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...
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Associação Brasileira de Divulgação Científica
2009-10-01
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Series: | Brazilian Journal of Medical and Biological Research |
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Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009001000005 |
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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. |
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issn | 0100-879X 1414-431X |
language | English |
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publishDate | 2009-10-01 |
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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 |
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