Free radical-mediated endothelial damage in blood vessels after electrical stimulation

F. S. Lamb, C. M. King, K. Harrell, W. Burkel, R. C. Webb

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

The endothelium plays an important role in mediating vasodilator effects of several agents (acetylcholine, thrombin, A23187, etc.). The goal of this study was to determine the ability of oxygen free radicals generated by electrical field stimulation to alter endothelial function in isolated tissue systems. Tail artery strips and the mesenteric microvasculature isolated from Sprague-Dawley rats were used. Following smooth muscle contraction induced by norepinephrine, these preparations relaxed in response to acetylcholine chloride or ionophore A23187. All vessels were then subjected to electrical stimulation (9 V, 1-2 ms, 4 Hz) of the physiological buffer in which they were bathed or perfused. In some of these preparations, an antioxidant, (10-4 M sodium ascorbate, 3.6 x 10-5 M glutathione, 1.3 x 10-2 M dimethyl sulfoxide) was included in the buffer. Relaxation responses persisted in vessels where an antioxidant had been included in the electrically stimulated buffer. Tissues stimulated without this protection did not relax on subsequent exposures to endothelium-dependent vasodilators. Scanning-electron microscopy of the tissues revealed significant endothelial damage (cell membrane pitting) in tissues exposed to electrical stimulation without antioxidant protection. These results suggest that electrical stimulation causes endothelial damage in isolated vascular preparations. This seemingly adverse effect proves to be a useful tool for removing the endothelium in studies of isolated vascular tissues.

Original languageEnglish (US)
Pages (from-to)21/5
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume252
Issue number5
StatePublished - Jul 30 1987

Fingerprint

Electric Stimulation
Free Radicals
Blood Vessels
Buffers
Antioxidants
Calcimycin
Endothelium
Endothelium-Dependent Relaxing Factors
Mesenteric Arteries
Ionophores
Muscle Contraction
Dimethyl Sulfoxide
Microvessels
Vasodilator Agents
Thrombin
Electron Scanning Microscopy
Cholinergic Agents
Ascorbic Acid
Acetylcholine
Glutathione

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Free radical-mediated endothelial damage in blood vessels after electrical stimulation. / Lamb, F. S.; King, C. M.; Harrell, K.; Burkel, W.; Webb, R. C.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 252, No. 5, 30.07.1987, p. 21/5.

Research output: Contribution to journalArticle

@article{5afebc7f01e64138856bb9535539e5c1,
title = "Free radical-mediated endothelial damage in blood vessels after electrical stimulation",
abstract = "The endothelium plays an important role in mediating vasodilator effects of several agents (acetylcholine, thrombin, A23187, etc.). The goal of this study was to determine the ability of oxygen free radicals generated by electrical field stimulation to alter endothelial function in isolated tissue systems. Tail artery strips and the mesenteric microvasculature isolated from Sprague-Dawley rats were used. Following smooth muscle contraction induced by norepinephrine, these preparations relaxed in response to acetylcholine chloride or ionophore A23187. All vessels were then subjected to electrical stimulation (9 V, 1-2 ms, 4 Hz) of the physiological buffer in which they were bathed or perfused. In some of these preparations, an antioxidant, (10-4 M sodium ascorbate, 3.6 x 10-5 M glutathione, 1.3 x 10-2 M dimethyl sulfoxide) was included in the buffer. Relaxation responses persisted in vessels where an antioxidant had been included in the electrically stimulated buffer. Tissues stimulated without this protection did not relax on subsequent exposures to endothelium-dependent vasodilators. Scanning-electron microscopy of the tissues revealed significant endothelial damage (cell membrane pitting) in tissues exposed to electrical stimulation without antioxidant protection. These results suggest that electrical stimulation causes endothelial damage in isolated vascular preparations. This seemingly adverse effect proves to be a useful tool for removing the endothelium in studies of isolated vascular tissues.",
author = "Lamb, {F. S.} and King, {C. M.} and K. Harrell and W. Burkel and Webb, {R. C.}",
year = "1987",
month = "7",
day = "30",
language = "English (US)",
volume = "252",
pages = "21/5",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Free radical-mediated endothelial damage in blood vessels after electrical stimulation

AU - Lamb, F. S.

AU - King, C. M.

AU - Harrell, K.

AU - Burkel, W.

AU - Webb, R. C.

PY - 1987/7/30

Y1 - 1987/7/30

N2 - The endothelium plays an important role in mediating vasodilator effects of several agents (acetylcholine, thrombin, A23187, etc.). The goal of this study was to determine the ability of oxygen free radicals generated by electrical field stimulation to alter endothelial function in isolated tissue systems. Tail artery strips and the mesenteric microvasculature isolated from Sprague-Dawley rats were used. Following smooth muscle contraction induced by norepinephrine, these preparations relaxed in response to acetylcholine chloride or ionophore A23187. All vessels were then subjected to electrical stimulation (9 V, 1-2 ms, 4 Hz) of the physiological buffer in which they were bathed or perfused. In some of these preparations, an antioxidant, (10-4 M sodium ascorbate, 3.6 x 10-5 M glutathione, 1.3 x 10-2 M dimethyl sulfoxide) was included in the buffer. Relaxation responses persisted in vessels where an antioxidant had been included in the electrically stimulated buffer. Tissues stimulated without this protection did not relax on subsequent exposures to endothelium-dependent vasodilators. Scanning-electron microscopy of the tissues revealed significant endothelial damage (cell membrane pitting) in tissues exposed to electrical stimulation without antioxidant protection. These results suggest that electrical stimulation causes endothelial damage in isolated vascular preparations. This seemingly adverse effect proves to be a useful tool for removing the endothelium in studies of isolated vascular tissues.

AB - The endothelium plays an important role in mediating vasodilator effects of several agents (acetylcholine, thrombin, A23187, etc.). The goal of this study was to determine the ability of oxygen free radicals generated by electrical field stimulation to alter endothelial function in isolated tissue systems. Tail artery strips and the mesenteric microvasculature isolated from Sprague-Dawley rats were used. Following smooth muscle contraction induced by norepinephrine, these preparations relaxed in response to acetylcholine chloride or ionophore A23187. All vessels were then subjected to electrical stimulation (9 V, 1-2 ms, 4 Hz) of the physiological buffer in which they were bathed or perfused. In some of these preparations, an antioxidant, (10-4 M sodium ascorbate, 3.6 x 10-5 M glutathione, 1.3 x 10-2 M dimethyl sulfoxide) was included in the buffer. Relaxation responses persisted in vessels where an antioxidant had been included in the electrically stimulated buffer. Tissues stimulated without this protection did not relax on subsequent exposures to endothelium-dependent vasodilators. Scanning-electron microscopy of the tissues revealed significant endothelial damage (cell membrane pitting) in tissues exposed to electrical stimulation without antioxidant protection. These results suggest that electrical stimulation causes endothelial damage in isolated vascular preparations. This seemingly adverse effect proves to be a useful tool for removing the endothelium in studies of isolated vascular tissues.

UR - http://www.scopus.com/inward/record.url?scp=0023254954&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023254954&partnerID=8YFLogxK

M3 - Article

C2 - 3107403

AN - SCOPUS:0023254954

VL - 252

SP - 21/5

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 5

ER -