Relationship between free radical production and lipid peroxidation during ischemia-reperfusion injury in the rat brain.
Forebrain ischemia was produced in the rat by bilateral occlusion of the common carotid arteries combined with hemorrhagic hypotension (30 mmHg). The whole cerebral cortex was homogenized in the presence of the spin trap agent N-tert-butyl-alpha-phenyl-nitrone, followed by a Folch extract. Spin-adducts were detected using electron spin resonance spectroscopy. The lipid peroxidation was estimated from both the amount of thiobarbituric acid reactive substance and the formation of conjugated diene. After 10 or 20 min of ischemia, reperfusion was initiated which induced an abrupt burst of free radical formation. The formation peaked at 5 min, and the peak value increased with the ischemia time. The degree of lipid peroxidation, which was measured after 20 min of reperfusion, also increased with the ischemia time. The results suggest that the lipid peroxidation may be the direct consequence of the action of free radicals formed during ischemia and reperfusion periods.
Sakamoto
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A
Philadelphia Biomedical Research Institute, King of Prussia, PA 19406.
Ohnishi
S T
ST
Ohnishi
T
T
Ogawa
R
R
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002245:Carbon Dioxide / Q000097:blood; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology*; D003497:Cyclic N-Oxides; D004578:Electron Spin Resonance Spectroscopy; D005609:Free Radicals; D006339:Heart Rate; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D015227:Lipid Peroxidation; D008297:Male; D009589:Nitrogen Oxides; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D015427:Reperfusion Injury / Q000503:physiopathology*; D013113:Spin Labels
D003497:Cyclic N-Oxides; D005609:Free Radicals; D009589:Nitrogen Oxides; D013113:Spin Labels; D002245:Carbon Dioxide; C029217:phenyl-N-tert-butylnitrone; D010100:Oxygen