Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats

Brazilian Journal of Medical and Biological Research

I. Stefanon¹  J.r. Cade¹  A.a. Fernandes¹  R.f. Ribeiro Junior¹  G.p. Targueta¹  J.g. Mill¹  D.v. Vassallo¹ 

[1] ,Universidade Federal do Espírito Santo Departamento de Ciências Fisiológicas Vitória ES ,Brasil

关键词: Heart failure;    Ouabain;    Na+-K+ ATPase;    Myocardial infarction;    Calcium handling;   

DOI  :  10.1590/S0100-879X2009005000015

来源: SciELO

【 摘 要 】

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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