Chronic low frequency electrical activation for one week corrects nerve conduction velocity deficits in rats with diabetes of three months duration

Abstract

Summary. This study examined the effect of chronic electrical activation on conduction velocity deficits after three months of streptozotocin-induced diabetes. There were 30% and 20% reductions in conduction velocity in diabetic animals for tibialis anterior and saphenous nerves, respectively (p <0.01). Unilateral electrical stimulation of the common peroneal nerve, which contains axons supplying tibialis anterior but not saphenous nerve, was carried out in a group of diabetic and a group of normal control rats. Stimulation was given over seven days, at 10 Hz for 8 h/day. Final experiments were carried out at least 17 h after the last stimulation session. In normal rats stimulation had no effect on conduction velocity in either nerve. In diabetic animals, however, tibialis anterior conduction was within the normal control range for the stimulated nerve. In contrast, the contralateral unstimulated nerve had reduced conduction velocity (p < 0.001), which was within the unoperated diabetic control range. There were no effects on saphenous nerve conduction, comparing stimulated and unstimulated legs. We conclude that chronic increases in nerve electrical activation promote mechanisms that reverse conduction deficits in diabetic rats.Key words: Diabetic neuropathy, chronic electrical stimulation, nerve conduction, streptozotocin-diabetes.Reduced nerve conduction velocity (NCV) is an early neuropathic change in diabetic patients and animals. Its aetiology is unclear although several hypotheses have been considered. One viewpoint is that neuropathy results from hyperglycaemia stimulating the polyol pathway, which leads to loss of myo-inositol from nerve fibres. This in turn reduces nerve Na-K ATPase pump activity: fibres become Na loaded, Na channels inactivate, and NCV decreases [1]. Another hypothesis suggests that reduced nerve blood flow caused by rheological changes coupled with vasa nervosum microangiopathy leads to endoneurial hypoxia sufficient to impair function [21.In this communication we present data demonstrating that chronic nerve stimulation normalises NCV in streptozotocin-diabetic rats. We employed nerve stimulation to activate skeletal muscles as part of an investigation into changes in capillarisation and oxidative potential [3]. We also monitored NCV in stimulated and unstimulated nerve branches, and this previously unreported effect of electrical activation may have some beating on the mechanisms underlying diabetic neuropathy. Materials and methodsMale Sprague-Dawley rats aged 19 weeks, obtained from the Aberdeen University breeding colony, were divided into normal and diabetic groups. Normal animals acted as ,onset controls and were studied in final experiments one week later. A further group of normal rats was not subjected to stimulation or any operative procedures but was left for a further three months to act as unstimulated age-matched controls. The other animals were given a single i.p. injection of streptozotocin (45 mg/kg) in 20 mmol/1 sodium citrate buffer (pH 4.5). Diabetes was verified...

The effects of evening primrose oil on nerve function and capillarization in streptozotocin‐diabetic rats: modulation by the cyclo‐oxygenase inhibitor flurbiprofen

“…The NCV deficit also appears to be readily and rapidly reversible by EPO treatment, at least during the first 3-4 months of diabetes. The time-course of reversal is similar to that found for chronic electrical nerve stimulation (Cameron et al, 1989b), and for vasodilator treatment with lisinopril (Cameron, Cotter & Robertson, unpublished observations). The washout of EPO effects on NCV was also extremely rapid, with a return to diabetic control levels within 24 h. This suggests that EPO's action relies in the first instance on fairly rapidly synthesized metabolic products, rather than depending on structural changes of nerve fibres or vasa nervorum.…”

The Electrical Response to Injury: Molecular Mechanisms and Wound Healing

“…Phasic electrical stimulation is often employed, which favors nerve activation, and indeed improves nerve function in diabetic rat, 106,107 as well as increasing wound healing in diabetic mice 108 and man. 109 Less is known about the effects of prolonged DC stimulation at a level to mimic naturally occurring wound potentials, although in nondiabetic patients and animals there is usually an improvement in wound tensile strength.…”

Changes in purinergic responses of the rabbit isolated central ear artery after chronic electrical stimulation in vivo

“…Few studies have investigated the effects of chronic electrical stimulation in vivo on the local control of the vasculature which is important in terms of how best the procedure can be used to alleviate disorders such as peripheral vascular disease (Tallis et al, 1983). It is known, however, that prolonged electrical stimulation increases tissue blood flow and induces structural changes in the vasculature, including neovascularization (Brown et al, 1976;Cameron et al, 1989;Hudlicka et al, 1991). The rabbit isolated central ear artery is a useful model since the great auricular nerve which supplies the artery (Feldberg, 1926) is easily accessible for stimulation in vivo.…”