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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.

Oxygen and glucose consumption related to Na+-K+ transport in canine brain.