|Título:||Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats|
Cade, J. R.
Fernandes, A. A.
Ribeiro Junior, Rogerio Faustino
Targueta, Gabriel Pelegrineti
Mill, José Geraldo
Vassallo, Dalton Valentim
Infarto do miocárdio
|Data do documento:||Out-2009|
|Citação:||STEFANON, I. et al. Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats. Braz J Med Biol Res, Ribeirão Preto, v. 42, n. 10, p. 902-911, out. 2009. Disponível em: <http://www.scielo.br/pdf/bjmbr/v42n10/7618.pdf>. Acesso em: 7 fev. 2011.|
|Resumo:||Myocardial infarction leads to compensatory ventricular remodeling. Disturbances in myocardial contractility depend on the active transport of Ca2+ and Na+, which are regulated by Na+-K+ ATPase. Inappropriate regulation of Na+-K+ ATPase activity leads to excessive loss of K+ and gain of Na+ by the cell. We determined the participation of Na+-K+ ATPase in ventricular performance early and late after myocardial infarction. Wistar rats (8-10 per group) underwent left coronary artery ligation (infarcted, Inf) or sham-operation (Sham). Ventricular performance was measured at 3 and 30 days after surgery using the Langendorff technique. Left ventricular systolic pressure was obtained under different ventricular diastolic pressures and increased extracellular Ca2+ concentrations (Ca2+e) and after low and high ouabain concentrations. The baseline coronary perfusion pressure increased 3 days after myocardial infarction and normalized by 30 days (Sham 3 = 88 ± 6; Inf 3 = 130 ± 9; Inf 30 = 92 ± 7 mmHg; P < 0.05). The inotropic response to Ca2+e and ouabain was reduced at 3 and 30 days after myocardial infarction (Ca2+ = 1.25 mM; Sham 3 = 70 ± 3; Inf 3 = 45 ± 2; Inf 30 = 29 ± 3 mmHg; P < 0.05), while the Frank-Starling mechanism was preserved. At 3 and 30 days after myocardial infarction, ventricular Na+-K+ ATPase activity and contractility were reduced. This Na+-K+ ATPase hypoactivity may modify the Na+, K+ and Ca2+ transport across the sarcolemma resulting in ventricular dysfunction.|
|Aparece nas coleções:||DCFSI - Artigos publicados em periódicos|
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