An early and consistent finding is impaired vasoregulation of peripheral nerve trunk. Nerve blood flow to peripheral nerve is reduced to about 50% of normal. The reduction occurs early and is sustained. In a recent review (1) of studies of peripheral nerve blood flow in experimental diabetic neuropathy, a reduction was demonstrated in 19/21 research programs (Table 1) and typically on multiple occasions. The two laboratories that failed to demonstrate this deficit had methodological problems such as inexperience with a label or contaminating nutritive flow with arteriovenous shunt flow. This reduction is because of impairment of nitric oxide synthase activity (2,3) and is initially reversible. To address the issue of whether the impaired perfusion is pathophysiologically important, Cameron et al. (4) regressed nerve blood flow against nerve conduction velocity. There is a close relationship between nerve blood flow and nerve conduction slowing (Fig. 1). This relationship highlights the importance of a reduction in endoneurial perfusion, either reflecting the effect of the same primary process (oxidative stress) affecting both microvessels and large somatic nerves or the primary role of nerve ischemia. The importance of oxidative stress is highlighted by correction of this perfusion deficit by the antioxidant a-lipoic acid (5,6).
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