title: Effect of glucose administration on contusion volume after moderate cortical impact injury in rats.
abstract: Previous studies had shown that pre- and postinjury glucose administration increased brain injury caused by a mild cortical impact injury only when the traumatic injury was complicated by a secondary ischemic insult. The purpose of this study was to examine the effect of pre- and postinjury glucose administration on a more severe cortical impact injury, where primary ischemia occurs at the site of the impact. Long Evans rats who were fasted overnight and anesthetized with isoflurane were subjected to a 5-m/sec, 2.5-mm impact injury. The animals were randomly assigned one of the following treatments: (1) 2.2 g/kg glucose in 4 ml of saline, 20 min prior to injury; (2) 2.0 g/kg glucose in 4 ml of saline, 20 min after injury; or (3) 4 ml of saline either 20 min before injury or 20 min after the injury. At 2 weeks, the animals were sacrificed and the brains were examined for contusion volume and for neuronal loss in CA1 and CA3 regions of the hippocampus. Contusion volume was increased from a median value of 23 mm3 in the saline-infused animals to 34 mm3 in the preimpact glucose infusion animals (p=0.005). Postimpact glucose infusion had no effect on contusion volume. Neuron density in CA1 and CA3 regions of the hippocampus was similar in all three treatment groups. These studies support the hypothesis that glucose administration adversely affects experimental traumatic brain injury in those circumstances where the trauma is complicated by primary cerebral ischemia, such as around cortical contusions.
authors.affiliation: Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: L
authors.initials: L
authors.lastname: Cherian
authors.forename: J C
authors.initials: JC
authors.lastname: Goodman
authors.forename: C S
authors.initials: CS
authors.lastname: Robertson
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001930:Brain Injuries / Q000188:drug therapy* / Q000473:pathology; D002245:Carbon Dioxide / Q000097:blood; D002540:Cerebral Cortex / Q000098:blood supply / Q000293:injuries*; D003288:Contusions / Q000188:drug therapy*; D005947:Glucose / Q000494:pharmacology*; D006624:Hippocampus / Q000098:blood supply / Q000293:injuries / Q000473:pathology; D006863:Hydrogen-Ion Concentration; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007773:Lactates / Q000097:blood; D017966:Pyramidal Cells / Q000098:blood supply / Q000473:pathology; D051381:Rats; D020318:Rats, Long-Evans
chemical_list: D007004:Hypoglycemic Agents; D007773:Lactates; D002245:Carbon Dioxide; D005947:Glucose