The study of some guanidine derivatives influence on free radical oxidation intensity and aconitase activity during the development of brain ischemia-reperfusion at rats has been carried out. The biochemiluminescence parameters increasing at the brain pathology changed toward normal values under the influence of N-[4-(chlorbenzoyl)benztiazol-2-yl]guanidine, N-[imino(1-piperidinyl)methyl]guanidine and N-[imino(4-morpholinyl)methyl]guanidine. The aconitase specific activity decreased in brain and blood of animals with ischemia-reperfusion. Administration of guanidine derivatives during brain ischemia-reperfusion development increased aconitase specific activity. These results suggest that investigated substances can play a role of neuroprotectors, preventing free radical oxidation development.