Peripheral vasodilatation after spinal cord stimulation: animal studies of putative effector mechanisms.

Spinal cord stimulation has been reported to relieve ischemic pain and to enhance peripheral circulation. To elucidate the still unknown mechanisms behind these effects, changes in the peripheral blood flow in the skin of the hind paw after stimulation applied to the dorsal column was studied in the normal rat. A substantial flow increase, monitored by laser Doppler technique, was observed in response to stimulation with an intensity comparable to that used clinically in man, recruiting only low-threshold neuronal elements. The response remained after transection of the dorsal roots, as well as after spinal cord section rostrally to the stimulating electrode. Furthermore, monitoring of antidromic compound action potentials in a peripheral nerve indicated that the stimulus intensity applied to dorsal columns recruited solely low-threshold, large-diameter fibers. Stimulation failed to produce an increase in blood flow in addition to that produced by guanethidine and hexamethonium, but high-intensity dorsal column or dorsal root stimulation still was effective. The results indicate that spinal mechanisms are essential and that antidromic activation of primary afferent fibers is unlikely to account for the peripheral vasodilatation induced by low-intensity spinal cord stimulation. Our observations suggest a transitory inhibition of sympathetic vasoconstriction as the principal underlying mechanism.