title: Effects of hyperglycemia on small cerebral infarctions in awake rabbits.
abstract: This study concerns the effects of hyperglycemia on small infarctions in the rabbit brain. Small ischemic foci were produced in both normoglycemic (6 mM) and hyperglycemic (25 mM) rabbits, by injecting small plastic beads into the left heart ventricle under short-acting anaesthesia. 2-deoxy-D-[14C]glucose (2-DG) autoradiography was used to trace ischemic regions in which glucose uptake was increased, either shortly after, or six hours after, the embolization (in awake rabbits). A lesion was characterized by a 2-DG activity > 120%. The obtained freeze-dried sections were inspected for infarcts (with lost tissue structure and increased transparency to light). In the short experiments (< 1 hour), lesions could be detected throughout the brains, indicating hypoxic regions with enhanced glycolysis. In some foci, mostly located in the basal ganglia (the region containing the largest lesions), a central dip could be seen in the 2-DG accumulation, suggesting a poor glucose supply to the ischemic core. The lesions in the basal ganglia of rabbits that were made hyperglycemic were smaller and did not show such dips. No infarcts could be found in the tissue sections. In the long experiments (6 hours), both infarcts and lesions could be found. The impact of hyperglycemia on the infarction process in different brain regions was evaluated by measuring the infarct volumes, and by evaluating the fraction of infarcts--number of infarcts found in freeze-dried sections/number of foci (both lesions and infarcts) found in the 2-DG autoradiograms. Hyperglycemia reduced the fraction of infarcts in the cortex, and reduced the size of infarcted areas in the brain stem. In summary, this study shows that the impact of hyperglycemia on the ischemic outcome depends on where in the brain the ischemic focus is located. This adds interesting information as to what is known about the general effects of glucose on cerebral ischemia.
authors.affiliation: Department of Physiology, Uppsala University, Sweden.
authors.forename: M W
authors.initials: MW
authors.lastname: Roos
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002544:Cerebral Infarction / Q000097:blood / Q000150:complications / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D006943:Hyperglycemia / Q000097:blood / Q000150:complications*; D008297:Male; D011817:Rabbits
chemical_list: D001786:Blood Glucose