title: Endothelial cell activation after subarachnoid hemorrhage.
abstract: OBJECTIVE
  Evidence from animal experiments suggests that endothelial cell activation plays a pathogenetic role in the development of cerebral ischemia after subarachnoid hemorrhage (SAH). We measured plasma concentrations of two markers of endothelial cell activation, i.e., ED1-fibronectin (ED1-fn) and von Willebrand factor (vWf), among patients with aneurysmal SAH. We analyzed the relationships of concentrations to initial clinical conditions, treatment modalities, and the occurrence of delayed cerebral ischemia.
  
  
  METHODS
  We collected 123 blood samples from 27 patients with aneurysmal SAH. Aneurysms were treated surgically in 19 cases, were treated endovascularly in 7 cases, and remained untreated in 1 case. Twelve patients developed symptomatic delayed cerebral ischemia.
  
  
  RESULTS
  Initial concentrations of ED1-fn (4.3 +/- 3.7 microg/ml) and vWf (17.8 +/- 8.2 microg/ml) were higher than the reference values (ED1-fn, 1.7 +/- 0.9 microg/ml, P < 0.001; vWf, 11.5 +/- 5.2 microg/ml, P = 0.003). Concentrations were higher among patients in poor clinical condition at admission, compared with patients in good clinical condition (mean difference, ED1-fn, 5.7 microg/ml, P = 0.04; vWf, 10.4 microg/ml, P = 0.02). Levels of both markers increased significantly after surgery (mean increase, ED1-fn, 7.5 microg/ml, P = 0.01; vWf, 13.2 microg/ml, P = 0.05) and after ischemic episodes (mean increase, ED1-fn, 8.3 microg/ml, P = 0.02; vWf, 5.0 microg/ml, P = 0.04).
  
  
  CONCLUSIONS
  Plasma concentrations of markers of endothelial cell activation were increased early after SAH and were significantly associated with the clinical condition at admission. We also observed a significant increase in concentrations after surgery and after ischemic episodes. Whether endothelial cell activation is a causal or indirectly related factor in the pathogenesis of delayed cerebral ischemia after SAH is still uncertain.
authors.affiliation: Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. C.J.M.Frijns@azu.nl
authors.forename: Catharina J M
authors.initials: CJ
authors.lastname: Frijns
authors.forename: Gabriël J E
authors.initials: GJ
authors.lastname: Rinkel
authors.forename: Domenico
authors.initials: D
authors.lastname: Castigliego
authors.forename: Jan
authors.initials: J
authors.lastname: Van Gijn
authors.forename: Jan J
authors.initials: JJ
authors.lastname: Sixma
authors.forename: Rob
authors.initials: R
authors.lastname: Fijnheer
mesh_terms: D000328:Adult; D000368:Aged; D002545:Brain Ischemia / Q000097:blood; D004621:Embolization, Therapeutic; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005353:Fibronectins / Q000097:blood; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications / Q000601:surgery / Q000628:therapy; D008297:Male; D008875:Middle Aged; D019635:Neurosurgical Procedures; D009994:Osmolar Concentration; D011184:Postoperative Period; D013345:Subarachnoid Hemorrhage / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D005353:Fibronectins; D014841:von Willebrand Factor