title: Interstitial lactate in the peritraumatic penumbra of rat brain.
abstract: A traumatic brain tissue necrosis is expanding to approximately 150% within 24 h after lesion. This process is accompanied by marked reduction of the perifocal cerebral blood flow likely to activate anaerobic glycolysis from a reduced O2-supply leading to an accumulation of lactic acid. The current study was carried out to assess the interstitial levels of lactic acid as a potential factor of secondary brain damage. A microdialysis probe was stereotactically implanted approximately 2 mm below the brain surface of the parietal cortex in Sprague Dawley rats (250-300 g bw; n = 6) in chloralhydrate anaesthesia. The position of the probe was controlled by histology. 24 h later a standardised cortical cold injury was induced above the probe in halothane/N2O anaesthesia. Dialysate (2 microliters/min) was collected in 15 min intervals, starting 1 h prior to and continuing until 4 hrs after trauma. The lactate concentration in the dialysate was fluorometrically determined by an enzymatic assay. Under baseline conditions dialysate concentrations of 324 +/- 48 microM were observed. A release of lactate was not found initially after trauma. Between 70 and 105 min later, however, the interstitial lactate levels briefly increased to 416 +/- 34 microM (n.s.), while reaching baseline levels again thereafter. Thus, the current results do not confirm an increased accumulation of lactate in the interstitial compartment of the penumbra despite a marked perifocal hypoperfusion of the brain after focal injury. The transitory increase in lactate at 90 min after trauma is unlikely to have caused a severe tissue acidosis which might be held liable for the secondary growth of the brain lesion induced by the focal injury.
authors.affiliation: Institute for Surgical Research, Klinikum Grosshadern, Ludwig-Maximilians-Universität, München, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Eriskat
authors.forename: M
authors.initials: M
authors.lastname: Stoffel
authors.forename: N
authors.initials: N
authors.lastname: Plesnila
authors.forename: M
authors.initials: M
authors.lastname: Rinecker
authors.forename: A
authors.initials: A
authors.lastname: Baethmann
mesh_terms: D000818:Animals; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D001929:Brain Edema / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000293:injuries* / Q000503:physiopathology; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D009336:Necrosis; D010101:Oxygen Consumption / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000502:physiology
chemical_list: D019344:Lactic Acid