Abstract
Ischemia and anoxia are associated with decreased concentrations of cellular antioxidants. The hypothesis that recirculation of oxygenated blood to previously ischemic tissue may result in enhanced free-radical reactions leading to lipid peroxidation and tissue damage was investigated. Elevated hepatic conjugated diene concentrations were detected 60 min after treatment of rats with carbon tetrachloride, a positive control, but were not found after 90 min ischemia or at 5 or 60 min after reperfusion of ischemic tissue. These findings suggest that lipid peroxidation may not be an early event in ischemia-induced necrosis but do not rule out a role of other free-radical reactions in the pathogenesis of ischemic necrosis.
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