Postischemic Na+-K+-ATPase reactivation is delayed in the absence of glycolytic ATP in isolated rat hearts
Autor: | Jan G. Van Emous, Carmen L. A. M. Vleggeert-Lankamp, Marcel G. J. Nederhoff, Tom J. C. Ruigrok, Cees J. A. Van Echteld |
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Rok vydání: | 2001 |
Předmět: |
Male
medicine.medical_specialty Magnetic Resonance Spectroscopy Physiology Sodium chemistry.chemical_element Myocardial Reperfusion Injury Oxidative phosphorylation In Vitro Techniques Biology Oxidative Phosphorylation Contractility chemistry.chemical_compound Adenosine Triphosphate Physiology (medical) Internal medicine Pyruvic Acid medicine Animals Glycolysis Rats Wistar Na+/K+-ATPase Glycogen Myocardium Pyruvate dehydrogenase complex Rats Enzyme Activation Perfusion Glucose Endocrinology chemistry Biochemistry Sodium Isotopes Sodium-Potassium-Exchanging ATPase Cardiology and Cardiovascular Medicine Homeostasis |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 280:H2189-H2195 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.2001.280.5.h2189 |
Popis: | Normalization of intracellular sodium (Na[Formula: see text]) after postischemic reperfusion depends on reactivation of the sarcolemmal Na+-K+-ATPase. To evaluate the requirement of glycolytic ATP for Na+-K+-ATPase function during postischemic reperfusion, 5-s time-resolution23Na NMR was performed in isolated perfused rat hearts. During 20 min of ischemia, Na[Formula: see text] increased approximately twofold. In glucose-reperfused hearts with or without prior preischemic glycogen depletion, Na[Formula: see text]decreased immediately upon postischemic reperfusion. In glycogen-depleted pyruvate-reperfused hearts, however, the decrease of Na[Formula: see text] was delayed by ∼25 s, and application of the pyruvate dehydrogenase (PDH) activator dichloroacetate (DA) did not shorten this delay. After 30 min of reperfusion, Na[Formula: see text]had almost normalized in all groups and contractile recovery was highest in the DA-treated hearts. In conclusion, some degree of functional coupling of glycolytic ATP and Na+-K+-ATPase activity exists, but glycolysis is not essential for recovery of Na[Formula: see text] homeostasis and contractility after prolonged reperfusion. Furthermore, the delayed Na+-K+-ATPase reactivation observed in pyruvate-reperfused hearts is not due to inhibition of PDH. |
Databáze: | OpenAIRE |
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