title: Cerebral vascular and metabolic response to sustained systemic inflammation in ovine traumatic brain injury.
abstract: Traumatic brain injury (TBI) is frequently accompanied by a systemic inflammatory response secondary to multiple trauma, shock, or infections. This study investigated the impact of sustained systemic inflammation on cerebral hemodynamics and metabolism in ovine traumatic brain injury. Fifteen sheep were investigated for 14 hours. Head injury was induced with a nonpenetrating stunner in anesthetized, ventilated animals. One group (TBI/Endo, n = 6) subsequently received a continuous endotoxin infusion for 12 hours, whereas a second group (TBI, n = 6) received the carrier. Three instrumented animals served as sham controls. Head impact significantly increased intracranial pressure from 9 +/- 4 mm Hg to 21 +/- 15 mm Hg (TBI/Endo) and from 10 +/- 3 mm Hg to 24 +/- 19 mm Hg (TBI) (means +/- SD). Internal carotid blood flow increased and cerebral vascular resistance decreased (P < 0.05) during the hyperdynamic inflammatory response between 10 and 14 hours in the TBI/Endo group, whereas these parameters were at baseline level in the TBI group. Intracranial pressure remained unchanged during this period, but increased during hypercapnia. The CMRO2, PaCO2, and arterial hematocrit values were identical among the groups between 10 and 14 hours. It is concluded that chronic endotoxemia in ovine traumatic brain injury was associated with cerebral vasodilation uncoupled from global brain metabolism. Different mechanisms appear to induce cerebral vasodilation in response to inflammation and hypercapnia.
authors.affiliation: Department of Anesthesiology and Intensive Care, University Hospital, Münster, Germany. hstubbe@uni-muenster.de
authors.forename: Henning D
authors.initials: HD
authors.lastname: Stubbe
authors.forename: Christoph
authors.initials: C
authors.lastname: Greiner
authors.forename: Hugo
authors.initials: H
authors.lastname: Van Aken
authors.forename: Christian H
authors.initials: CH
authors.lastname: Rickert
authors.forename: Martin
authors.initials: M
authors.lastname: Westphal
authors.forename: Hansdetlef
authors.initials: H
authors.lastname: Wassmann
authors.forename: Ali
authors.initials: A
authors.lastname: Akcocuk
authors.forename: Fritz
authors.initials: F
authors.lastname: Daudel
authors.forename: Michael
authors.initials: M
authors.lastname: Erren
authors.forename: Frank
authors.initials: F
authors.lastname: Hinder
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001831:Body Temperature; D001921:Brain / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000378:metabolism; D002560:Cerebrovascular Circulation; D006439:Hemodynamics; D007249:Inflammation / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D019344:Lactic Acid / Q000378:metabolism; D012756:Sheep; D014947:Wounds and Injuries / Q000378:metabolism* / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D002245:Carbon Dioxide; D019344:Lactic Acid