title: Local cooling alters neural mechanisms producing changes in peripheral blood flow by spinal cord stimulation.
abstract: This study was performed to investigate the respective role of sensory afferent and sympathetic fibers in peripheral vasodilatation induced by spinal cord stimulation at different hindpaw skin temperatures. Cooling the skin was used as a strategy to enhance sympathetic activity [Am. J. Physiol.: Heart Circ. Physiol. 263 (1992) H1197]. Cutaneous blood flow in the footpad of anesthetized rats was recorded using laser Doppler flowmetry. Local cooling (<25 degrees C) or moderate local cooling (25-28 degrees C) of the hindpaw was produced with a cooling copper coil. Spinal cord stimulation delivered at clinically relevant parameters and with 30%, 60%, and 90% of motor threshold induced the early phase of vasodilatation in the cooled and the moderately cooled hindpaw. In addition, spinal cord stimulation at 90% of motor threshold produced the late phase of vasodilatation only in the cooled hindpaw, which was possible to block by the autonomic ganglion-blocking agent, hexamethonium. The early responses to spinal cord stimulation in the moderately cooled hindpaw were not affected by hexamethonium. In contrast, both the early and the late phase responses were eliminated by CGRP (8-37), an antagonist of the calcitonin gene-related peptide receptor. After dorsal rhizotomy, spinal cord stimulation at 90% of motor threshold elicited hexamethonium-sensitive vasodilatation in the cooled hindpaw (late phase). These results suggest that spinal cord stimulation-induced vasodilatation in the cooled hindpaw (<25 degrees C) is mediated via both the sensory afferent (early phase of vasodilatation) and via suppression of the sympathetic efferent activity (late phase) although the threshold for vasodilatation via the sympathetic efferent fibers is higher than that via sensory nerves. In contrast, vasodilatation via sensory afferent fibers may predominate with moderate temperatures (25-28 degrees C). Thus, two complementary mechanisms for spinal cord stimulation-induced vasodilatation may exist depending on the basal sympathetic tone.
authors.affiliation: Department of Physiology, University of Oklahoma Health Sciences Center, PO Box 26901, Oklahoma City, OK 73190, USA.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tanaka
authors.forename: Kirk W
authors.initials: KW
authors.lastname: Barron
authors.forename: Margaret J
authors.initials: MJ
authors.lastname: Chandler
authors.forename: Bengt
authors.initials: B
authors.lastname: Linderoth
authors.forename: Robert D
authors.initials: RD
authors.lastname: Foreman
mesh_terms: D000818:Animals; D001775:Blood Circulation / Q000502:physiology*; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology; D003080:Cold Temperature; D004558:Electric Stimulation; D005528:Foot / Q000098:blood supply; D005730:Ganglionic Blockers / Q000494:pharmacology; D018738:Hexamethonium / Q000494:pharmacology; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D019051:Rhizotomy; D013116:Spinal Cord / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D005730:Ganglionic Blockers; D010446:Peptide Fragments; C058636:calcitonin gene-related peptide (8-37); D018738:Hexamethonium; D015740:Calcitonin Gene-Related Peptide