Sepsis: Going to the Heart of the Matter

Autor(es)

Celes, Mara R. N. ^[1] ; Prado, Cibele M. ^[1] ; Rossi, Marcos A. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Dept Pathol, Fac Med Ribeirao Preto, Lab Cellular & Mol Cardiol, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: PATHOBIOLOGY; v. 80, n. 2, p. 70-86, 2013.
• Citações Web of Science: 46

Resumo

Although myocardial depression is the predominant cause of death in severe sepsis/septic shock, it remains disputed whether the functional changes are a consequence of structural alterations. If we look at myocardial dysfunction from the perspective of a critically ill patient, there are a few questions to be asked: What causes myocardial dysfunction? What is the pathophysiology of cardiac dysfunction and death? Is there something that could be done to prevent the outcome? Each of these questions is interrelated and the answers will be more easily addressed if we continue to understand the basic mechanisms that are implicated. The principal mechanisms proposed for the pathogenesis of myocardial dysfunction support a prominent role for functional rather than anatomical abnormalities. However, attempts to reduce the high mortality in septic patients by manipulating the functional alterations have provided limited success. In recent years, the concept of septic cardiomyopathy has evolved, which implies alterations in the myocardial phenotype. This review includes an overview on the activation of the immune system and therapeutic approaches in sepsis, myocardial structural changes in the human septic heart, experimental models of sepsis, and cellular, molecular and functional myocardial changes seen in a variety of experimental sepsis models. The abnormal parameters discussed may emerge as therapeutic targets, for which modulation might provide beneficial effects on cardiovascular outcome and mortality in sepsis in the future. Copyright (C) 2012 S. Karger AG, Basel (AU)

• Processo FAPESP: 10/19216-5 - Hipertensão arterial, hipertrofia e falência cardíaca e complexo de glicoproteínas associadas à distrofina
• Beneficiário: Cibele Maria Prado Zinni
• Modalidade de apoio: Bolsas no Brasil - Jovens Pesquisadores
• Processo FAPESP: 09/54010-1 - EMU: sepsis e choque séptico: alterações funcionais e morfológicas do coração. Estudo experimental em camundongos
• Beneficiário: Helio Cesar Salgado
• Modalidade de apoio: Auxílio à Pesquisa - Programa Equipamentos Multiusuários
• Processo FAPESP: 07/58843-2 - O possivel papel do calcio no mecanismo intrinseco de perda primaria de distrofina na patogenese da disfuncao cardiaca na sepsis experimental.
• Beneficiário: Mara Rúbia Nunes Celes
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 09/17787-8 - Hipertensão arterial, hipertrofia e falência cardíaca e complexo de glicoproteínas associadas à distrofina.
• Beneficiário: Cibele Maria Prado Zinni
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores