Hyperglycemia enhances excessive superoxide anion radical generation, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats.
The aim of this study was to confirm the effect of acute hyperglycemia on the superoxide anion radical (O(2)(-)) generation, using a novel electrochemical O(2)(-) sensor in forebrain ischemia/reperfusion rats. Fourteen male Wistar rats were allocated to a normoglycemia group (n= 7) and a hyperglycemia group (n=7). Hyperglycemia was induced by intravenous infusion of glucose solution. Forebrain ischemia was induced by bilateral common carotid arteries occlusion with hemorrhagic hypotension for 10 min and then was reperfused. The generated O(2)(-) was measured as the current produced, which was integrated as a quantified partial value of electricity (Q), in the jugular vein using the O(2)(-) sensor. The reacted O(2)(-) current and the Q began to increase gradually during the forebrain ischemia in both groups. These values increased remarkably just after reperfusion in the normoglycemia group and were further increased significantly in the hyperglycemia group after the reperfusion. Concentrations of malondialdehyde (MDA) and high-mobility group box 1 (HMGB1) in the brain and plasma, and soluble intercellular adhesion molecule-1 (ICAM-1) in the plasma in the hyperglycemia group were significantly higher than those in the normoglycemia group. Brain and plasma MDA, HMGB1, and ICAM-1 were correlated with a sum of Q during ischemia and after reperfusion. In conclusion, acute transient hyperglycemia enhanced the O(2)(-) generation in blood and exacerbated oxidative stress, early inflammation, and endothelial injury after the forebrain ischemia/reperfusion in the rats.
Tsuruta
Ryosuke
R
Advanced Medical Emergency and Critical Care Center, Yamaguchi University Hospital, 1-1-1, Minami-Kogushi, Ube, Yamaguchi, Japan.
Fujita
Motoki
M
Ono
Takeru
T
Koda
Yoichi
Y
Koga
Yasutaka
Y
Yamamoto
Takahiro
T
Nanba
Masahiro
M
Shitara
Masaki
M
Kasaoka
Shunji
S
Maruyama
Ikuro
I
Yuasa
Makoto
M
Maekawa
Tsuyoshi
T
D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology; D002536:Cerebral Arteries / Q000378:metabolism / Q000503:physiopathology; D048909:Diabetes Complications / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D004560:Electricity; D004563:Electrochemistry / Q000379:methods; D004660:Encephalitis / Q000378:metabolism* / Q000503:physiopathology; D042783:Endothelial Cells / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D013481:Superoxides / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
D001786:Blood Glucose; D013481:Superoxides; D005947:Glucose