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Updated: Jun 20, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats
I Stefanon1, J R Cade, A A Fernandes
1Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil. ivanita@pq.cnpq.br
Insights
Myocardial infarction reduces Na+-K+ ATPase activity, impairing ventricular contractility and ion transport. This dysfunction persists long after heart attack, affecting cardiac performance.
Area of Science:
- Cardiovascular Physiology
- Cardiac Metabolism
- Myocardial Infarction Research
Background:
- Myocardial infarction (MI) triggers ventricular remodeling, impacting cardiac contractility.
- Cardiac contractility relies on ion transport, particularly Na+ and Ca2+, regulated by Na+-K+ ATPase.
- Dysregulated Na+-K+ ATPase activity can lead to cellular ion imbalance (K+ loss, Na+ gain).
Purpose of the Study:
- To investigate the role of Na+-K+ ATPase in ventricular performance after myocardial infarction.
- To assess early (3 days) and late (30 days) effects of MI on Na+-K+ ATPase activity and cardiac function.
- To determine if Na+-K+ ATPase hypoactivity contributes to post-MI ventricular dysfunction.
Main Methods:
- Wistar rats underwent myocardial infarction (coronary ligation) or sham surgery.
- Ventricular performance was evaluated using the Langendorff technique.
- Measurements included left ventricular pressure, response to extracellular Ca2+ and ouabain, and Na+-K+ ATPase activity.
Main Results:
- Coronary perfusion pressure increased early post-MI but normalized by 30 days.
- The inotropic response to Ca2+ and ouabain was significantly reduced at both 3 and 30 days post-MI.
- Ventricular Na+-K+ ATPase activity and contractility were decreased at 3 and 30 days after MI.
- The Frank-Starling mechanism remained preserved post-MI.
Conclusions:
- Reduced Na+-K+ ATPase activity (hypoactivity) is evident early and late after myocardial infarction.
- This hypoactivity likely impairs Na+, K+, and Ca2+ transport across the sarcolemma.
- Na+-K+ ATPase dysfunction contributes significantly to post-myocardial infarction ventricular dysfunction.
Abstract:
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.
