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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

INCREASED SARCOLEMMAL PERMEABILITY AS AN EARLY EVENT IN EXPERIMENTAL SEPTIC CARDIOMYOPATHY: A POTENTIAL ROLE FOR OXIDATIVE DAMAGE TO LIPIDS AND PROTEINS

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Autor(es):
Celes, Mara R. N. [1] ; Torres-Duenas, Diego [2] ; Prado, Cibele M. [1] ; Campos, Erica C. [1] ; Moreira, Jorge E. [1, 3] ; Cunha, Fernando Q. [2] ; Rossi, Marcos A. [1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Pathol, BR-14049900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Pharmacol, BR-14049900 Sao Paulo - Brazil
[3] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Mol & Cell Biol, BR-14049900 Sao Paulo - Brazil
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: Shock; v. 33, n. 3, p. 322-331, MAR 2010.
Citações Web of Science: 21
Resumo

This study describes increased sarcolemmal permeability and myofilamentar damage that occur together with lipid peroxidation and protein nitration in the myocardium in severe sepsis induced by cecal ligation and puncture. Male C57BL/6 mice were submitted to moderate and severe septic injury and sham operation. Using light and laser confocal microscopy, diffuse foci of myocytolysis associated with focal disruption of the actin/myosin contractile apparatus could be seen in hearts with severe septic injury. The myocardial expressions of the sarcomeric proteins myosin and actin were downregulated by both severe and moderate injuries. The detection of albumin staining in the cytoplasm of myocytes to evaluate sarcolemmal permeability provided evidence of severe and mild injury of the plasma membrane in hearts with severe and moderate septic injury, respectively. The administration of a superoxide scavenger caused marked reduction of sarcolemmal permeability, indicating the involvement of free radicals in its genesis. On electron microscopy, these changes were seen to correspond to spread blocks of a few myocytes with fragmentation and dissolution of myofibrils, intracellular edema, and, occasionally, rupture of the sarcolemma. In addition, oxidative damage to lipids, using anti-4-hydroxynonenal, an indicator of oxidative stress and disruption of plasma membrane lipids, and to proteins, using antinitrotyrosine, a stable biomarker of peroxynitrite-mediated protein nitration, was demonstrated. These findings make plausible the hypothesis that increased sarcolemmal permeability might be a primary event in myocardial injury in severe sepsis possibly due to oxidative damage to lipids and proteins that could precede phenotypic changes that characterize a septic cardiomyopathy. (AU)

Processo FAPESP: 07/58843-2 - O possível papel do cálcio no mecanismo intrínseco de perda primária de distrofina na patogênese da disfunção cardíaca na sépsis experimental
Beneficiário:Mara Rúbia Nunes Celes
Linha de fomento: Bolsas no Brasil - Pós-Doutorado
Processo FAPESP: 06/52882-3 - O possível papel do complexo de glicoproteínas associadas à distrofina na morte súbita na tripanosomíase americana experimental
Beneficiário:Cibele Maria Prado Zinni
Linha de fomento: Bolsas no Brasil - Pós-Doutorado
Processo FAPESP: 06/59618-0 - O possível papel do complexo de glicoproteínas associadas à distrofia na morte súbita na tripanossomiase americana experimental
Beneficiário:Marcos Antonio Rossi
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 07/59448-0 - O possível papel do complexo distrofina-glicoproteínas associadas na cardiomiopatia dilatada experimental induzida pelo antineoplásico doxorrubicina
Beneficiário:Erica Carolina Campos Pulici
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 07/52556-1 - Imunopatogênese da lesão periapical experimentalmente induzida em camundongos knockout de citocinas Th1 (IFNy) e Th2 (IL-4 and IL-10), molécula de adesão intercelular (ICAM-1) e receptor de quimiocina (CCR5): panorama geral de possíveis mecanismos envolvidos no estímulo ou proteção da reabsorção óssea
Beneficiário:Marcos Antonio Rossi
Linha de fomento: Auxílio à Pesquisa - Regular