Vol. 280, Issue 5, H2189-H2195, May 2001
Postischemic
Na+-K+-ATPase reactivation is
delayed in the absence of glycolytic ATP in isolated
rat hearts
Jan G.
Van Emous,
Carmen L. A. M.
Vleggeert-Lankamp,
Marcel G. J.
Nederhoff,
Tom J. C.
Ruigrok, and
Cees J. A.
Van Echteld
Interuniversity Cardiology Institute of The Netherlands and
Department of Cardiology, Heart Lung Institute, University Medical
Center, 3508 GA Utrecht, The Netherlands
Normalization of intracellular sodium (Na
)
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-resolution 23Na NMR was performed in isolated perfused rat hearts.
During 20 min of ischemia, Na increased
approximately twofold. In glucose-reperfused hearts with or without
prior preischemic glycogen depletion, Na
decreased immediately upon postischemic reperfusion. In
glycogen-depleted pyruvate-reperfused hearts, however, the decrease of
Na 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
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 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.
23Na NMR spectroscopy; oxidative phosphorylation; glycogen; compartmentalization
