Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of pyrimido-pyrimidine derivatives (dipyridamole, RA-642 and mopydamole) on lipid peroxidation (inhibition of the production of malondialdehyde, MDA) in different regions of the rat brain were studied. Ferrous sulfate and ascorbic acid (FeAs) were used to induce lipid peroxidation via the formation of hydroxyl anions. The antiperoxidative effect of RA-642 (in the microM range) was 10 times more potent than that of dipyridamole. Mopydamole did not exert any inhibitory effect on MDA production. In a model of ischemia reperfusion with bilateral occlusion of the common carotid arteries for 1 h and restoration of circulation for a period of 2 h, dipyridamole inhibited FeAs-induced MDA production but did not protect from postischemic brain tissue damage (measured by mitochondrial reduction of tetraphenyl tetrazolium). RA-642 inhibited FeAs-induced MDA production and showed 50-67% protection from tissue damage as compared with untreated animals, while mopydamole did not inhibit MDA production and showed 30-48% protection. No correlation was found between inhibition of lipid peroxidation and protection from brain tissue damage.
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PMID:The pyrimido-pyrimidine derivative RA-642 protects from brain injury in a combined model of permanent focal ischemia and global ischemia reperfusion. 147 97

The antioxidant effect of alpha-tocopherol was assessed in a model of ischemia-reperfusion in the rat brain. In this model, permanent ischemia of the cortical branches of the middle cerebral artery was combined with bilateral occlusion of the common carotid arteries for 1 h and restoration of circulation for a period of 2 h. Lipid peroxidation and mitochondrial reduction of tetraphenyl tetrazolium (TPT) were determined in both untreated and d-alpha-tocopherol treated rats. Ferrous sulfate and ascorbic acid (FeAs) were used to induce lipid peroxidation via the formation of hydroxyl anions. Malondialdehyde (MDA) increased in the ischemia-reperfusion areas (+101%), but FeAs-induced MDA did not vary in the area of permanent ischemia. Brain tissue undergoing ischemia-reperfusion was about 50% less sensitive to the antioxidant effect of ascorbic acid. The reduction of TPT showed 52% mitochondrial damage in the area of ischemia-reperfusion, whereas mitochondrial activity in the area of permanent ischemia was 177 times lower as compared to controls. d-alpha-tocopherol caused a 40% inhibition of MDA production and 16.5% and 21.5% decrease in mitochondrial activity in the areas of ischemia-reperfusion and permanent ischemia, respectively.
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PMID:Effects of alpha-tocopherol on lipid peroxidation and mitochondrial reduction of tetraphenyl tetrazolium in the rat brain. 829 15