Cutaneous vasodilation during dorsal column stimulation is mediated by dorsal roots and CGRP

John E. Groom, Robert D. Foreman, Margaret J. Chandler, Kirk W. Barron

Research output: Contribution to journalArticle

81 Citations (Scopus)

Abstract

Dorsal column stimulation (DCS) is used clinically to provide pain relief from peripheral vascular disease and has the benefit of increasing cutaneous blood flow to the affected lower extremities. The purpose of this study was to examine the role of dorsal roots, calcitonin gene-related peptide (CGRP), and substance P in the cutaneous vasodilation induced by DCS. Male rats were anesthetized with pentobarbital sodium (60 mg/kg ip). A unipolar ball electrode was placed unilaterally on the spinal cord at the L1-L2 spinal segment. Blood flow was recorded in each hindpaw foot pad with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (either 0.2 mA subdural or 0.6 mA epidural at 50 Hz, 0.2-ms pulse duration). Dorsal rhizotomy of L3-L5 (n = 5) abolished the cutaneous vasodilation to subdural DCS, whereas removal of T10-T12 (n = 5) and T13-L2 dorsal roots (n = 5) did not attenuate the DCS-induced vasodilation. The CGRP antagonist, CGRP-(837) (2.6 mg/kg iv, n = 7), eliminated the epidural DCS-induced vasodilation, whereas the substance P receptor antagonist, CP-96345 (1 mg/kg iv, n = 6), had no effect. In summary, L3-L5 dorsal roots and CGRP are essential for the DCS-induced vasodilation. We propose that DCS antidromitally activates afferent fibers in the dorsal roots, thus causing peripheral release of CGRP, which produces cutaneous vasodilation.

Original languageEnglish
Pages (from-to)H950-H957
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume272
Issue number2 41-2
StatePublished - 1 Feb 1997

Fingerprint

Calcitonin Gene-Related Peptide
Spinal Nerve Roots
Vasodilation
Skin
Neurokinin-1 Receptor Antagonists
Rhizotomy
Flowmeters
Peripheral Vascular Diseases
Pentobarbital
Substance P
Foot
Lower Extremity
Spinal Cord
Electrodes
Lasers
Pain

Keywords

  • antidromic vasodilation
  • calcitonin gene- related peptide
  • cutaneous blood flow
  • laser Doppler flowmetry
  • microcirculation
  • skin vasodilation
  • spinal cord
  • spinal cord stimulation
  • substance P

Cite this

@article{7a327704eba94b14b864685e6536e567,
title = "Cutaneous vasodilation during dorsal column stimulation is mediated by dorsal roots and CGRP",
abstract = "Dorsal column stimulation (DCS) is used clinically to provide pain relief from peripheral vascular disease and has the benefit of increasing cutaneous blood flow to the affected lower extremities. The purpose of this study was to examine the role of dorsal roots, calcitonin gene-related peptide (CGRP), and substance P in the cutaneous vasodilation induced by DCS. Male rats were anesthetized with pentobarbital sodium (60 mg/kg ip). A unipolar ball electrode was placed unilaterally on the spinal cord at the L1-L2 spinal segment. Blood flow was recorded in each hindpaw foot pad with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (either 0.2 mA subdural or 0.6 mA epidural at 50 Hz, 0.2-ms pulse duration). Dorsal rhizotomy of L3-L5 (n = 5) abolished the cutaneous vasodilation to subdural DCS, whereas removal of T10-T12 (n = 5) and T13-L2 dorsal roots (n = 5) did not attenuate the DCS-induced vasodilation. The CGRP antagonist, CGRP-(837) (2.6 mg/kg iv, n = 7), eliminated the epidural DCS-induced vasodilation, whereas the substance P receptor antagonist, CP-96345 (1 mg/kg iv, n = 6), had no effect. In summary, L3-L5 dorsal roots and CGRP are essential for the DCS-induced vasodilation. We propose that DCS antidromitally activates afferent fibers in the dorsal roots, thus causing peripheral release of CGRP, which produces cutaneous vasodilation.",
keywords = "antidromic vasodilation, calcitonin gene- related peptide, cutaneous blood flow, laser Doppler flowmetry, microcirculation, skin vasodilation, spinal cord, spinal cord stimulation, substance P",
author = "Groom, {John E.} and Foreman, {Robert D.} and Chandler, {Margaret J.} and Barron, {Kirk W.}",
year = "1997",
month = "2",
day = "1",
language = "English",
volume = "272",
pages = "H950--H957",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "2 41-2",

}

Cutaneous vasodilation during dorsal column stimulation is mediated by dorsal roots and CGRP. / Groom, John E.; Foreman, Robert D.; Chandler, Margaret J.; Barron, Kirk W.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 272, No. 2 41-2, 01.02.1997, p. H950-H957.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Cutaneous vasodilation during dorsal column stimulation is mediated by dorsal roots and CGRP

AU - Groom, John E.

AU - Foreman, Robert D.

AU - Chandler, Margaret J.

AU - Barron, Kirk W.

PY - 1997/2/1

Y1 - 1997/2/1

N2 - Dorsal column stimulation (DCS) is used clinically to provide pain relief from peripheral vascular disease and has the benefit of increasing cutaneous blood flow to the affected lower extremities. The purpose of this study was to examine the role of dorsal roots, calcitonin gene-related peptide (CGRP), and substance P in the cutaneous vasodilation induced by DCS. Male rats were anesthetized with pentobarbital sodium (60 mg/kg ip). A unipolar ball electrode was placed unilaterally on the spinal cord at the L1-L2 spinal segment. Blood flow was recorded in each hindpaw foot pad with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (either 0.2 mA subdural or 0.6 mA epidural at 50 Hz, 0.2-ms pulse duration). Dorsal rhizotomy of L3-L5 (n = 5) abolished the cutaneous vasodilation to subdural DCS, whereas removal of T10-T12 (n = 5) and T13-L2 dorsal roots (n = 5) did not attenuate the DCS-induced vasodilation. The CGRP antagonist, CGRP-(837) (2.6 mg/kg iv, n = 7), eliminated the epidural DCS-induced vasodilation, whereas the substance P receptor antagonist, CP-96345 (1 mg/kg iv, n = 6), had no effect. In summary, L3-L5 dorsal roots and CGRP are essential for the DCS-induced vasodilation. We propose that DCS antidromitally activates afferent fibers in the dorsal roots, thus causing peripheral release of CGRP, which produces cutaneous vasodilation.

AB - Dorsal column stimulation (DCS) is used clinically to provide pain relief from peripheral vascular disease and has the benefit of increasing cutaneous blood flow to the affected lower extremities. The purpose of this study was to examine the role of dorsal roots, calcitonin gene-related peptide (CGRP), and substance P in the cutaneous vasodilation induced by DCS. Male rats were anesthetized with pentobarbital sodium (60 mg/kg ip). A unipolar ball electrode was placed unilaterally on the spinal cord at the L1-L2 spinal segment. Blood flow was recorded in each hindpaw foot pad with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (either 0.2 mA subdural or 0.6 mA epidural at 50 Hz, 0.2-ms pulse duration). Dorsal rhizotomy of L3-L5 (n = 5) abolished the cutaneous vasodilation to subdural DCS, whereas removal of T10-T12 (n = 5) and T13-L2 dorsal roots (n = 5) did not attenuate the DCS-induced vasodilation. The CGRP antagonist, CGRP-(837) (2.6 mg/kg iv, n = 7), eliminated the epidural DCS-induced vasodilation, whereas the substance P receptor antagonist, CP-96345 (1 mg/kg iv, n = 6), had no effect. In summary, L3-L5 dorsal roots and CGRP are essential for the DCS-induced vasodilation. We propose that DCS antidromitally activates afferent fibers in the dorsal roots, thus causing peripheral release of CGRP, which produces cutaneous vasodilation.

KW - antidromic vasodilation

KW - calcitonin gene- related peptide

KW - cutaneous blood flow

KW - laser Doppler flowmetry

KW - microcirculation

KW - skin vasodilation

KW - spinal cord

KW - spinal cord stimulation

KW - substance P

UR - http://www.scopus.com/inward/record.url?scp=0030938912&partnerID=8YFLogxK

M3 - Article

C2 - 9124459

AN - SCOPUS:33750882725

VL - 272

SP - H950-H957

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 2 41-2

ER -