Data/hora: 12/06/2024 10:33:15

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