Nerve conduction velocity and evoked potential latencies in streptozotocin-diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor

Background Diabetes mellitus is associated with deficits in cerebral function. Vascular disorders may play a role in the pathogenesis and provide a potential target for treatment. The present study examined if prevention and intervention treatment with the angiotensin converting enzyme inhibitor enalapril could improve peripheral and central neurophysiological deficits in streptozotocin-diabetic rats. Methods Sciatic nerve conduction velocities were measured prior to diabetes induction and again every three weeks. In the prevention study, the final nerve conduction measurements were performed at 15 weeks and in the intervention study at 24 weeks. Brain stem auditory and visual evoked potential latencies were measured every 3 weeks from 10 weeks after diabetes induction. In the prevention study, the final evoked potential measurements were performed at 16 weeks and in the intervention study at 25 weeks. Treatment with the angiotensin converting enzyme inhibitor enalapril was started directly after diabetes induction (prevention treatment) and after 15 weeks of diabetes (intervention treatment). Results Nerve conduction velocity, brain stem auditory and visual evoked potential latencies were impaired in diabetic rats. Enalapril prevented deficits in nerve conduction velocity (p < 0.001), brain stem auditory evoked potential latencies (p < 0.01) and visual evoked potential latencies (p < 0.005). Enalapril intervention treatment had no effect on nerve conduction velocity and on visual evoked potential latencies, but improved brain stem auditory evoked potential latencies (p < 0.05) after 10 weeks of treatment. Conclusion Enalapril partially prevents the development of neurophysiological alterations in the peripheral and central nervous system and partially reverses deficits in brain stem auditory evoked potential latencies in STZ-diabetic rats. Copyright (C) 2003 John Wiley Sons, Ltd.