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Fig. 9. Local measurements of erythrocyte flux (LDF) made in patients with mild diabetic polyneuropathy before a sural nerve biopsy in comparison with patients without diabetes with other polyneuropathies or with vasculitic polyneuropathy. Note that patients with diabetes had trends toward higher flux whereas patients with vasculitis had significant reductions in local blood flow. One patient with a sural nerve that was treated with epinephrine had reduced flux whereas a patient with diabetes with severe lumbosacral plexopathy had significantly reduced local blood flow. (Reproduced with permission from ref. 152.)

Fig. 9. Local measurements of erythrocyte flux (LDF) made in patients with mild diabetic polyneuropathy before a sural nerve biopsy in comparison with patients without diabetes with other polyneuropathies or with vasculitic polyneuropathy. Note that patients with diabetes had trends toward higher flux whereas patients with vasculitis had significant reductions in local blood flow. One patient with a sural nerve that was treated with epinephrine had reduced flux whereas a patient with diabetes with severe lumbosacral plexopathy had significantly reduced local blood flow. (Reproduced with permission from ref. 152.)

morphological work have not identified such alterations in a variety of models or in a human study. Very few interventional studies have gone beyond short-term rat models, where structural evidence of axon damage is very limited. Indeed the sheer numbers and varieties of agents proposed for human therapy based on some of the experimental work is so large as to question specificity of the corrections they have identified and proposed. Similarly, few studies have explored the possibility that interventions directed primarily toward microvessels might more importantly target events in ganglia, rather than nerve trunks. Many human diabetic subjects already undergo chronic therapy for a number of macrovascular complications and hypertension, yet it is unclear if they are protected from polyneuropathy by these agents. Other interventions without vascular actions have substantially altered the development of neuropathy or reversed it through mechanisms that directly target neurons, rather than blood vessels.

Future work should likely de-emphasize exclusive attention toward microvessels in the pathogenesis of diabetic neuropathy. Thinking about diabetic polyneuropathy needs to be flexible, multidisciplinary, and not exclusive. It should emphasize rigorous, long-term models in more than one species, several clinically relevant end points beyond changes in nerve conduction, and should consider the range of potential actions of pharmacological interventions applied. It might be that shared molecular mechanisms, not yet thoroughly worked out, of microvessel dysfunction and direct neuron targeting, best explains the development of this complex and intractable problem.

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