title: Ischemia in normoglycemic and hyperglycemic rats: plasma energy substrates and hormones.
abstract: Seizures are a documented complication to cerebral ischemia. After 10 min of forebrain ischemia in rats, preischemic hyperglycemia invariably leads to severe, most often fatal epileptic attacks. This outcome is related to the exaggerated lactic acidosis, which has been suggested as a possible contributor to severe membrane changes and widespread edema. To find out if circulating hormones or plasma energy substrates modulate this additive damage caused by the hyperglycemia, plasma concentrations of of corticosterone, epinephrine, norepinephrine, dopamine, glucagon, insulin, glucose, free fatty acids (FFA), 3-hydroxybutyrate, and acetoacetate were measured before and in the early recirculation period after 15 min of forebrain ischemia in the rat. Plasma corticosterone levels did not differ between the normo- and hyperglycemic groups. Although not significantly different from control, the catecholamine levels showed a tendency to be higher in the hyperglycemic groups. Therefore, because catecholamines have been reported to have a protective effect during ischemia the present result cannot explain why hyperglycemia aggravates the ischemic damage. Insulin levels seemed to increase during ischemia but not significantly. Levels quickly returned to normal after 30 min of recirculation. FFA concentrations were reduced after the induction of ischemia and appeared lower in all hyperglycemic groups. The level of one of the ketone bodies, 3-hydroxybutyrate, showed a significant decrease in hyperglycemic ischemia in all groups compared with normoglycemic ischemia. The same tendency was seen for acetoacetate. Results are compatible with a protective role of ketone bodies in ischemia. It is concluded that among the hormones and substrates studied only the ketone body concentrations qualify as a modulator of the exaggerated brain damage after ischemia in hyperglycemic subjects.
authors.affiliation: Laboratory for Experimental Brain Research, University of Lund, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Lundgren
authors.forename: A
authors.initials: A
authors.lastname: Mans
authors.forename: B K
authors.initials: BK
authors.lastname: Siesjö
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D003345:Corticosterone / Q000097:blood; D004837:Epinephrine / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005934:Glucagon / Q000097:blood; D006728:Hormones / Q000097:blood*; D006943:Hyperglycemia / Q000097:blood* / Q000150:complications; D007328:Insulin / Q000097:blood; D002546:Ischemic Attack, Transient / Q000097:blood* / Q000150:complications; D007657:Ketone Bodies / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D007328:Insulin; D007657:Ketone Bodies; D002245:Carbon Dioxide; D005934:Glucagon; D010100:Oxygen; D003345:Corticosterone; D009638:Norepinephrine; D004837:Epinephrine