DOI 10.1189/jlb.0806542-
hcfmusp.relation.referenceRivers E, 2001, NEW ENGL J MED, V345, P1368, DOI 10.1056/NEJMoa010307-
hcfmusp.relation.referenceSILVA MRF, 1987, AM J PHYSIOL, V253, pH751-
hcfmusp.relation.referenceShimazu R, 1999, J EXP MED, V189, P1777, DOI 10.1084/jem.189.11.1777-
hcfmusp.relation.referenceSoriano FG, 2002, SHOCK, V17, P286, DOI 10.1097/00024382-200204000-00008-
hcfmusp.relation.referenceSoriano FG, 2001, CRIT CARE MED, V29, P703-
hcfmusp.relation.referenceSoriano FG, 2011, SHOCK, V35, P560, DOI 10.1097/SHK.0b013e31820fe5d5-
hcfmusp.relation.referenceTakeuchi O, 1999, IMMUNITY, V11, P443, DOI 10.1016/S1074-7613(00)80119-3-
hcfmusp.relation.referencevan Haren FMP, 2012, SHOCK, V37, P268, DOI 10.1097/SHK.0b013e31823f152f-
hcfmusp.relation.referenceVELASCO IT, 1989, CRIT CARE MED, V17, P261, DOI 10.1097/00003246-198903000-00012-
hcfmusp.relation.referenceVELASCO IT, 1980, AM J PHYSIOL, V239, pH664-
hcfmusp.relation.referenceWEISS SJ, 1989, NEW ENGL J MED, V320, P365-
hcfmusp.relation.referenceWiedemann HP, 2006, NEW ENGL J MED, V354, P2564-
hcfmusp.relation.referenceZAPATASIRVENT RL, 1995, BURNS, V21, P185, DOI 10.1016/0305-4179(95)80006-A-
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Artigos e Materiais de Revistas Científicas - FM/MCM
Departamento de Clínica Médica - FM/MCM

Artigos e Materiais de Revistas Científicas - HC/ICHC
Instituto Central - HC/ICHC

Artigos e Materiais de Revistas Científicas - HC/InCor
Instituto do Coração - HC/InCor

Artigos e Materiais de Revistas Científicas - LIM/51
LIM/51 - Laboratório de Emergências Clínicas

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