Is vasodilatation following dorsal column stimulation mediated by antidromic activation of small diameter afferents?

It is well-known that high intensity electrical stimulation of peripheral nerves and dorsal root fibres causes vasodilatation. However, the mechanisms underlying the vasodilatory effect of stimulation applied to the dorsal columns (DCS), with an intensity insufficient to recruit small diameter, high threshold fibres are virtually unknown. The present project was planned to elucidate underlying neural mechanisms. Albino rats, anaesthetized, paralyzed and artificially ventilated were used. Electrical stimulation with different parameters was applied to various sites of the exposed spinal cord, root fibres and peripheral nerves. In some experiments the spinal cord, root fibres or peripheral nerves were transected. Peripheral blood flow was recorded using laser Doppler technique. With stimulation of the lower thoracic region at low intensity substantially increased blood flow in the ipsilateral hind paw. The compound action potentials from the gural nerve displayed only components from low threshold, rapidly conducting fibres without detectable late components. Transection of the spinal cord above the stimulation site did not affect the blood flow changes. Also low intensity stimulation of the proximal part of a sectioned dorsal root resulted in a substantial rise in peripheral blood flow, whereas the same intensity proved ineffective when applied to the distal stump. High intensity stimulation of the distal stump not unexpectedly, caused a major increase in blood flow. The findings in the present study implicate the importance of a central circuit for the effect, whereas antidromic activation of primary afferents seems to be a less likely explanation. Possibly, stimulation induces a transitory inhibition of sympathetic vasoconstrictor tone, though activation of sympathetic vasodilatory efferents cannot be excluded.