| Registro completo |
| Provedor de dados: |
56
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| País: |
Brazil
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| Título: |
Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
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| Autores: |
Stefanon,I.
Cade,J.R.
Fernandes,A.A.
Ribeiro Junior,R.F.
Targueta,G.P.
Mill,J.G.
Vassallo,D.V.
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| Data: |
2009-10-01
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| Ano: |
2009
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| Palavras-chave: |
Heart failure
Ouabain
Na+-K+ ATPase
Myocardial infarction
Calcium handling
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| 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.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009001000005
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| Editor: |
Associação Brasileira de Divulgação Científica
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| Relação: |
10.1590/S0100-879X2009005000015
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| Formato: |
text/html
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| Fonte: |
Brazilian Journal of Medical and Biological Research v.42 n.10 2009
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| Direitos: |
info:eu-repo/semantics/openAccess
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