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Sepsis and septic shock: functional and morphological changes in the heart. An experimental study in mice

Grant number: 09/54010-1
Support type:Multi-user Equipment Program
Duration: October 01, 2010 - September 30, 2012
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Helio Cesar Salgado
Grantee:Helio Cesar Salgado
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
As informações de acesso ao Equipamento Multiusuário são de responsabilidade do Pesquisador responsável
EMU web page: Página do Equipamento Multiusuário não informada
Tipo de equipamento: Tipo de Equipamento Multiusuário não informado
Fabricante: Fabricante não informado
Modelo: Modelo não informado

Abstract

Sepsis produces pathophysiological changes, with marked hypotension, cardiac depression and decreased systemic perfusion, which contributes to multiple organ dysfunction. Although the cause of death in septic shock is probably multifactorial, myocardial dysfunction is a common complication, occurring prior to the shock. Even if studies in humans suggest the absence of ischemic myocardial alterations in sepsis, abnormal microcirculation induces a disturbance in regional blood flow and poor tissue oxygenation, which could cause relative ischemia in various organs, including the heart. The occurrence of microvascular changes is an issue that has been raised recently in our laboratory: the microcirculation might be implicated in the mechanism of myocyte cell injury, with subsequent cardiac dysfunction and death. Therefore, the objective of this project is to use the model of sepsis induced by the technique of cecal ligation and puncture (CLP) in mice to assess functional, structural and morphological characteristics of myocardial. (AU)

Scientific publications (7)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
PRADO, FERNANDA P.; DOS SANTOS, DANIELE O.; BLEFARI, VALDECIR; SILVA, CARLOS A.; MACHADO, JULIANO; KETTELHUT, ISIS DO CARMO; RAMOS, SIMONE G.; BARUFFI, MARCELO DIAS; SALGADO, HELIO C.; PRADO, CIBELE M. Early dystrophin loss is coincident with the transition of compensated cardiac hypertrophy to heart failure. PLoS One, v. 12, n. 12 DEC 21 2017. Web of Science Citations: 2.
DAL-SECCO, DANIELA; DALBO, SILVIA; LAUTHERBACH, NATALIA E. S.; GAVA, FABIO N.; CELES, MARA R. N.; BENEDET, PATRICIA O.; SOUZA, ADRIANA H.; AKINAGA, JULIANA; LIMA, VANESSA; SILVA, KATIUSSIA P.; KIGUTI, LUIZ RICARDO A.; ROSSI, MARCOS A.; KETTELHUT, ISIS C.; PUPO, ANDRE S.; CUNHA, FERNANDO Q.; ASSREUY, JAMIL. Cardiac hyporesponsiveness in severe sepsis is associated with nitric oxide-dependent activation of G protein receptor kinase. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, v. 313, n. 1, p. H149-H163, JUL 2017. Web of Science Citations: 11.
DOS SANTOS, DANIELE O.; BLEFARI, VALDECIR; PRADO, FERNANDA P.; SILVA, CARLOS A.; FAZAN, JR., RUBENS; SALGADO, HELIO C.; RAMOS, SIMONE G.; PRADO, CIBELE M. Reduced expression of adherens and gap junction proteins can have a fundamental role in the development of heart failure following cardiac hypertrophy in rats. Experimental and Molecular Pathology, v. 100, n. 1, p. 167-176, FEB 2016. Web of Science Citations: 6.
CELES, MARA R. N.; MALVESTIO, LYGIA M.; SUADICANI, SYLVIA O.; PRADO, CIBELE M.; FIGUEIREDO, MARIA J.; CAMPOS, ERICA C.; FREITAS, ANA C. S.; SPRAY, DAVID C.; TANOWITZ, HERBERT B.; DA SILVA, JOAO S.; ROSSI, MARCOS A. Disruption of Calcium Homeostasis in Cardiomyocytes Underlies Cardiac Structural and Functional Changes in Severe Sepsis. PLoS One, v. 8, n. 7 JUL 23 2013. Web of Science Citations: 18.
CELES, MARA R. N.; PRADO, CIBELE M.; ROSSI, MARCOS A. Sepsis: Going to the Heart of the Matter. PATHOBIOLOGY, v. 80, n. 2, p. 70-86, 2013. Web of Science Citations: 46.
PRADO, CIBELE M.; CELES, MARA R. N.; MALVESTIO, LYGIA M.; CAMPOS, ERICA C.; SILVA, JOAO S.; JELICKS, LINDA A.; TANOWITZ, HERBERT B.; ROSSI, MARCOS A. Early dystrophin disruption in the pathogenesis of experimental chronic Chagas cardiomyopathy. Microbes and Infection, v. 14, n. 1, p. 59-68, JAN 2012. Web of Science Citations: 7.
CAMPOS, ERICA C.; O'CONNELL, JOAO L.; MALVESTIO, LYGIA M.; DIAS ROMANO, MINNA M.; RAMOS, SIMONE G.; CELES, MARA RUBIA N.; PRADO, CIBELE M.; SIMOES, MARCUS V.; ROSSI, MARCOS A. Calpain-mediated dystrophin disruption may be a potential structural culprit behind chronic doxorubicin-induced cardiomyopathy. European Journal of Pharmacology, v. 670, n. 2-3, p. 541-553, NOV 30 2011. Web of Science Citations: 20.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.