Lesion-remote metabolic changes after neocortical cold injury in rats

Lesion-remote metabolic changes were examined 1-7 days after neocortical cold injury using tissue ATP, glucose and lactate bioluminescent imaging, pH-dependent fluoroscopy and cerebral protein synthesis (CPS) autoradiography. One day after lesioning an alkaline pH shift (0.35 +/- 0.19 units above contralateral) was noticed in the lesion-remote cortex, the underlying white matter, the striatum, hippocampus and thalamus, which slowly resolved within 7 days and probably reflected the spread of vasogenic edema. Closely associated with the pH shift, elevations in tissue glucose and lactate levels were found, which reached maximum levels after 3 days (7.4 +/- 2.4 vs 4.2 +/- 1.2 micromol/g glucose, 6.6 +/- 2.3 vs 2.1 +/- 0.6 micromol/g lactate) but, in contrast to the alkalosis, remained elevated after 1 week. Thus, neocortical trauma is associated with long-lasting metabolic changes, which are intimately linked with the distribution of post-traumatic alkalosis.