Data/hora: 11/06/2024 02:35:30

Provedor de dados: | Brazilian Journal of Medical and Biological Research
País: | Brazil
Título: | Expression of inducible nitric oxide synthase is increased in patients with heart failure due to ischemic disease
Autores: | Ferreiro,C.R.; Chagas,A.C.P.; Carvalho,M.H.C.; Dantas,A.P.; Scavone,C.; Souza,L.C.B.; Buffolo,E.; Luz,P.L. da.
Data: | 2004-09-01
Ano: | 2004
Palavras-chave: | Nitric oxide synthase; Left ventricle ejection fraction; Heart failure.
Resumo: | The objective of the present study was to determine the relationship between nitric oxide synthases (NOS) and heart failure in cardiac tissue from patients with and without cardiac decompensation. Right atrial tissue was excised from patients with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) &lt;35% (N = 10), and from patients with CAD and LVEF &gt;60% (N = 10) during cardiac surgery. NOS activity was measured by the conversion of L-[H³]-arginine to L-[H³]-citrulline. Gene expression was quantified by the competitive reverse transcription-polymerase chain reaction. Both endothelial NOS (eNOS) activity and expression were significantly reduced in failing hearts compared to non-failing hearts: 0.36 ± 0.18 vs 1.51 ± 0.31 pmol mg-1 min-1 (P &lt; 0.0001) and 0.37 ± 0.08 vs 0.78 ± 0.09 relative cDNA absorbance at 320 nm (P &lt; 0.0001), respectively. In contrast, inducible NOS (iNOS) activity and expression were significantly higher in failing hearts than in non-failing hearts: 4.00 ± 0.90 vs 1.54 ± 0.65 pmol mg-1 min-1 (P &lt; 0.0001) and 2.19 ± 0.27 vs 1.43 ± 0.13 cDNA absorbance at 320 nm (P &lt; 0.0001), respectively. We conclude that heart failure down-regulates both eNOS activity and expression in cardiac tissue from patients with LVEF &lt;35%. In contrast, iNOS activity and expression are increased in failing hearts and may represent an alternative mechanism for nitric oxide production in heart failure due to ischemic disease.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004000900005
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2004000900005
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.37 n.9 2004
Fonte: | info:eu-repo/semantics/openAccess