The reduction in nerve free myoinositol, microvascular abnormalities, endoneurial hypoxia, vulnerability of the nerve to compression and entrapment, and resistance to ischemic conduction failure are the characteristics of diabetic neuropathy.

The aim of the present study is to assess the response of peripheral nerve to transient ishemia in streptozotocin-induced diabetic rats by the use of electrophysiologic and histopathologic studies.

The latency of compound muscle action potentials (CMAPs) of the tail was significantly prolonged in diabetic group as 2.26⁑0.46 msec compared with control group as 1.89⁑0.35 msec (p=0.009).

Ishemia was produced at the base of the tail and maintained for 180 minutes. CMAPs were recorded at 6 cm distal to the point of electrical stimulus. During ischemia, there were significant increments of latency and decrements of amplitude until the time to disappearance of CMAPs. the mean time to persistence of CMAPs was significantly prolonged in diabetic group as 75.8⁑25.4 minutes than control group as 30.0⁑5.1 minutes (p=0.000).

CMAPs were recorded again, after 180 minutes of ischemia. The mean time CMAPs evoked was shorter in diabetic group as 7.25⁑4.72 minutes than control group as 13.00⁑11.96 minutes (p=0.057). For an hour, there were decrements of latency and increments of amplitude in control and diabetic group, but to the half degree of those before ischemia the recovery rate was not different significantly (p>0.05). Histopathologic study showed ꁁ few attenuated nerve fibers in both groups similarly after 180 minutes' ischemia.

The results demonstrate that resistance to ischemic conduction failure is produced and no susceptibility to ischemia is noted in the peripheral nerve of 4 week-duration diabetic rats.