Effects of blood glucose on ischemic brain damage in mature gerbils.
- Author:
Seung Hee HONG
1
;
Hea Soo KOO
Author Information
1. Department of Neurology, Top clinic, Wonju.
- Publication Type:Original Article
- Keywords:
hyperglycemia;
focal cerebral ischemia;
global cerebral ischemia
- MeSH:
Arteries;
Blood Glucose*;
Brain Ischemia;
Brain*;
Carotid Artery, Common;
Gerbillinae*;
Glucose;
Hippocampus;
Hyperglycemia;
Hypoglycemia;
Incidence;
Infarction;
Ischemia;
Ligation;
Mortality;
Necrosis;
Neurons;
Reperfusion;
Starvation;
Thalamus
- From:Journal of the Korean Neurological Association
1998;16(2):119-130
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND PURPOSE: Many clinical and experimental studies showed that in global ischemic encephalopathy, hyperglycemia consistently excacerbate ischemic brain damages with high mortality and morbidity. In contrast, the results of experiments on focal ischemic lesions were controversial or contradictory to each other according to various conditions. In addition, there have been few studies on the effects of hyperglycemia on delayed neuronal necrosis of hippocampus, which is one of characteristic patterns of selective neuronal necrosis. METHODS: Mongolian gerbils were used and divided into 4 groups ; control(group 1) with 4ml of intraperitoneal(ip) saline injection, hypoglycemia(group 2) was induced by 36-hour of starvation, marked hyperglycemia(group 3) was induced by 20ml/kg ip injection of 50% dextrose solution, and moderate hyperglycemia (group 4) was induced by 5ml/kg ip injection of 50% dextrose solution. Each hyperglycemia group was devided into 2 subgroups (A&B) according to the injection time, either 15 minutes before or after the ligation of arteries, respectively. Focal ischemic lesions were induced by 4-hour ligation of left common carotid artery (CCA) followed by 24 hour reperfusion. Global ischemic encephalopathy was induced by 10 min occlusion of bilateral CCAs followed by reperfusion for 1 or 3 days. RESULTS: In this study, hyperglycemia groups showed high incidence of mortality. Hypoglycemia group showed slightly less damages than control group and the damages were significantly decreased in group 3A. The gerbils in group 4 showed significantly aggravated damages than group 2 and 3. Timing of injection did not show significant difference. The thalamus was the only area showing significant differences among experimental groups. The gerbils with 10-min occlusion of bilateral CCAs with 1 or 3 days of reperfusion showed typical bilateral delayed neuronal damages in control group. In contrast, the hyperglycemia groups showed high incidence of infarction and mortality as well as unilateral delayed neuronal damages. CONCLUSION: This study showed different effects of hyperglycemia on focal cerebral ischemia according to blood glucose level and the difference in thalamus suggests the possibility of effects of glucose on local physicochemical factors. Mechanism of decreased delayed neuronal damages in group 4A with global ischemia was not clear and further studies would be helpful.
