Regional changes in cerebral extracellular glucose and lactate concentrations following severe cortical impact injury and secondary ischemia in rats

Traumatic brain injury (TBI) causes the brain to be more susceptible to sec ondary insults, and the occurrence of a secondary insult after trauma incre ases the damage that develops in the brain. To study the synergistic effect of trauma and ischemia on brain energy metabolites, regional changes in th e extracellular concentrations of glucose and lactate following a severe co rtical impact injury were measured employing a microdialysis technique. Thr ee microdialysis probes were placed in center of the impact site, in an are a adjacent to the impact site, and in the contralateral parietal cortex, an d perfused with artificial cerebrospinal fluid (CSF) at 2 mu l/min. Rats we re assigned to one of the following experimental groups (n = 7 per group): (1) combined impact injury and secondary insult, (2) impact injury with sha m secondary insult, (3) sham impact with secondary insult, or (4) sham impa ct and sham secondary insult. The impact injury was produced with a pneumat ic impactor (5 m/sec, 3-mm deformation). One hour following the impact inju ry, a secondary insult was produced by bilateral carotid occclusion for 1 h . The impact injury resulted in a three- to fivefold global increase in dia lysate lactate concentrations, with a corresponding fall in dialysate gluco se concentration by 50% compared to no change in lactate or glucose concent rations in sham-injured animals (p < .0001 for both lactate and glucose). T he 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.