title: Absence of early proinflammatory cytokine expression in experimental intracerebral hemorrhage.
abstract: OBJECTIVE
  We sought to analyze the regional concentrations of proinflammatory cytokines in the acute period of intracerebral hemorrhage (ICH) and to test the hypothesis that ICH is associated with the expression of proinflammatory cytokines in the acute period. Although the expression of cytokines and their role in neuronal injury and inflammation is well characterized in cerebral ischemia and head injury, no information exists regarding expression of cytokines in ICH.
  
  
  METHODS
  We introduced ICH in eight anesthetized mongrel dogs by autologous blood injection (6 ml) under arterial pressure in the deep white matter adjacent to the left basal ganglia. Samples of arterial blood and cerebrospinal fluid were collected, and tissue extracts were prepared from different regions of the brain for immunoassay of tumor necrosis factor alpha, interleukin (IL)-1beta, and IL-6 concentrations in animals with and without ICH.
  
  
  RESULTS
  The tumor necrosis factor a levels (+/- standard error) in the cerebrospinal fluid 1 hour after ICH did not differ significantly between the ICH group and the control group (7.1 +/- 1.3 pg/ml versus 10.8 +/- 2.3 pg/ml, P = 0.22). Levels in the perihematoma region in the ICH group (96.6 +/- 3.1 pg/ml) were not significantly different from those in the control group (93.4 +/- 6.7 pg/ml, P = 0.7). IL-6 levels (+/- standard error) in the perihematoma region in the ICH group (116.3 +/- 13.3 pg/ml) did not differ significantly from those in corresponding regions in the control group (122.3 +/- 12.8 pg/ml, P = 0.7). IL-1beta levels were below 5 pg/ml in serum, cerebrospinal fluid, and extracts of different brain regions.
  
  
  CONCLUSIONS
  The early pathophysiology of ICH does not involve significant expression of tumor necrosis factor a either in the perihematoma region or other regions of the brain. The observation suggests that the pathophysiology of ICH in the acute period is different from both cerebral ischemia and traumatic brain injury.
authors.affiliation: Department of Neurosurgery and Toshiba Stroke Research Center, University at Buffalo, The State University of New York, USA. aiqureshi@hotmail.com
authors.forename: A I
authors.initials: AI
authors.lastname: Qureshi
authors.forename: M F
authors.initials: MF
authors.lastname: Suri
authors.forename: G S
authors.initials: GS
authors.lastname: Ling
authors.forename: J
authors.initials: J
authors.lastname: Khan
authors.forename: L R
authors.initials: LR
authors.lastname: Guterman
authors.forename: L N
authors.initials: LN
authors.lastname: Hopkins
mesh_terms: D000818:Animals; D002543:Cerebral Hemorrhage / Q000378:metabolism*; D004285:Dogs; D005260:Female; D006406:Hematoma / Q000378:metabolism; D018836:Inflammation Mediators / Q000134:cerebrospinal fluid / Q000378:metabolism*; D007375:Interleukin-1 / Q000134:cerebrospinal fluid / Q000378:metabolism*; D015850:Interleukin-6 / Q000134:cerebrospinal fluid / Q000378:metabolism*; D008297:Male; D012016:Reference Values; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000134:cerebrospinal fluid / Q000378:metabolism*
chemical_list: D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha