Diabetic nerve exhibits morphological vulnerability to ischemia and reperfusion, in contrast to its physiological resistance to ischemic conduction failure (RICF). To examine the sequence of ischemic conduction failure after reperfusion in diabetic nerve, we measured sciatic-tibial nerve conduction before and during 30-180 min of ischemia and after reperfusion for up to 1 week in streptozocin (STZ)-induced diabetic rats. RICF in diabetic rats was confirmed during ischemia. After reperfusion, control nerves showed an immediate recovery in amplitude of compound muscle action potential (CMAP) following ischemia for 120 min or less, and delayed recovery after 150 min of ischemia. In contrast, recovery in diabetic nerves was delayed even after 1 h of ischemia. Ischemia for 75 min in diabetic nerve resulted in either delayed or no recovery of the CMAP upon reperfusion. Following ischemia for 90 or 120 min, axonal degeneration was observed in diabetic nerve. Thus, severe ischemia for 60 or 75 min causes prolonged ischemic conduction failure in diabetic nerve, compared with 150 min in control nerve. In conclusion, diabetic nerve shows delayed recovery of ischemic conduction failure after brief ischemia, compared to controls, suggesting that patients with diabetic neuropathy have a worse prognosis when faced with nerve ischemia.

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SHR showed slowed nerve conduction velocity and pathological abnormalities of hindlimb nerves. Sustained severe hypertension may cause axonal atrophy and endoneurial microangiopathy. Muscle Nerve 54: 756-762, 2016.