Influence of Preischemic Hyperglycemia on Osmolality and Early Postischemic Edema in the Rat Brain

Preischemic hyperglycemia, which raises tissue lactate content during ischemia, is known to aggravate ischemic brain damage. To explore the possibility that the enhanced lactic acidosis gives rise to osmotic damage, we studied the influence of a varied preischemic plasma glucose concentration on the early postischemic edema. Brain edema was measured by the specific-gravity technique. Brain and plasma osmolality were measured with a vapor pressure osmometer. We examined different brain regions in hyperglycemic and moderately hypoglycemic rats subjected to 15 min of forebrain ischemia, followed by recirculation for 5, 15, and 30 min. The decrease in specific gravity was compared with the increase in osmolality, to study whether the edema formation in the different groups correlated to the increase in tissue osmolality. We found edema formation to be most pronounced in frontoparietal cortex. In this structure and in hippocampus, statistically significant decreases of specific gravity were seen at all recirculation times studied. In caudoputamen, significant edema was seen only in the groups with 5 and 15 min of recirculation. Contrary to expectations, no difference was found between hyperglycemic and hyperglycemic animals. Tissue osmolality increased during ischemia in both the low and high glucose groups, but to a higher level in the latter (hypoglycemia 311 ± 1 mmol kg−1, hyperglycemia 328 ± 10 mmol kg−1; mean ± SD, p < 0.05). In the hyperglycemic group, brain osmolality remained elevated for the first 15 min of recirculation. Plasma osmolality also increased during ischemia in the two situations studied and remained increased during the first 15 min of recirculation. In spite of the higher brain osmolality during ischemia and the early recirculation phase in the hyperglycemic animals, theoretically favoring influx of water into brain tissue, we failed to observe increased edema formation in the hyperglycemic animals, probably due to the increased plasma osmolality, partly balancing the rise in brain osmolality and restricting water influx when cerebral blood flow was restored. We conclude that the fatal outcome in hyperglycemic animals is not likely caused by a more pronounced edema in the early recirculation phase.