We examined the effect of acute ischemia on peripheral nerve uptake of the glucose analog 2-deoxyglucose (2-DG). Endoneurial 2-DG incorporation was uniform at rest, but increased focally in areas subjected to moderate levels of ischemia which were not severe enough to impair nerve conduction. We believe these data are indicative of increased endoneurial glucose metabolism probably reflecting a compensatory shift to less efficient anaerobic glycolysis. This mechanism may in part account for peripheral nerve's ability to survive transient interruption of its blood supply.