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Biomedical subjects

Z Kleinrok

Publications and source records attributed to Z Kleinrok.

At least 397 records · Page 22Linked to original sources
PubMedDate not supplied

The influence of ethanol on pentetrazol-induced seizures and anticonvulsant activity of phenobarbital and valproate against maximal electroshock in mice.

The effect of acute (1, 2, and 3 g/kg) and chronic (2 g/kg) ethanol administration and ethanol withdrawal on pentetrazol-induced seizures and influence of ethanol in a dose of 2 g/kg upon the protective efficacy of valproate and phenobarbital against maximal electroshock-induced seizures was investigated. In the acute study ethanol increased, in the chronic study ethanol had no effect on ED50 values for pentetrazol. During withdrawal the ED50 was reduced. In the acute study ethanol reduced ED50 values for valproate and phenobarbital, in the chronic study had no effect. During withdrawal ED50 values for phenobarbital were elevated.

Animals↗
PubMedDate not supplied

Effect of nifedipine on lithium-pilocarpine-induced seizures in the rats.

Recent studies have shown that lithium pretreatment of rats potentiates the convulsant effect of pilocarpine. A large body of evidence support the hypothesis that calcium channel antagonists possess antiepileptic properties in various models of epilepsy. This study was designed to investigate effect of calcium channel antagonist, nifedipine on lithium-pilocarpine-induced convulsions in rats. Pretreatment of rats with nifedipine (5 or 10 mg/kg) as well as with a calcium channel agonist BAY k-8644 (2 mg/kg) increased convulsant effect induced by lithium and pilocarpine. The facilitating effect of nifedipine on lithium-pilocarpine-induced convulsions was prevented by pretreatment with a cholinergic antagonist atropine. It can be concluded that nifedipine facilitates convulsions in lithium-pilocarpine model of epilepsy and that cholinergic system may be involved in this effect.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Some pharmacological properties and cumulative, subchronic and chronic toxicity of 9-methyl-2-[3-(4-phenyl-1-piperazinylpropyl)] -1,2,3,4-tetrahydro-beta-carbolin-1-one (B-193).

The cumulative, subchronic and chronic toxicity of B-193 were studied on the rats and mice. It was found that this compound exerted weak tendency to cumulation in the body. Only the highest doses of B-193 (70, 40 mg/kg po for 12 weeks) caused the increase of animals mortality. Studies on subchronic and chronic toxicity have demonstrated, that B-193 administrated po or ip for 3 weeks, and po for 12 weeks, in general, neither affects the body weight gain nor the mass and morphology of heart, liver and kidneys, as well as spontaneous locomotor activity of animals. The weak depressant effect of B-193 on peripheral blood morphology was seen only after 3 weeks po or ip treatment with this compound. The moderate effect of B-193 on activity of alanine and aspartate transaminases (A1At and AspAt) and serum protein level found after 3 weeks of treatment, was no longer observed after 12 weeks of treatment. This could indicate that above effects of B-193 are reversible.

Animals↗
PubMedDate not supplied

Excitatory amino acid antagonists and the anticonvulsive activity of conventional antiepileptic drugs.

There is a great body of evidence, that excitatory amino acid antagonists, apart from their anticonvulsive properties per se, potentiate the protective activity of conventional antiepileptics against maximal electroshock-induced seizures in mice. It is worth stressing, that combinations of valproate with either CGP 37849 (a competitive NMDA antagonist) or dizocilpine (MK-801, a non-competitive NMDA antagonist), providing a 50% protection against maximal electroshock, resulted in no adverse effects, as measured in the chimney test (motor coordination) or passive avoidance task (long-term memory). On the other hand, valproate administered alone at its ED50, to protect against maximal electroshock, produced profound adverse effects. However, some NMDA antagonists (D-CPP-ene, memantine, procyclidine or trihexyphenidyl) did enhance the protection offered by common antiepileptics but these combined treatments were associated with considerable side-effects on motor coordination and long-term memory. Interestingly, ifenprodil (an antagonist of the polyamine site within the NMDA receptor complex) possessed some anticonvulsive activity against electroconvulsions but failed to enhance the antielectroshock efficacy of conventional antiepileptics. AMPA/KA receptor antagonists (NBQX and GYKI 52466), similarly to NMDA antagonists, potentiated the protective action of antiepileptic drugs against maximal electroshock and these combinations were generally devoid of unwanted effects.

Anticonvulsants↗
PubMedDate not supplied

Synthesis, chemical and pharmacological properties of some 2,4-dioxo-1,2,3,4,5,6,7,8-octahydropyrimido [4,5-d]pyrimidines.

Synthesis of 6-substituted 2,4-dioxo-1,2,3,4,5,6,7,8-octahydropyrimido[4,5-d]pyrimidines [III-VI] obtained by cyclocondensation of 1-phenyl-6-aminouracil with formaline and the primary amines is described. Compounds III, V, VI in the Mannich reaction with secondary cyclic amines yield the corresponding 3-substituted N-aminomethyl derivatives VII-X. Some of them were active pharmacologically.

Amines↗
PubMedDate not supplied

Effect of methionine on the brain biogenic monoamines and on the cortical bioelectrical activity of rabbits.

Methionine (150 and 300 mg/kg ip for 3 days) did not change the concentrations of striatal DA. It was also without effect on the levels of NA and 5-HT in the diencephalon and in the brain stem, while the 5-HIAA content was significantly increased in both structures after the dose 300 mg/kg. The single injection of methionine in doses of 10--300 mg/kg iv provoked dose-dependent changes in cortical bioelectrical activity. It was observed a considerable increase in the number of spindles, an increase in the amplitude and number of waves composing the spindles as well as a rise in their frequency characteristic.

Animals↗
PubMedDate not supplied

Central action of insect neuropeptide, periplanetin CC-1, in mice.

The central action of periplanetin CC-1 (Pea-HrTH) (Glp-Val-Asn-Phe-Ser-Pro-Asn-TrpNH2), octapeptide of the insect adipokinetic hormone family (AKH-family), isolated from American cockroach-Periplaneta americana, was studied in Albino Swiss mice (20-25 g). CC-1 was injected intracerebroventricularly (i.c.v.) in the volume of 5 microliters at the dose of 50 ng/mouse. It was found that CC-1 showed strong analgesic activity in "writhing syndrome" test and in "hot plate" test. In addition, periplanetin CC-1 decreased the threshold for tonic seizures and increased mortality in pentetrazole-induced seizures, having no influence on the electric convulsions. CC-1 is known to be a glucagon-like AKH in insects. However, administered i.c.v. to mice, it did not increase the peripheral blood glucose level. The obtained results indicate that periplanetin CC-1 shows a biological action in vertebrates, but its metabolic effects are different than in insects.

Animals↗
PubMedDate not supplied

Role of voltage dependent calcium channels and cholinergic receptors in the convulsant action of BAY k-8644.

The study was designed to investigate the effects of administration of cholinomimetic agents and nifedipine on seizures induced by BAY k-8644 in rats. Injection of pilocarpine (3 mg/kg) increased seizures induced by BAY k-8644 (2 mg/kg). Administration of nifedipine (10 mg/kg) did not affect the convulsions and mortality elicited by coadministration of BAY k-8644 and pilocarpine. However, the facilitating effect of pilocarpine on BAY k-8644-induced seizures was fully prevented by pretreatment of rats with a cholinergic antagonist atropine (5 mg/kg). No similar effects were observed after injection of another cholinomimetic agent physostigmine (0.3 mg/kg). This finding implies, that facilitation of convulsant action of BAY k-8644 by pilocarpine may be related to activity of cholinergic system, but not strictly to activity of voltage dependent calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗