E. K. Maxfield

TL;DR: The data suggest that vascular-mediated nerve dysfunction in diabetes depends on oxidative stress, and that similar effects in non-diabetic rats may be produced by pro-oxidant treatment, and provides evidence for the potentially important role of oxygen free radical activity in diabetic neuropathy.

TL;DR: It is concluded that oxidative stress makes an important contribution to the aetiology of early experimental diabetic neuropathy and amelioration of oxidative stress could potentially be a final common mechanism whereby a number of diverse treatments exert a beneficial effect on diabetic nerve function.

TL;DR: The data show that a very high degree of polyol pathway blockade is necessary to correct nerve functional deficits and that aldose reductase inhibitors have a neurovascular action that does not depend on restoration of nerve myo-inositol.

TL;DR: It is concluded that overproduction of nitric oxide is unlikely to be involved in the aetiology of experimental diabetic neuropathy, however, endothelial dysfunction resulting in impaired Nitric oxide and prostacyclin synthesis could make a substantial contribution.

TL;DR: The investigation has identified abnormalities in vasa nervorum reactivity which are ameliorated by angiotensin II receptor blockade and may contribute to experimental diabetic neuropathy.