title: Hemorrhage and intracranial hypertension in combination increase cerebral production of thromboxane A2.
abstract: METHODS
  To determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A2 (TxA2) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB2 (double-antibody radioimmunoassay technique), the major metabolite of TxA2. Data were obtained at baseline and at the beginning and end of the 30-min shock period.
  
  
  RESULTS
  Hemorrhagic shock significantly (p less than .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p less than .05) and venous-arterial differences in TxB2 increased significantly (p less than .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB2 remained significantly (p less than .05) higher in group 2.
  
  
  CONCLUSIONS
  Increased cerebral production of TxA2 during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock.
authors.affiliation: Section on Critical Care, Bowman Gray School of Medicine, Wake Forest University Medical Center, Winston-Salem, NC 27103.
authors.forename: D L
authors.initials: DL
authors.lastname: Kong
authors.forename: D S
authors.initials: DS
authors.lastname: Prough
authors.forename: J M
authors.initials: JM
authors.lastname: Whitley
authors.forename: C
authors.initials: C
authors.lastname: Taylor
authors.forename: S
authors.initials: S
authors.lastname: Vines
authors.forename: D D
authors.initials: DD
authors.lastname: Deal
authors.forename: D S
authors.initials: DS
authors.lastname: DeWitt
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D004285:Dogs; D005260:Female; D007022:Hypotension / Q000150:complications / Q000378:metabolism*; D007427:Intracranial Pressure / Q000502:physiology*; D008297:Male; D015999:Multivariate Analysis; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism*; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013929:Thromboxane B2 / Q000097:blood
chemical_list: D013929:Thromboxane B2; D013928:Thromboxane A2