[Model corasol-induced seizures are followed by increase of nitric oxide generation and are abolished by mexidol and alpha-tocopherol]. / Model'nye korazolovye sudorogi soprovozhdaiutsia usileniem generatsii okisi azota i ustraniaiutsia meksidolom i al'fa-tokoferolom.

The effect of mexidol and alpha-tocopherol on the onset and development of acute epilepsy model was studied in Wistar rats using penthylenetetrazole induced convulsions. The intensity of the nitric oxide (NO) production in the cerebral cortex was determined by a direct method using electron paramagnetic resonance. The rate of lipid peroxidation (LPO) was estimated by measuring the level of secondary products (thiobarbituric acid reactive species). The peak of penthylene-tetrazole convulsions is accompanied by a significant increase in the levels of both NO and LPO products. Mexidol (150 mg/kg) and alpha-tocopherol (100 mg/kg) hindered the development of model convulsions, prevented NO buildup, and inhibited LPO growth. It is suggested that suppression of the excess NO production in the cortex and inhibition of the LPO enhancement can be involved in the mechanism of action of antiepileptic drugs.

[The effect of anticonvulsants on the nitric oxide content and level of lipid peroxidation in the brain of rats in model seizure states]. / Vliianie antikonvul'santov na soderzhanie oksida azota i uroven' perekisnogo okisleniia lipidov v mozge krys pri model'nykh sudorozhnykh sostoianiiakh.

EPR spectroscopy was performed to study the effect of anticonvulsants lamotrigine and phenobarbital on nitric oxide generation in rat brain on models of a convulsive seizure caused by exposure to maximal electric shock or corasole injection. The intensity of lipid peroxidation (LPO) was studied at the same time. The anticonvulsants under study proved to be capable of suppressing to a various degree intensification of nitric oxide generation and increase of LPO intensity in the rat cerebral cortex induced by convulsions. This widens the existing idea of the mechanism of the effect of antiepileptic agents.

[The seizures induced by N-methyl-D,L-aspartate administration are accompanied by an enhancement of nitric oxide generation and of lipid peroxidation processes in the rat brain]. / Sudorogi, vyzvaemye vvedeniem N-metil-D,L-aspartata, soprovozhdaiutsia usileniem generatsii oksida azota i protsessov perekisnogo okisleniia lipidov v mozge krys.

EPR-spectrometry was performed to study the nitrous oxide (NO) content and the intensity of lipid peroxidation (LPO) in the brain cortex of rats during convulsions induced by intracerebral injection of N-methyl-D,L-aspartate (NMDLA). It was shown that the convulsions were attended with a fourfold increase in the NO content and activation of LPO in the rat brain cortex. Disocilpin injection fully prevented the development of convulsions as well as increase in the NO level and LPO activation caused by NMDLA injection. N-nitro-L-arginine had an anticonvulsive effect and prevented increase in the NO content but did not cause any noticeable effect on LPO intensity in the brain cortex.

[Nitric oxide in the rat cerebral cortex in seizure models: potential ways of pharmacological modulation]. / Oksid azota v kore mozga krys pri model'nykh sudorozhnykh sostoianiiakh: vozmozhnye puti farmakologicheskoi moduliatsii.

Seizures induced with Thiosemicarbaside, Pentylenetetrasole, N-methyl-D,L-aspartate were used as models. The NO content increased 4-5-fold in the brain cortex at the peak of seizures. The increase could be prevented by pre-treatment with N-nitro-L-arginine and the seizures were weakened. Anticonvulsant drugs reduced the seizure manifestations and partially prevented the NO generation enhancement. The latter seems to be involved in pathophysiological mechanisms underlying the seizures.