Blood glucose level and morphological brain damage following cerebral ischemia.

It is well known that various systemic parameters can modulate the deleterious effects of cerebral ischemia. We have reviewed the experimental data concerning the relationship between blood glucose concentration and brain ischemic morphological damage. Whereas the influence of hyperglycemia has been extensively investigated, the effect of a decrease in blood glucose concentration is not well documented. In models of transient ischemia, the cytologic damage is increased if the insult is induced in glucose-infused fed or fasted animals and decreased if it is induced in fasted animals. A more recent finding is the modulation of the extent of the cellular ischemic injury by manipulation of postischemic blood glucose concentration. In models of focal ischemia, conflicting results (a deleterious, a protective, or no effect) have been reported on the influence of elevated blood glucose concentration. Differences between the models of focal ischemia with respect to the possibility of collateral blood flow to enter the infarcted region may be an important factor for the explanation of the discrepant results. Because glycemia differences may explain some of the divergences on the susceptibility of the brain to ischemia, it becomes obvious (a) that the monitoring of glycemia before, during, and following the ischemic period is a prerequisite for the validation and the comparison of histological results, and (b) that every situation known to interfere with glycemia, such as food intake, anesthesia, or stress, have to be strictly controlled.