title: Reevaluation of the Role of the Sympathetic Nervous System in Cutaneous Vasodilation during Dorsal Spinal Cord Stimulation: Are Multiple Mechanisms Active?
abstract: Objective. In addition to treatment of refractory chronic pain in patients with peripheral vascular disease, dorsal spinal cord stimulation (DCS) increases cutaneous blood flow to the extremities and may have a limb-saving effect. The purpose of this study was to examine the role of the sympathetic nervous system in the cutaneous vasodilation due to DCS. Methods. Male Sprague-Dawley rats were anesthetized with pentobarbital (60 mg/kg, i.p.). A unipolar ball electrode was placed on the left side of the exposed spinal cord at approximately the L1-L2 level. Blood flow was concurrently recorded from both hindpaw foot pads with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (0.6 mA at 50 Hz, 0.2 msec pulse duration) at 10 min intervals. To determine the contribution of the sympathetic nervous system in the blood flow response to DCS, the role of ganglionic transmission, alpha-adrenergic receptors, beta-adrenergic receptors, and adrenal catecholamine secretion were investigated using adrenergic receptor antagonists. Results. Hexamethonium (10 mg/kg, i.v.), an autonomic ganglionic receptor antagonist, did not attenuate the cutaneous vasodilation during DCS. Phentolamine (3 mg/kg, i.v.), a nonselective alpha-adrenergic receptor antagonist, also did not attenuate the DCS-induced increase in peripheral cutaneous blood flow. On the other hand, prazosin (0.1 mg/kg, i.v.), a selective alpha-1-adrenergic receptor antagonist, attenuated the DCS response but this may, at least, be partly due to a vehicle effect. Propranolol (5 mg/kg, i.v.), a nonselective beta-adrenergic receptor antagonist, attenuated the DCS response while adrenal demedullation did not. Conclusion. Overall, our results show that DCS-induced vasodilation can occur through mechanisms that are independent of sympathetic outflow.
authors.affiliation: Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma USA.
authors.forename: J E
authors.initials: JE
authors.lastname: Croom
authors.forename: R D
authors.initials: RD
authors.lastname: Foreman
authors.forename: M J
authors.initials: MJ
authors.lastname: Chandler
authors.forename: K W
authors.initials: KW
authors.lastname: Barron