Reversible pulmonary trunk banding. VI: Glucose-6-phosphate dehydrogenase activity in rapid ventricular hypertrophy in young goats
Carregando...
Citações na Scopus
13
Tipo de produção
article
Data de publicação
2011
Título da Revista
ISSN da Revista
Título do Volume
Editora
MOSBY-ELSEVIER
Autores
ATIK, Fernando A.
OLIVEIRA, Fernanda S.
ABDUCH, Maria C. D.
SILVA, Gustavo J. J.
Citação
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, v.142, n.5, p.1108-U585, 2011
Resumo
Objective: Increased myocardial glucose-6-phosphate dehydrogenase (G6PD) activity occurs in heart failure. This study compared G6PD activity in 2 protocols of right ventricle (RV) systolic overload in young goats. Methods: Twenty-seven goats were separated into 3 groups: sham (no overload), continuous (continuous systolic overload), and intermittent (four 12-hour periods of systolic overload paired with a 12-hour resting period). During a 96-hour protocol, systolic overload was adjusted to achieve a 0.7 RV/aortic pressure ratio. Echocardiographic and hemodynamic evaluations were performed before and after systolic overload every day postoperatively. After the study period, the animals were humanely killed for morphologic and G6PD tissue activity assessment. Results: A 92.1% and 46.5% increase occurred in RV and septal mass, respectively, in the intermittent group compared with the sham group; continuous systolic overload resulted in a 37.2% increase in septal mass. A worsening RV myocardial performance index occurred in the continuous group at 72 hours and 96 hours, compared with the sham (P <.039) and intermittent groups at the end of the protocol (P <.001). Compared with the sham group, RV G6PD activity was elevated 130.1% in the continuous group (P = .012) and 39.8% in the intermittent group (P = .764). Conclusions: Continuous systolic overload for ventricle retraining causes RV dysfunction and upregulation of myocardial G6PD activity, which can elevate levels of free radicals by NADPH oxidase, an important mechanism in the pathophysiology of heart failure. Intermittent systolic overload promotes a more efficient RV hypertrophy, with better preservation of myocardial performance and and less exposure to hypertrophic triggers. (J Thorac Cardiovasc Surg 2011;142:1108-13)
Palavras-chave
Referências
- Abduch MCD, 2007, J THORAC CARDIOV SUR, V133, P1510, DOI 10.1016/j.jtcvs.2006.12.010
- Valente AS, 2008, REV BRAS CIR CARDIOV, V23, P60, DOI 10.1590/S0102-76382008000100011
- Gupte RS, 2007, J CARD FAIL, V13, P497, DOI 10.1016/j.cardfail.2007.04.003
- Gupte SA, 2006, J MOL CELL CARDIOL, V41, P340, DOI 10.1016/j.yjmcc.2006.05.003
- BISHOP SP, 1976, CIRC RES, V39, P238
- Dias CA, 2002, J THORAC CARDIOV SUR, V124, P999, DOI 10.1067/mtc.2002.124234
- Rajasekaran NS, 2007, CELL, V130, P427, DOI 10.1016/j.cell.2007.06.044
- Guzik TJ, 2002, CIRCULATION, V105, P1656, DOI 10.1161/01.CIR.0000012748.58444.08
- Serpillon S, 2009, AM J PHYSIOL-HEART C, V297, pH153, DOI 10.1152/ajpheart.01142.2008
- Recchia FA, 1998, CIRC RES, V83, P969
- Huss JM, 2005, J CLIN INVEST, V115, P547, DOI 10.1172/JCI200524405
- Park J, 2005, MOL CELL BIOL, V25, P5146, DOI 10.1128/MCB.25.12.5146-5157.2005
- Hink U, 2001, CIRC RES, V88, pE14
- Gupte SA, 2008, CURR OPIN INVEST DR, V9, P993
- Leong HS, 2002, AM J PHYSIOL-ENDOC M, V282, pE1039, DOI 10.1152/ajpendo.00507.2001
- Lopaschuk GD, 2007, CIRC RES, V101, P335, DOI 10.1161/CIRCRESAHA.107.150417
- An D, 2006, AM J PHYSIOL-HEART C, V291, pH1489, DOI 10.1152/ajpheart.00278.2006
- FULTON RM, 1952, BRIT HEART J, V14, P413
- Matsui R, 2005, CIRCULATION, V112, P257, DOI 10.1161/CIRCULATIONAHA.104.499095
- Bergmeyer HU, 1974, METHOD ENZYMAT AN, P1196
- Bonnet D, 1997, ARCH MAL COEUR VAISS, V90, P707
- Iemitsu M, 2003, HYPERTENS RES, V26, P829, DOI 10.1291/hypres.26.829
- LUZZATTO L, 1985, ADV HUM GENET, V14, P217
- Miana LA, 2010, ARQ BRAS CARDIOL, V95, P364, DOI 10.1590/S0066-782X2010005000105
- Zimmer Heinz-Gerd, 1996, Molecular and Cellular Biochemistry, V160-161, P101, DOI 10.1007/BF00240038