It is well documented that diabetic rats and subjects have a paradoxical resistance to ischemic conduction block although the nerves of diabetes are more susceptible to entrapment neuropathies. The aim of the present study was to further analyze the effect of anoxia on the diabetic nerve. Nerve conduction was measured in vitro in desheathed sciatic nerves from spontaneously diabetic rats (BB-Wistar) and age-matched controls. After onset of anoxia the compound action potential (CAP) decreased to 50% in 17 min in diabetic rat nerves and 8 min in normals. Following reoxygenation CAP recovered to 50% in 30 s in normal rat nerves and after 3 min the recovery was 92%. In nerves from diabetic animals 50% recovery took 4 min, but still after 12 min CAP was suppressed to a 60% level of the original. Longer periods of anoxia did not impair the recovery in normal nerve as it did in the diabetic ones. This defective recovery after anoxia in nerves from diabetic animals may be relevant for the understanding of the pathogenesis of entrapment neuropathies in diabetic subjects.