Endothelial cell expression of intercellular adhesion molecule 1 in experimental posthemorrhagic vasospasm

Allen K. Sills, Richard E. Clatterbuck, Reid C. Thompson, Paul L. Cohen, Rafael J Tamargo

Research output: Contribution to journalArticle

Abstract

OBJECTIVE: The exposure of large intracranial arteries to blood after an aneurysmal subarachnoid hemorrhage leads to a cascade of morphological and physiological changes in the vessels, a condition generally described as vasospasm. This response to the periadventitial deposition of blood is mediated in part by the endothelial layer of the vessel. This study was undertaken to examine the role of endothelial cell expression of intercellular adhesion molecule 1 (ICAM-1) in the initiation and regulation of this response. METHODS: The femoral artery model of vasospasm was used in rats (65 animals, 130 arteries). In each rat, one artery was exposed to blood and the contralateral vessel was exposed to saline, so that each animal served as its own control. Animals were perfused and killed at sequential time points, from 1 hour to 20 days after blood exposure. The vessels were examined immunohistochemically and histologically for the presence of ICAM-1 and morphological features of vasospasm, respectively. RESULTS: Endothelial cell ICAM-1 immunoreactivity was extensively increased in only the blood- exposed vessels, beginning 3 hours after clot placement and persisting for 24 hours. ICAM-1 immunoreactivity returned to baseline by 48 hours after blood exposure. The influx of inflammatory cells correlated directly with the time and location of increased ICAM-1 expression. Peak arterial remodeling was observed on the blood-exposed side 8 to 12 days after clot placement, as quantified by measurements of increased wall thickness, decreased lumen size, and increased collagen content. CONCLUSION: Endothelial cell ICAM-1 expression seems to be an early and specific signal used by a vessel in response to the deposition of blood periadventitially. This molecule may be a marker for vessels likely to undergo subsequent morphological remodeling and vasospasm.

Original languageEnglish (US)
Pages (from-to)453-461
Number of pages9
JournalNeurosurgery
Volume41
Issue number2
DOIs
StatePublished - Aug 1997

Fingerprint

Intercellular Adhesion Molecule-1
Endothelial Cells
Arteries
Cell Adhesion Molecules
Blood Vessels
Subarachnoid Hemorrhage
Femoral Artery
Collagen

Keywords

  • Cerebral vasospasm
  • Endothelium
  • Inflammation
  • Intercellular adhesion molecule 1 (ICAM-1)
  • Leukocytes
  • Subarachnoid hemorrhage

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Endothelial cell expression of intercellular adhesion molecule 1 in experimental posthemorrhagic vasospasm. / Sills, Allen K.; Clatterbuck, Richard E.; Thompson, Reid C.; Cohen, Paul L.; Tamargo, Rafael J.

In: Neurosurgery, Vol. 41, No. 2, 08.1997, p. 453-461.

Research output: Contribution to journalArticle

Sills, Allen K. ; Clatterbuck, Richard E. ; Thompson, Reid C. ; Cohen, Paul L. ; Tamargo, Rafael J. / Endothelial cell expression of intercellular adhesion molecule 1 in experimental posthemorrhagic vasospasm. In: Neurosurgery. 1997 ; Vol. 41, No. 2. pp. 453-461.
@article{3f6f0390a97147458eb1f955d42edd96,
title = "Endothelial cell expression of intercellular adhesion molecule 1 in experimental posthemorrhagic vasospasm",
abstract = "OBJECTIVE: The exposure of large intracranial arteries to blood after an aneurysmal subarachnoid hemorrhage leads to a cascade of morphological and physiological changes in the vessels, a condition generally described as vasospasm. This response to the periadventitial deposition of blood is mediated in part by the endothelial layer of the vessel. This study was undertaken to examine the role of endothelial cell expression of intercellular adhesion molecule 1 (ICAM-1) in the initiation and regulation of this response. METHODS: The femoral artery model of vasospasm was used in rats (65 animals, 130 arteries). In each rat, one artery was exposed to blood and the contralateral vessel was exposed to saline, so that each animal served as its own control. Animals were perfused and killed at sequential time points, from 1 hour to 20 days after blood exposure. The vessels were examined immunohistochemically and histologically for the presence of ICAM-1 and morphological features of vasospasm, respectively. RESULTS: Endothelial cell ICAM-1 immunoreactivity was extensively increased in only the blood- exposed vessels, beginning 3 hours after clot placement and persisting for 24 hours. ICAM-1 immunoreactivity returned to baseline by 48 hours after blood exposure. The influx of inflammatory cells correlated directly with the time and location of increased ICAM-1 expression. Peak arterial remodeling was observed on the blood-exposed side 8 to 12 days after clot placement, as quantified by measurements of increased wall thickness, decreased lumen size, and increased collagen content. CONCLUSION: Endothelial cell ICAM-1 expression seems to be an early and specific signal used by a vessel in response to the deposition of blood periadventitially. This molecule may be a marker for vessels likely to undergo subsequent morphological remodeling and vasospasm.",
keywords = "Cerebral vasospasm, Endothelium, Inflammation, Intercellular adhesion molecule 1 (ICAM-1), Leukocytes, Subarachnoid hemorrhage",
author = "Sills, {Allen K.} and Clatterbuck, {Richard E.} and Thompson, {Reid C.} and Cohen, {Paul L.} and Tamargo, {Rafael J}",
year = "1997",
month = "8",
doi = "10.1097/00006123-199708000-00025",
language = "English (US)",
volume = "41",
pages = "453--461",
journal = "Neurosurgery",
issn = "0148-396X",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Endothelial cell expression of intercellular adhesion molecule 1 in experimental posthemorrhagic vasospasm

AU - Sills, Allen K.

AU - Clatterbuck, Richard E.

AU - Thompson, Reid C.

AU - Cohen, Paul L.

AU - Tamargo, Rafael J

PY - 1997/8

Y1 - 1997/8

N2 - OBJECTIVE: The exposure of large intracranial arteries to blood after an aneurysmal subarachnoid hemorrhage leads to a cascade of morphological and physiological changes in the vessels, a condition generally described as vasospasm. This response to the periadventitial deposition of blood is mediated in part by the endothelial layer of the vessel. This study was undertaken to examine the role of endothelial cell expression of intercellular adhesion molecule 1 (ICAM-1) in the initiation and regulation of this response. METHODS: The femoral artery model of vasospasm was used in rats (65 animals, 130 arteries). In each rat, one artery was exposed to blood and the contralateral vessel was exposed to saline, so that each animal served as its own control. Animals were perfused and killed at sequential time points, from 1 hour to 20 days after blood exposure. The vessels were examined immunohistochemically and histologically for the presence of ICAM-1 and morphological features of vasospasm, respectively. RESULTS: Endothelial cell ICAM-1 immunoreactivity was extensively increased in only the blood- exposed vessels, beginning 3 hours after clot placement and persisting for 24 hours. ICAM-1 immunoreactivity returned to baseline by 48 hours after blood exposure. The influx of inflammatory cells correlated directly with the time and location of increased ICAM-1 expression. Peak arterial remodeling was observed on the blood-exposed side 8 to 12 days after clot placement, as quantified by measurements of increased wall thickness, decreased lumen size, and increased collagen content. CONCLUSION: Endothelial cell ICAM-1 expression seems to be an early and specific signal used by a vessel in response to the deposition of blood periadventitially. This molecule may be a marker for vessels likely to undergo subsequent morphological remodeling and vasospasm.

AB - OBJECTIVE: The exposure of large intracranial arteries to blood after an aneurysmal subarachnoid hemorrhage leads to a cascade of morphological and physiological changes in the vessels, a condition generally described as vasospasm. This response to the periadventitial deposition of blood is mediated in part by the endothelial layer of the vessel. This study was undertaken to examine the role of endothelial cell expression of intercellular adhesion molecule 1 (ICAM-1) in the initiation and regulation of this response. METHODS: The femoral artery model of vasospasm was used in rats (65 animals, 130 arteries). In each rat, one artery was exposed to blood and the contralateral vessel was exposed to saline, so that each animal served as its own control. Animals were perfused and killed at sequential time points, from 1 hour to 20 days after blood exposure. The vessels were examined immunohistochemically and histologically for the presence of ICAM-1 and morphological features of vasospasm, respectively. RESULTS: Endothelial cell ICAM-1 immunoreactivity was extensively increased in only the blood- exposed vessels, beginning 3 hours after clot placement and persisting for 24 hours. ICAM-1 immunoreactivity returned to baseline by 48 hours after blood exposure. The influx of inflammatory cells correlated directly with the time and location of increased ICAM-1 expression. Peak arterial remodeling was observed on the blood-exposed side 8 to 12 days after clot placement, as quantified by measurements of increased wall thickness, decreased lumen size, and increased collagen content. CONCLUSION: Endothelial cell ICAM-1 expression seems to be an early and specific signal used by a vessel in response to the deposition of blood periadventitially. This molecule may be a marker for vessels likely to undergo subsequent morphological remodeling and vasospasm.

KW - Cerebral vasospasm

KW - Endothelium

KW - Inflammation

KW - Intercellular adhesion molecule 1 (ICAM-1)

KW - Leukocytes

KW - Subarachnoid hemorrhage

UR - http://www.scopus.com/inward/record.url?scp=0343307027&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0343307027&partnerID=8YFLogxK

U2 - 10.1097/00006123-199708000-00025

DO - 10.1097/00006123-199708000-00025

M3 - Article

C2 - 9257314

AN - SCOPUS:0343307027

VL - 41

SP - 453

EP - 461

JO - Neurosurgery

JF - Neurosurgery

SN - 0148-396X

IS - 2

ER -