title: Regional changes in cerebral extracellular glucose and lactate concentrations following severe cortical impact injury and secondary ischemia in rats.
abstract: Traumatic brain injury (TBI) causes the brain to be more susceptible to secondary insults, and the occurrence of a secondary insult after trauma increases the damage that develops in the brain. To study the synergistic effect of trauma and ischemia on brain energy metabolites, regional changes in the extracellular concentrations of glucose and lactate following a severe cortical impact injury were measured employing a microdialysis technique. Three microdialysis probes were placed in center of the impact site, in an area adjacent to the impact site, and in the contralateral parietal cortex, and perfused with artificial cerebrospinal fluid (CSF) at 2 microl/min. Rats were assigned to one of the following experimental groups (n = 7 per group): (1) combined impact injury and secondary insult, (2) impact injury with sham secondary insult, (3) sham impact with secondary insult, or (4) sham impact and sham secondary insult. The impact injury was produced with a pneumatic impactor (5 m/sec, 3-mm deformation). One hour following the impact injury, a secondary insult was produced by bilateral carotid occlusion for 1 h. The impact injury resulted in a three- to fivefold global increase in dialysate lactate concentrations, with a corresponding fall in dialysate glucose concentration by 50% compared to no change in lactate or glucose concentrations in sham-injured animals (p < .0001 for both lactate and glucose). The secondary insult resulted in a second increase in dialysate lactate and decrease in dialysate glucose concentration that was significantly greater in the animals that had suffered the impact injury than in the sham-injured animals. Ischemia and traumatic injury have synergistic effects on lactate accumulation and on glucose depletion in the brain that probably reflects persisting ischemia, but may also indicate mitochondrial abnormalities and inhibition of oxidative metabolism.
authors: Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA. Indrak@bcm.tmc.edu
authors: I K
authors: IK
authors: Krishnappa
authors: C F
authors: CF
authors: Contant
authors: C S
authors: CS
authors: Robertson
mesh_terms: D000140:Acidosis, Lactic / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001784:Blood Gas Analysis; D001831:Body Temperature / Q000502:physiology; D001923:Brain Chemistry / Q000502:physiology*; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism*; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism*; D016893:Carotid Stenosis / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000293:injuries*; D005110:Extracellular Space / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D051381:Rats; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology
chemical_list: D019344:Lactic Acid; D005947:Glucose