title: Pentobarbital fails to reduce cerebral oxygen consumption early after non-hemorrhagic closed head injury in rats.
abstract: It is unknown whether barbiturates suppress cerebral oxygen metabolism after cerebral trauma as they do in normal individuals. We evaluated the influence of pentobarbital on cerebral oxygen handling of normal rats and rats subjected to non-hemorrhagic closed head injury (CHI). Oxygen delivery was assessed by measuring cerebral perfusion and oxygen extraction, enabling the calculation of cerebral metabolic rate of oxygen (CMRO2). Mitochondrial function was assessed by studying changes in the oxidized cytochrome oxidase concentration. CHI caused changes in both systemic and cerebral hemodynamics. Cerebral blood flow was reduced to 66% of its control value, but the cerebral metabolic rate of oxygen remained unchanged. Pentobarbital administration induced a significant lowering of the cerebral oxygen consumption in normal rats associated with a secondary decrease in cerebral perfusion. In rats subjected to CHI, pentobarbital was unable to lower the cerebral metabolic demand and did not cause a further decrease in perfusion. Pentobarbital was unable to significantly modulate mitochondrial function in traumatized rats, whereas it exerted this effect in all control animals. We therefore conclude that, in rats subjected to CHI, pentobarbital is unable to perform its beneficial effects on the cerebral metabolism.
authors: Laboratory for Cardiovascular Research, CEHA, Catholic University of Leuven, Belgium.
authors: Geofrey
authors: G
authors: De Visscher
authors: Servan
authors: S
authors: Rooker
authors: Philippe
authors: P
authors: Jorens
authors: Jan
authors: J
authors: Verlooy
authors: Marcel
authors: M
authors: Borgers
authors: Robert S
authors: RS
authors: Reneman
authors: Koen
authors: K
authors: Van Rossem
authors: Willem
authors: W
authors: Flameng
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D003576:Electron Transport Complex IV / Q000187:drug effects / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D016489:Head Injuries, Closed / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006993:Hypnotics and Sedatives / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects* / Q000502:physiology; D010424:Pentobarbital / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D017211:Treatment Failure
chemical_list: D006993:Hypnotics and Sedatives; D003576:Electron Transport Complex IV; D010424:Pentobarbital