TY - JOUR
T1 - Mechanisms of sustained cutaneous vasodilation induced by spinal cord stimulation
AU - Tanaka, Satoshi
AU - Komori, Naoka
AU - Barron, Kirk W.
AU - Chandler, Margaret J.
AU - Linderoth, Bengt
AU - Foreman, Robert D.
N1 - Funding Information:
We would like to thank Diana Holston (OUHSC) and Göte Hammarström (KI) for their expert technical assistance, and Julie Marley for excellent secretarial assistance. We are grateful to Dr. Jay P. Farber for his support on the progress of this project. This research was supported by NIH grant NS36775 (R.D.F.) and Presbyterian Health Foundation grant 1401 (N.K.).
PY - 2004/7/30
Y1 - 2004/7/30
N2 - This study was performed to investigate whether spinal cord stimulation (SCS) at intensities below motor threshold prolongs cutaneous vasodilation and whether sustained vasodilation by SCS is mediated through sympathetic inhibition and/or antidromic activation of sensory fibers. SCS was applied to the dorsal surface of the L 2-L 3 spinal cord of anesthesized rats with stimulus parameters used clinically (i.e., 50 Hz, 0.2 ms duration, and stimulus intensity at 30%, 60%, or 90% of motor threshold). Peripheral vasodilation induced by 5-min SCS was not attenuated by hexamethonium, an autonomic ganglion-blocking agent, but was abolished by dorsal rhizotomy. SCS at ≤60% of motor threshold increased cutaneous blood flow to the level similar to that obtained at 90% of motor threshold, but the vasodilation did not last for 5 min. SCS-induced vasodilation at 90% of motor threshold persisted for the entire stimulation period up to 30 min, and the vasodilation was not attenuated by hexamethonium. It is concluded that sustained vasodilation, which is induced by SCS at only 90% of motor threshold, in this study was mediated via antidromic activation of sensory fibers.
AB - This study was performed to investigate whether spinal cord stimulation (SCS) at intensities below motor threshold prolongs cutaneous vasodilation and whether sustained vasodilation by SCS is mediated through sympathetic inhibition and/or antidromic activation of sensory fibers. SCS was applied to the dorsal surface of the L 2-L 3 spinal cord of anesthesized rats with stimulus parameters used clinically (i.e., 50 Hz, 0.2 ms duration, and stimulus intensity at 30%, 60%, or 90% of motor threshold). Peripheral vasodilation induced by 5-min SCS was not attenuated by hexamethonium, an autonomic ganglion-blocking agent, but was abolished by dorsal rhizotomy. SCS at ≤60% of motor threshold increased cutaneous blood flow to the level similar to that obtained at 90% of motor threshold, but the vasodilation did not last for 5 min. SCS-induced vasodilation at 90% of motor threshold persisted for the entire stimulation period up to 30 min, and the vasodilation was not attenuated by hexamethonium. It is concluded that sustained vasodilation, which is induced by SCS at only 90% of motor threshold, in this study was mediated via antidromic activation of sensory fibers.
KW - Antidromic afferent activation
KW - Skin vasodilation
KW - Spinal cord stimulation (SCS)
KW - Sympathetic inhibition
UR - http://www.scopus.com/inward/record.url?scp=4344691790&partnerID=8YFLogxK
U2 - 10.1016/j.autneu.2004.07.004
DO - 10.1016/j.autneu.2004.07.004
M3 - Article
C2 - 15331045
AN - SCOPUS:4344691790
SN - 1566-0702
VL - 114
SP - 55
EP - 60
JO - Autonomic Neuroscience: Basic and Clinical
JF - Autonomic Neuroscience: Basic and Clinical
IS - 1-2
ER -