[Model corasol-induced seizures are followed by increase of nitric oxide generation and are abolished by mexidol and alpha-tocopherol].

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 influence of anticonvulsant and antioxidant drugs on nitric oxide level and lipid peroxidation in the rat brain during penthylenetetrazole-induced epileptiform model seizures.

Nitric oxide (NO) generation in the brain cortex of Wistar rats was measured by direct method of electron paramagnetic resonance (EPR) spectroscopy. Dramatic (fivefold) elevation of NO production was found during penthylenetetrazole (PTZ)-induced epileptiform seizures. The level of secondary products of lipid peroxidation (LPO; thiobarbituric acid reactive substances, TBARS) was also significantly increased in the cerebral cortex of rats with PTZ-evoked seizures.

Role of nitric oxide and lipid peroxidation in mechanisms of febrile convulsions in Wistar rat pups.

Generation of nitric oxide and the content of lipid peroxidation products in the brain are increased in rat pups during febrile convulsions. NO-synthase inhibitor N-nitro-L-arginine in a dose of 250 mg/kg prevented hyperthermia-induced accumulation of nitric oxide, increased the latency febrile convulsions, and had no effect on the content of lipid peroxidation products.

Nitric oxide content measured by ESR-spectroscopy in the rat brain is increased during pentylenetetrazole-induced seizures.

Nitric oxide (NO) content in rat cerebral cortex was measured using Electron Spin Resonance (ESR) spectroscopy. A nearly fivefold elevation in NO content was found at the peak time of pentylenetetrazole (PTZ)-induced seizures. The administration of N-nitro-L-arginine (L-NNA), a competitive inhibitor of NO-synthase, at the dose of 250 mg/kg, completely prevented the NO increase induced by PTZ, although clonic convulsions in the animals have been observed.

[The effect of anticonvulsants on the nitric oxide content and level of lipid peroxidation in the brain of rats in model seizure states].

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.