Isolated Stimulation of Glycolysis Following Traumatic Brain Injury

Abstract

Clinical investigators have postulated that head trauma causes cerebral metabolic derangement, as evidenced by the presence of CSF lactate and brain acidosis (DeSalles et al. 1986). Work in our laboratory (Unterberg et al. 1988) reported decreased tissue pH within 15 minutes following trauma that eventually normalizes. Post traumatic tissue acidosis has been reported to correlate tightly with increased brain lactate (McIntosh et al. 1987). We have also found (Inao et al. 1988) increased cerebrospinal fluid and brain tissue lactate at 15 minutes posttrauma. We hypothesized from these studies that the metabolic derangement responsible for cerebral lactic acidosis occurs within minutes of trauma. To investigate this hypothesis, we focused our investigation on the first 15 minutes following trauma and measured global cerebral blood flow, cerebral metabolic rate of oxygen utilization, cerebral metabolic rate of glucose utilization, and performed 31P magnetic resonance spectroscopy in traumatized, ventilated cats. Data was obtained immediately following trauma and serially for the first hour posttrauma.