AbstractWe have developed a reliable, reproducible model of hypoxia in the gerbil.1H and31P NMR spectroscopy demonstrates that cerebral energy metabolism is very 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 untilpaO2was below 40 mm Hg. In 50% of the animals lactate increased prior to any change in the phosphorus metabolites or intracellular pH, suggesting that1H NMR may be more sensitive than31P 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 lactat