Stroke, Vol 12, 726-730, Copyright © 1981 by American Heart Association
J Astrup, PM Sorensen and HR Sorensen
This study examines the relation between Na+-K+ transport and metabolism in
the canine brain. Cerebral oxygen and glucose consumption was measured by
the sagittal sinus outflow technique. Synaptic transmission and related
metabolism was blocked by pentobarbital 40 mg/kg (EEG flat). Lidocaine
blocked an additional 15-20%, presumable by restricting Na+-K+ leak fluxes
and reducing the demand for Na+-K+ transport. Ouabain blocked an additional
20-25% of metabolism. Ouabain also inhibited the Na+-K+ sensitive ATPase
associated transport and caused a net efflux of K+ from the cellular
compartment as evidenced by an increasing extracellular K+ concentration in
the cortex. Accordingly, a total of 40% of metabolism in te EEG-arrested
barbiturate inhibited brain could be related to Na+-K+ leak fluxes and
associated transport. The remaining 60% are related to processes
unidentified by this study. It is concluded that cerebral metabolism may be
reduced below the hitherto described barbiturate minimum.
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Oxygen and glucose consumption related to Na+-K+ transport in canine brain
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