BRAIN METABOLISM AND BLOOD-FLOW IN ACUTE CEREBRAL HYPOXIA STUDIED BY NMR-SPECTROSCOPY AND HYDROGEN CLEARANCE

We have developed a reliable, reproducible model of hypoxia in the gerbil. H-1 and P-31 NMR spectroscopy demonstrates that cerebral energy metabolism is verv resistant to hypoxia. Cerebral blood flow (measured by hydrogen clearance) began to increase when the arterial oxygen tension (paO2) was reduced to 40-50 mm Hg, and there was no change in phosphorus metabolites or lactate until paO2 was below 40 mm Hg. In 50% of the animals lactate increased prior to any change in the phosphorus metabolites or intracellular pH, suggesting that H-1 NMR may be more sensitive than P-31 NMR at detecting hypoxic or ischaemic changes. The calculated rate of oxygen delivery at a time when phosphorus energy metabolism becomes impaired is similar in both hypoxia and ischaemia (ca 4 mL/100 g/min). We suggest that the critical factor in ischaemia is the reduction in oxygen supply, rather than the accumulation of toxic metabolites, such as lactate.