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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Hunterian Neurosurgical Laboratory, Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
authors.forename: A K
authors.initials: AK
authors.lastname: Sills
authors.forename: R E
authors.initials: RE
authors.lastname: Clatterbuck
authors.forename: R C
authors.initials: RC
authors.lastname: Thompson
authors.forename: P L
authors.initials: PL
authors.lastname: Cohen
authors.forename: R J
authors.initials: RJ
authors.lastname: Tamargo
mesh_terms: D000818:Animals; D001167:Arteritis / Q000473:pathology; D002465:Cell Movement; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D005263:Femoral Artery / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006470:Hemorrhage / Q000503:physiopathology*; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D051381:Rats; D011916:Rats, Inbred F344; D014661:Vasoconstriction
chemical_list: D018799:Intercellular Adhesion Molecule-1