Cardiac changes in experimental sepsis (2005)
- Authors:
- USP affiliated authors: CUNHA, FERNANDO DE QUEIROZ - FMRP ; ROSSI, MARCOS ANTONIO - FMRP
- Unidade: FMRP
- Subjects: DOENÇAS CARDIOVASCULARES; SEPTICEMIA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: The journal of coronary artery disease
- Volume/Número/Paginação/Ano: v. 6, n. 1, p. 24, res. 074, 2005
- Conference titles: International congress on coronary artery disease : from prevention to intervention
-
ABNT
CELES, M. R. N.; TORRES-DUENAS, D.; CUNHA, Fernando de Queiroz; ROSSI, Marcos Antonio. Cardiac changes in experimental sepsis. The journal of coronary artery disease[S.l: s.n.], 2005. -
APA
Celes, M. R. N., Torres-Duenas, D., Cunha, F. de Q., & Rossi, M. A. (2005). Cardiac changes in experimental sepsis. The journal of coronary artery disease. Istambul. -
NLM
Celes MRN, Torres-Duenas D, Cunha F de Q, Rossi MA. Cardiac changes in experimental sepsis. The journal of coronary artery disease. 2005 ; 6( 1): 24. -
Vancouver
Celes MRN, Torres-Duenas D, Cunha F de Q, Rossi MA. Cardiac changes in experimental sepsis. The journal of coronary artery disease. 2005 ; 6( 1): 24. - Reduction of GAP junction proteins and intercalated disc structural remodeling in the hearts of mice submitted to sepsis
- Aorta remodeling due to stretch or turbulent flow/low wall shear stress: distinctly different biological phenomena ?
- Reduction of gap junction proteins and intercalated disc structural remodeling in the hearts of mice submitted to sepsis
- Sepsis and the heart
- Reduction of gap and adherens junction proteins and intercalated disc structural remodeling in the hearts of mice submitted to severe cecal ligation and puncture sepsis
- Sepsis and the heart
- Intercalated disc and dystrophin-glycoprotein complex remodeling in the hearts of mice submitted to severe sepsis
- Verapamil ameliorates septic cardiomyopathy induced by cecal ligation and puncture in mice
- Sepsis and the heart
- Cardiovascular hyporresponsiveness in severe sepsis is related with augment of G-protein receptor kinase (GRK)-2 expression via a nitric oxide-dependent mechanism
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