Models For Hyperglycemia And Stroke

Clinical studies clearly show that admission hyperglycemia is related to the outcome after stroke (Chapter 9). It is less clear, however, if this relation is causal, i.e., high admission glucose causes poor outcome. Issues that need to be resolved are as follows: (i) whether stroke-related hyperglycemia reflects pre-existent metabolic abnormalities, such as impaired glucose tolerance, (ii) whether such pre-existent metabolic abnormalities already compromise the brain, which might explain the relatively poorer functional outcome in relation to hyperglycemia, (iii) if hyperglycemia in the days after the initial event is still harmful to the brain or may even represent a compensatory event for reductions in energy supply to the ischemic area, and (iv) if correction of hyperglycemia improves outcome. Studies in animal models can help to clarify these issues.

The timing and severity of hyperglycemia in relation to stroke can be readily manipulated in rodent models. A range of rodent models of stroke is available (11). A detailed discussion of the pros and cons of these models can be found elsewhere (12,13). This paragraph only deals with induction of hyperglycemia in these models. Hyperglycemia can be induced within minutes in rodents by an intraperitoneal injection of a concentrated glucose solution (14-16), prior to stroke or at any time after the stroke. Hyperglycemia can also be maintained for a prolonged period prior to the induction of a stroke. A stable elevation of blood glucose levels can, for example, be achieved within days after injection of f-cytotoxic compounds (14). If so desired, glucose levels can also be rapidly normalized again by intravenous insulin infusion (17) and chronic hyperglycemia may also be combined with other conditions that co-occur with disturbances in glucose metabolism in patients, such as hypertension.

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