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

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 c...

Full description

Bibliographic Details
Main Authors: I. Stefanon, J.R. Cade, A.A. Fernandes, R.F. Ribeiro Junior, G.P. Targueta, J.G. Mill, D.V. Vassallo
Format: Article
Language:English
Published: Associação Brasileira de Divulgação Científica 2009-10-01
Series:Brazilian Journal of Medical and Biological Research
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009001000005
_version_ 1819208372016119808
author I. Stefanon
J.R. Cade
A.A. Fernandes
R.F. Ribeiro Junior
G.P. Targueta
J.G. Mill
D.V. Vassallo
author_facet I. Stefanon
J.R. Cade
A.A. Fernandes
R.F. Ribeiro Junior
G.P. Targueta
J.G. Mill
D.V. Vassallo
author_sort I. Stefanon
collection DOAJ
description 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.
first_indexed 2024-12-23T05:38:20Z
format Article
id doaj.art-4f6ad84fde4548d2acdb3b7729cbad22
institution Directory Open Access Journal
issn 0100-879X
1414-431X
language English
last_indexed 2024-12-23T05:38:20Z
publishDate 2009-10-01
publisher Associação Brasileira de Divulgação Científica
record_format Article
series Brazilian Journal of Medical and Biological Research
spelling doaj.art-4f6ad84fde4548d2acdb3b7729cbad222022-12-21T17:58:15ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X1414-431X2009-10-014210902911Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in ratsI. StefanonJ.R. CadeA.A. FernandesR.F. Ribeiro JuniorG.P. TarguetaJ.G. MillD.V. VassalloMyocardial 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.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009001000005Heart failureOuabainNa+-K+ ATPaseMyocardial infarctionCalcium handling
spellingShingle I. Stefanon
J.R. Cade
A.A. Fernandes
R.F. Ribeiro Junior
G.P. Targueta
J.G. Mill
D.V. Vassallo
Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
Brazilian Journal of Medical and Biological Research
Heart failure
Ouabain
Na+-K+ ATPase
Myocardial infarction
Calcium handling
title Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
title_full Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
title_fullStr Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
title_full_unstemmed Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
title_short Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
title_sort ventricular performance and na k atpase activity are reduced early and late after myocardial infarction in rats
topic Heart failure
Ouabain
Na+-K+ ATPase
Myocardial infarction
Calcium handling
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009001000005
work_keys_str_mv AT istefanon ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats
AT jrcade ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats
AT aafernandes ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats
AT rfribeirojunior ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats
AT gptargueta ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats
AT jgmill ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats
AT dvvassallo ventricularperformanceandnakatpaseactivityarereducedearlyandlateaftermyocardialinfarctioninrats