ALPHA-TOCOPHEROL AND GINKGO-BILOBA TREATMENT PROTECTS LIPID-PEROXIDATION DURING ISCHEMIC PERIOD IN RAT GROIN ISLAND SKIN FLAPS

Oxygen-derived free radicals have been implicated in the causation of cellular injury during low-flow ischemia and during reperfusion of pre viously completely ischemic tissue; they are also believed to be the c ausative factor in the no-reflow phenomena. Modulation of these free r adical substances has been suggested as a means of decreasing the amou nt of tissue loss due to ischemia and subsequent reperfusion. Pretreat ment of tissues with a variety of agents has been reported to minimize the production of oxygen radicals and augment tissue survival after a n ischemic insult. Further evidence of free radical involvement in ski n flap necrosis in a rat groin island skin flap model is presented. In addition, the effects of two different free radical scavengers, alpha tocopherol (20 mg/kg intraperitoneally once daily for a week) and gin kgo biloba (5 mg/kg orally twice a day for a week) have been investiga ted and compared. Since malonyldialdehyde (MDA) is the end product of lipoperoxidation which occurs in cellular membranes in an ischemic per iod - dependent manner, MDA levels in tissue homogenates were measured 60, 90, and 120 min after an ischemic insult. MDA levels significantl y increased in a time-dependent manner during the ischemic period in t he control group. Results from the determination of tissue MDA levels at biopsy sites of radical scavenger treated groups compared with the placebo group showed that the ginkgo biloba-treated rat samples had si gnificantly lower MDA levels than control samples only at the 120 min ischemic period (p<0.01). However, protection of lipoperoxidation in a lpha tocopherol-treated rat samples was detected after both the 90 and 12 min ischemic periods (p<0.01), and the magnitude of these decrease d MDA levels in alpha tocopherol-treated samples was found to be great er than it was after ginkgo biloba treatment. Decreasing free radicals during reperfusion by using these agents, preferably alpha tocopherol , may be beneficial in modulating the no-reflow phenomenon and subsequ ent reperfusion injury, and may help to improve tissue salvage.