The effects of α-receptor blockade on nerve conduction, hypoxic resistance, ouabain-sensitive Na+)-K+)-ATPase, nerve polyols, and capillary density were examined in streptozocin-induced diabetic (STZ-D) rats. Nondiabetic and untreated diabetic control groups were used. Diabetes duration was 2 mo. There were two treated diabetic groups. A “prevention” group received 5 mg/kg prazosin for 2 mo from the induction of diabetes. A “reversal” group was untreated for the 1st mo and was given prazosin for the subsequent month. Conduction was measured in motor nerves supplying tibialis anterior and gastrocnemius muscles and sensory saphenous nerve. Diabetes resulted in 15–29% reductions in conduction velocity (P < 0.01). In the prevention group, conduction deficits were minimal compared with untreated diabetes (P < 0.01). In the reversal group, motor conduction was also substantially improved, although sensory conduction was not significantly affected. In vitro measurement of sciatic nerve hypoxic resistance revealed a 49% increase in the time taken for compound action potential amplitude to reach half its initial value with diabetes (P < 0.01). This was largely prevented by prazosin treatment (P < 0.01), although treatment had a lesser effect in the reversal group. Treatment had no effect on nerve polyol levels or Na+-K+-ATPase activity. Functional improvements with prazosin were probably based on increased vasa nervorum perfusion. There was a 20% elevation of endoneurial capillary density (P < 0.01) in both prevention and reversal groups. We conclude that vascular factors play an important role in the etiology of experimental diabetic neuropathy, and functional changes may be corrected by chronic vasodilator treatment.

This content is only available via PDF.