Effects of nerve compression or ischaemia on conduction properties of myelinated and nonmyelinated nerve fibres. An experimental study in the rabbit common peroneal nerve

Compound action potentials of both myelinated (A) and non-myelinated (C) fibres in the common peroneal nerve of rabbits were studied during and after acute, graded compression of the nerve at 200 or 400 mmHg applied for 2 h or during ischaemia created by nitrogen inhalation or aortic occlusion. Compression of the nerve at 200 mmHg blocked the Ai component (large myelinated fibres) after about 23 min, while compression at 400 mmHg shortened this time to 11 min. The A2 component (thinner myelinated fibres) had a lower conduction velocity and a higher resistance to compression. There was just a slight decrease in conduction velocity of the nonmyelinated fibres when the nerves were compressed at 200 mmHg for 2 h. However, compression at 400 mmHg for 2 h induced a marked deterioration of amplitude and conduction velocity of the C-fibres. There was an incomplete restitution of function of A- and C-fibres during 2 h of recovery. The thinner myelinated fibres were more susceptible to deprivation of oxygen than the thicker ones, while non-myelinated fibres differed in response according to method of ischaemia induction. It is concluded that non-myelinated fibres are very resistant to compression and a very high pressure (> 400 mmHg) is needed to affect these fibres.     

Renal sympathetic nerve responses to stimulation, inhibition and destruction of the ventrolateral medulla in the rabbit

The role of the sympathetic nervous system in the cardiovascular responses to lesions of the caudal ventrolateral medulla of the rabbit was investigated by measurement of renal sympathetic nerve activity. In addition, the effect of chemical stimulation and inhibition on renal sympathetic nerve activity was assessed. The results show that lesions or chemical inhibition of the caudal ventrolateral medulla result in an increase in sympathetic nerve activity and blood pressure, whilst excitation results in a decrease in blood pressure and nerve activity. These findings contrast with chemical stimulation or inhibition of the rostral ventrolateral medulla in the region of the C1 cells where stimulation results in a rise in blood pressure and renal nerve activity, and inhibition, a fall in blood pressure and nerve activity.     

Effects of propionyl-l-carnitine and insulin on the electroretinogram,nerve conduction and nerve blood flow in rats with streptozotocin-induced diabetes

The effect of an analogue ofl-carnitine, propionyl-l-carnitine, on the electroretinogram, motor nerve conduction velocity and nerve blood flow was determined in rats with streptozotocin-induced diabetes, and was compared with the effects of insulin alone or combined therapy. Oral administration of propionyl-l-carnitine (3 g/kg daily for 4 weeks) significantly increased caudal nerve motor conduction velocity and sciatic nerve blood flow in diabetic rats. There were no differences in the effects of insulin (8–10 U daily for 4 weeks), propionyl-l-carnitine and combined therapy. Although propionyl-l-carnitine significantly shortened the peak latency of the electroretinogram b-wave in diabetic rats, its effect was far weaker than that of insulin or combined therapy, with combined therapy producing the greatest improvement. These effects of propionyl-l-carnitine were accompanied by a decrease of serum lipid levels, an increase of the sciatic nerve carnitine content, and no changes of the tissue (nerve and retinal) sorbitol andmyo-inositol concentrations. In contrast, insulin significantly reduced the tissue sorbitol content and markedly increasedmyo-inositol. These findings suggest that propionyl-l-carnitine may improve diabetic neuropathy and retinopathy without influencing the polyol pathway, and that this beneficial effect may be mediated through the amelioration of microcirculation and tissue carnitine content, thus probably increasing fatty acid oxidation.