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PubMed1980

Decreased convulsant potency of picrotoxin and pentetrazol and enhanced [3H]flunitrazepam cortical binding following stressful manipulations in rats.

Various stressful manipulations in rats (cold-water swim, electric foot-shock administration, imparied access to food reward) were found to reduce the convulsant potency of drugs which interfere with GABA or benzodiazepine central processes. The convulsant threshold dosages of picrotoxin (0.4 mg/ml) or pentetrazol (10 mg/ml) administered after the stress by infusion (0.2 ml/min) via a vein of the tail were enhanced. The onset of generalized seizures induced by isoniazid (800 mg/kg) or by thiosemicarbazide (64 mg/kg) i.p. was delayed after cold-water swim. However, convulsant threshold dosages of bemegride or strychnine perfused at 2 and 0.2 mg/ml respectively were not changed by stress. Cold-water swim increased the number of cortical (but not cerebellar) [3H]flunitrazepam binding sites (+ 24%) but failed to alter cortical [3H]muscimol binding. This post-stress enhancement of binding sties, although suppressed by bicuculline (10(-4) M) seems not to be dependent on GABAergic mechanisms. Indeed cold-water stress did not reduce the ability of muscimol (10(-6) and 10(-5) M) and GABA (5 x 10(-6) and 5 x 10(-5) M) to increase flunitrazepam binding. Finally, this post-stress enhancement of benzodiazepine binding was not found to be paralleled by changes in the protective effects of diazepam against picrotoxin- or pentetrazol-induced seizures.

Animals↗
PubMed1995

The novel antiepileptic drug levetiracetam (ucb L059) appears to act via a specific binding site in CNS membranes.

Levetiracetam ((S)-alpha-ethyl-2-oxo-pyrrolidine acetamide, ucb L059) is a novel potential antiepileptic agent presently in clinical development with unknown mechanism of action. The finding that its anticonvulsant activity is highly stereoselective (Gower et al., 1992) led us to investigate the presence of specific binding sites for [3H]levetiracetam in rat central nervous system (CNS). Binding assays, performed on crude membranes, revealed the existence of a reversible, saturable and stereoselective specific binding site. Results obtained in hippocampal membranes suggest that [3H]levetiracetam labels a single class of binding sites (nH = 0.92 +/- 0.06) with modest affinity (Kd = 780 +/- 115 nM) and with a high binding capacity (Bmax = 9.1 +/- 1.2 pmol/mg protein). Similar Kd and Bmax values were obtained in other brain regions (cortex, cerebellum and striatum). ucb L060, the (R) enantiomer of levetiracetam, displayed about 1000 times less affinity for these sites. The binding of [3H]levetiracetam is confined to the synaptic plasma membranes in the central nervous system since no specific binding was observed in a range of peripheral tissues including heart, kidneys, spleen, pancreas, adrenals, lungs and liver. The commonly used antiepileptic drugs carbamazepine, phenytoin, valproate, phenobarbital and clonazepam, as well as the convulsant agent t-butylbicyclophosphorothionate (TBPS), picrotoxin and bicuculline did not displace [3H]levetiracetam binding. However, ethosuximide (pKi = 3.5 +/- 0.1), pentobarbital (pKi = 3.8 +/- 0.1), pentylenetetrazole (pKi = 4.1 +/- 0.1) and bemegride (pKi = 5.0 +/- 0.1) competed with [3H]levetiracetam with pKi values comparable to active drug concentrations observed in vivo. Structurally related compounds, including piracetam and aniracetam, also displaced [3H]levetiracetam binding. (S) Stereoisomer homologues of levetiracetam demonstrated a rank order of affinity for [3H]levetiracetam binding in correlation with their anticonvulsant activity in the audiogenic mouse test (r2 = 0.84, n = 12, P < 0.0001). These results support a possible role of this binding site in the anticonvulsant activity of levetiracetam and substantiate the singular pharmacological profile of this compound. This site remains however to be further characterised.

Animals↗
PubMed1985

Comparative effects of convulsant drugs on the sensory responses of neurons in the amygdala and brainstem reticular formation.

The sensory responses of neurons in the amygdala and mesencephalic reticular formation in the cat were enhanced following the intravenous administration of subconvulsant doses of bicuculline, strychnine, bemegride, pentylenetetrazol and physostigmine. The degree and intensity of the enhancement of the response was considerably greater in the reticular formation than in the amygdala. The latency of the response in simultaneously-recorded pairs of neurons in the amygdala and reticular formation was significantly shorter in the mesencephalic reticular formation. The enhancement induced by convulsants does not appear to be transmitter-specific, since enhancement was produced with sequential administration of convulsant drugs which affect gamma-aminobutyric acid (GABA), glycine or acetylcholine. These findings suggest that the reticular formation is involved, to a larger degree than the amygdala, in the ability of sensory stimuli to initiate generalized convulsive seizures in animals treated with these convulsant drugs. The enhancement of the response in the hippocampus and cortex, which has previously been shown to exhibit a longer latency and a lower degree of enhancement than the reticular formation, coupled with the findings in the amygdala, suggest that the reticular formation may mediate the enhancement of the response of these other regions of the brain. The spread of the enhancement of the response to other structures in the brain via the widely distributed output pathways from the reticular formation may lead to initiation of generalized seizures by a recruitment-like process, which may involve enlargement of the sensory hyperresponsive neural network of the brain until a critical neural mass is reached and initiation of seizures results.

Amygdala↗
PubMed1987

Antagonists of GABA responses, studied using internally perfused frog dorsal root ganglion neurons.

Responses of frog dorsal root ganglion neurons to GABA were studied under conditions of internal perfusion. Conductances to Na, Ca and K were pharmacologically blocked, C1 concentrations were maintained equal on both sides of the membrane and a small holding potential was used. Under these conditions GABA-induced C1 currents could be studied in isolation without shifts in EC1 occurring after GABA application. GABA currents were blocked by a variety of agents. The blockade by bicuculline and Zn was competitive, while that to penicillin was competitive at low concentrations (6 x 10(-5) M) and non-competitive at high concentrations (3 x 10(-4) M). Picrotoxin was non-competitive at all concentrations studied. The time course of the GABA-induced currents was changed in the presence of antagonists, including those that were competitive. These actions appear to be due to a change in the rates of receptor desensitization rather than shifts in EC1. Pretreatment with antagonists increased the degree of inhibition only for picrotoxin as compared to simultaneous application of GABA plus antagonist. The voltage dependence of the GABA response was altered by penicillin but not by other antagonists. GABA responses on frog dorsal root ganglion cell were also depressed by a variety of other metal ions (Cd, Ni, Cu, Co, Mn) and other drugs (strychnine, curare, 4-acetamide, 4'-isothiocyano-stilbene-2,2'-dilsulfonic acid disodium salt, 4,4'-diisothiocyano-stilbene-2,2'-dilsulfonic acid disodium salt trihydrate, bemegride and folic acid). In this preparation bicuculline and the heavy metal ions appear to block at or very near to the agonist binding site, while penicillin probably blocks the ion channel. The non-competitive action of picrotoxin appears not to be channel blockade, but to be due to a slowly equilibrating action at a site different from either the agonist binding site or the channel.

Animals↗
PubMed2006

Binding characteristics of levetiracetam to synaptic vesicle protein 2A (SV2A) in human brain and in CHO cells expressing the human recombinant protein.

A specific binding site for the antiepileptic drug levetiracetam (2S-(oxo-1-pyrrolidinyl)butanamide, Keppra) in rat brain, referred to as the levetiracetam binding site, was discovered several years ago. More recently, this binding site has been identified as the synaptic vesicle protein 2A (SV2A), a protein present in synaptic vesicles [Lynch, B., Lambeng, N., Nocka, K., Kensel-Hammes, P., Bajjalieh, S.M., Matagne, A., Fuks, B., 2004. The synaptic vesicle protein SV2A is the binding site for the antiepileptic drug levetiracetam. Proc. Natl. Acad. Sci. USA, 101, 9861-9866.]. In this study, we characterized the binding properties of levetiracetam in post-mortem human brain and compared them to human SV2A expressed in Chinese hamster ovary (CHO) cells. The results showed that the binding properties of levetiracetam and [3H]ucb 30889, an analogue that was previously characterized as a suitable ligand for levetiracetam binding site/SV2A in rat brain [Gillard, M., Fuks, B., Michel, P., Vertongen, P., Massingham, R. Chatelain, P., 2003. Binding characteristics of [3H]ucb 30889 to levetiracetam binding sites in rat brain. Eur. J. Pharmacol. 478, 1-9.], are almost identical in human brain samples (cerebral cortex, hippocampus and cerebellum) and in CHO cell membranes expressing the human SV2A protein. Moreover, the results are also similar to those previously obtained in rat brain. [3H]ucb 30889 binding in human brain and to SV2A was saturable and reversible. At 4 degrees C, its binding kinetics were best fitted assuming a two-phase model in all tissues. The half-times of association for the fast component ranged between 1 to 2 min and represent 30% to 36% of the sites whereas the half-times for the slow component ranged from 20 to 29 min. In dissociation experiments, the half-times were from 2 to 4 min for the fast component (33% to 49% of the sites) and 20 to 41 min for the slow component. Saturation binding curves led to Kd values for [3H]ucb 30889 of 53+/-7, 55+/-9, 70+/-11 and 75+/-33 nM in human cerebral cortex, hippocampus, cerebellum and CHO cells expressing SV2A respectively. Bmax values around 3-4 pmol/mg protein were calculated in all brain regions. Some of the saturation curves displayed curvilinear Scatchard plots indicating the presence of high and low affinity binding sites. When this was the case, Kd values from 25 to 30 nM for the high affinity sites (24% to 34% of total sites) and from 200 to 275 nM for the low affinity sites were calculated. This was observed in all brain regions and in CHO cell membranes expressing the SV2A protein. It cannot be explained by putative binding of [3H]ucb 30889 to SV2B or C isoforms but may reflect different patterns of SV2A glycosylation or the formation of SV2A oligomers. Competition experiments were performed to determine the affinities for SV2A of a variety of compounds including levetiracetam, some of its analogues and other molecules known to interact with levetiracetam binding sites in rat brain such as bemegride, pentylenetetrazol and chlordiazepoxide. We found an excellent correlation between the affinities of these compounds measured in human brain, rat brain and CHO cells expressing human SV2A. In conclusion, we report for the first time that the binding characteristics of native levetiracetam binding sites/SV2A in human brain and rat brain share very similar properties with human recombinant SV2A expressed in CHO cells.

Animals↗
PubMedDate not supplied

[Tele-E.E.G. recordings of three epileptic attacks classified as episodes of PM status (author's transl)].

The authors present the tele-E.E.G. resording of three episodes of PM status, occurring in three known epileptics (ages: 16, 20 and 22 years). One episode was induced by an injection of bemegride and the other two by overbreathing. Their duration was 27, 31 and 44 minutes respectively. The development of abnormalities was progressive in all three cases, whilst they disappeared suddenly in two cases. Study of these three episodes was made in two ways: an electrical study and a clinical study. In addition, a brief retrospective study of the psychological experience of the episodes was carried out. The main finding was that the three episodes recorded and observed represented prolonged attacks and not a succession of attacks. The authors concluded that episodes classified under the name of PM Status may be studied in two ways: either considering them as prolonged attacks which are not status epilepticus, or considering them as repeated attacks, their repetition resulting in the appearance of unusual additional signs and which are status epilepticus.

Adolescent↗
PubMed1991

Early and delayed I-123 IMP SPECT in epileptic patients with partial seizures and normal CT.

Forty-six epileptic patients with partial seizures and normal CT underwent 48 examinations of early and delayed SPECT using I-123 IMP in the interictal phase. One of them underwent a follow-up SPECT in a more stable state compared to the first SPECT. Another patient, with informed consent, underwent a follow-up SPECT in combination with pharmacologic activation with bemegride. Early SPECT was performed 30 minutes after an IMP injection and delayed SPECT 4 to 4 1/2 hours later. Temporal changes in uptake pattern were visually classified into six types and compared with known patterns of SPECT uptake in relation to ischemic, hyperemic, and other changes. These were also correlated with the amount of epileptic activity seen on the EEG.

Adolescent↗
PubMed1969

Taloximine, a new respiratory stimulant with brochodilator properties.

1. A novel phthalazine analogue taloximine (1-hydroxyimino-4(2-dimethyl-aminoethoxy)-1,2-dihydrophthalazine monohydrochloride monohydrate) stimulated respiration in conscious rabbits at doses of 7 mg/kg and above.2. Taloximine antagonized the depressant action of morphine on respiration in rabbits at doses of 10 mg/kg. At high doses it resuscitated rabbits after they had been given lethal doses of sodium pentobarbitone.3. In in vitro preparations of the trachea or bronchus taloximine was about equiactive with aminophylline. In the Konzett-Rössler preparation the intravenous ED50 for taloximine was about 18% of that of aminophylline, whereas after oral administration the two drugs were equiactive.4. Taloximine, unlike aminophylline, did not protect guinea-pigs against anaphylactic microshock to egg albumen.5. Taloximine shortened the duration of the loss of righting reflex in mice due to hexobarbitone more effectively than bemegride, nikethamide or vanillic acid diethylamide.6. In the dose required to stimulate respiration taloximine had only slight cardiovascular effects. Up to four times this dose produced no evidence of general excitation of the central nervous system.

Anaphylaxis↗
PubMed1976

Antagonism of gamma-aminobutyric acid and glycine by convulsants in the cuneate nucleus of cat.

1. Some convulsant substances have been applied to single neurones in the cat cuneate nucleus by microiontophoresis. Numerical values were derived for the effectiveness and selectivity of the substances as antagonists of gamma-aminobutyric acid (GABA) and glycine. 2. (+)-Bicuculline methochloride was the most effective GABA antagonist and it also excited many neurones. It antagonized GABA in 93% of experiments but also antagonized glycine in 41% of experiments. In most experiments the antagonism of GABA was greater than the antagonism of glycine resulting in an overall selective antagonism of GABA that was statistically significant. Nevertheless, in only about one quarter of the individual experiments was the GABA antagonism substantial and the selectivity clearcut. 3. (+)-Bicuculline and picrotoxin were less easily applied to neurones by microiontophoresis and were found to antagonize GABA in 30% and 35% of experiments, respectively. They also antagonized glycine in 25% and 30% of experiments, respectively. Overall, neither substance could be shown to be selective, statistically, although in the few individual experiments where the GABA antagonism was substantial the antagonism was clearly selective. 4. (+)-Tubocurarine antagonized GABA in 59% and glycine in 32% of experiments and it also excited many neurones. Penicillin antagonized GABA in 33% of experiments without antagonizing glycine. Neither antagonist caused any substantial antagonisms of GABA and neither showed significant selectivity overall. (-)-Bicuculline methochloride, leptazol and bemegride antagonized GABA or glycine in less than 10% of experiments, although (-)-bicuculline methochloride excited most neurones. 5. Strychnine antagonized glycine in every experiment while antagonizing GABA in only 5% of experiments. In each individual experiment the antagonism of glycine was substantial and clearly selective, resulting in a statistically significant selectivity overall. 6. It is concluded that the selective glycine antagonist strychnine is considerably better than the presently available GABA antagonists for distinguishing between responses to GABA and glycine, when the antagonists are applied by microiontophoresis.

Action Potentials↗
PubMed1975

The pharmacology of Avena sativa.

The pharmacology of Avena sativa has been investigated in laboratory animals following a report that tincture of Avena sativa reduced the craying for cigarettes in man. The tincture, evaporated to dryness, craving for cigarettes in man. The tincture, evaporated to dryness, re-constituted in an equal volume of water and administered by stomach tube or intraperitoneal injection, antagonized the antinociceptive effect of morphine in two separate test (hot-plate and tail flick). Compared with animals made depedent on morphine alone, mice pretreated with repeated injections of morphine plus extract passed a smaller number of stools and tended to jump less after administration of nalorphine. The pressor response to intravenously administered nicotine in urethane-anaesthetized rats was also antagonized by prior administration of Avena sativa. However, the aqueous extract prepared from the tincture did not affect the seizure threshold to bemegride or nicotine or the sleeping time induced by barbitone sodium.

Animals↗
PubMed2000

Noninvasive cerebral blood volume measurement during seizures using multichannel near infrared spectroscopic topography.

Near infrared spectroscopic topography (NIRS) is widely recognized as a noninvasive method to measure the regional cerebral blood volume (rCBV) dynamics coupled with neuronal activities. We analyzed the rCBV change in the early phase of epileptic seizures in 12 consecutive patients with medically intractable epilepsy. Seizure was induced by bemegride injection. We used eight-channel NIRS in nine cases and 24 channel in three cases. In all of the cases, rCBV increased rapidly after the seizure onset on the focus side. The increased rCBV was observed for about 30-60 s. The NIRS method can be applied to monitor the rCBV change continuously during seizures. Therefore, this method may be combined with ictal SPECT as one of the most reliable noninvasive methods of focus diagnosis.

Adult↗
PubMed1980

Effects of CS-386 and diazepam upon the gastric contraction and excitation of lumbar gamma-motoneurons following stimulation of the hypothalamus in the cat.

Effects of a new minor tranquilizer, CS-386 and diazepam were studied upon the gastric contraction and excitation of lumbar gamma-motoneurons following stimulation of some of the brain structures as well as upon the spontaneous gastric motility in the cat. CS-386 inhibited the hypothalamus-induced gastric contraction with little changes in spontaneous motility at doses of 5 and 10 mg/kg (i.d.). Diazepam inhibited both the hypothalamus-induced contraction and spontaneous motility at these doses. The vagal nerve-induced gastric contraction was suppressed by diazepam (5 mg/kg, i.d.) but not by the same dose of CS-386. Bemegride (5 mg/kg, i.v.) antagonized almost completely the depression caused by 5 mg/kg of CS-386, but not that by a dose of 10 mg/kg or 5 as well as 10 mg/kg of diazepam. Excitation of the lumbar gamma-motoneuron following stimulation of the posterior hypothalamus or the mesencephalic reticular formation was depressed by CS-386 or diazepam (10 mg/kg, p.o.), but not by lower doses. Based on the these evidences, it was suggested that CS-386 could be effective in stress-induced gastric lesions with lower side effects in digestive organs than diazepam.

Animals↗
PubMed1978

Anti-convulsant effect of phthalazino-2,3b-phthalazine-5(14H),12(7h)-dione (L-5418). I. Behavioral effect.

Since it had been demonstrated that L5418 has an anti-convulsant effect with no relation to its anti-inflammatory properties, comparative studies were carried out with the use of currently available anti-convulsant agents as controls. L-5418 inhibited tonic convulsions induced by maximal electroshock and strychinine in mice and prevented animals from the death sequence. L-5418 had an inhibitory effect on tonic convulsions induced by pentetrazol and N-sulfamoyl-hexahydroazepine (SaH 41-178), but not on clonic convulsions by those compounds at even a high dosage or on clonic convulsions induced by picrotoxin and bemegride. Trimethadione produced an inhibitory effect on both tonic and clonic convulsions. The hypnotic agents, phenobarbital and glutethimide inhibited both convulsions, but a higher dose was required in the case of clonic convulsions. Anti-convulsant agents are classified into three different groups according to their mode of action. L-5418 had the same mode of action as seen with diphenylhydantoin and carbamazepine. As L-5418 did not inhibit tremor induced by tremorine, an anti-Parkinson effect was ruled out. When L-5418 was administered alone, the animals did not lose the righting reflex nor show muscle relaxation observed in inclined screen and rotarod tests. Moreover, the compound had no influence on the aggressive behavior induced by electrical stimulation or olfactory bulb ablation. L-5418 possesses a selective anti-convulsant effect, yet has no sedative, tranquilizing or disturbing effects on movement such as equilibrium disturbance or muscle relaxation. L-5418 may prove useful for grand mal epilepsy as it is less toxic than diphenylhydantoin and carbamazepine.

Aggression↗
PubMed1984

Effects of brotizolam, a new thieno-triazolo-diazepine derivative, on the central nervous system.

The effects of brotizolam, a new thieno-triazolo-diazepine derivative, on the central nervous system were analyzed in mice, rats and rabbits. Diazepam, estazolam and triazolam were used as control drugs. Brotizolam inhibited spontaneous motor activities; performances in the rotarod test, staircase test, and maximal electroshock seizure test; and pentetrazol- or bemegride-induced convulsion. Moreover, catalepsy inducing action and potentiating effect on sleep elicited by pentobarbital or ethanol were observed. Following intraperitoneal or oral administration of brotizolam to rabbits with chronically implanted electrodes, the electroencephalographic profile in spontaneous EEG was characterized by slow waves with high amplitudes in the neocortex. The arousal responses by stimulation of the midbrain reticular formation and posterior hypothalamus were slightly inhibited, but the recruiting responses induced by stimulation of the diffuse thalamic projecting system were not inhibited, and seizure discharges induced by stimulation of the dorsal hippocampus were inhibited markedly. When motor activities and pentetrazol-induced convulsions were observed as indices of tolerance for brotizolam, tolerance was not developed by repeated administration of brotizolam up to 14 days. These results suggested that brotizolam, a new thieno-triazolo-diazepine derivative, is judged to be a safer and stronger sleep inducer than diazepam and estazolam.

Animals↗
PubMed2006

False lateralization of mesial temporal lobe epilepsy by noninvasive neurophysiological examinations.

Mesial temporal lobe epilepsy (mTLE) is the most common form of symptomatic localization-related epilepsy and is surgically remediable. Lateralization of the seizure onset is particularly important to determine from a surgical perspective. A 39-year-old woman with intractable mTLE first exhibited seizure at the age of 3 years. She experienced epigastric sensation and placed her right hand on her abdomen before falling backward. Although interictal scalp electroencephalography (EEG), sphenoidal scalp ictal EEG, and magnetoencephalography showed right temporal side focus, computed tomography and magnetic resonance imaging showed atrophy of the left cerebral hemisphere. Single photon emission computed tomography with technetium-99m ethyl cysteinate dimmer and I-123 iomazenil showed obscure focus on the left side. As a discrepancy existed between the results of neurophysiological examinations and imaging, we performed subdural electrode implantation on the bilateral temporal lobe. Although a bemegride-induced seizure arose from the right side during the subdural recording, the onset of 5 habitual seizures was observed in the left hippocampus. On the basis of these results, the seizure was diagnosed as left mTLE, and left anterior temporal lobectomy and amygdalohippocampectomy were performed. The patient has been free from the seizures for more than 1.5 years of follow up. Bilateral subdural electrode measurement of habitual seizures is indispensable for clarifying the actual focus when a discrepancy exists between neuroimaging and noninvasive neurophysiological examinations.

Adult↗
PubMed1997

Analeptic use in clinical toxicology: a historical appraisal.

BACKGROUND: The introduction and increasing popularity of the barbiturates during the first two decades of the 20th century was associated with a new life threatening toxicological problem: the barbiturate overdose. METHODS: This paper reviews the four major phases of analeptic use. As interest in the principles of physiologic antagonism between stimulants and depressants grew, analeptic agents were increasingly used to treat the obtundation and respiratory depression of barbiturate overdose. At first, naturally occurring stimulants such as camphor, strychnine, picrotoxin, and caffeine were used in desperate attempts to awaken patients. During the 1930s, and continuing at some centers into the 1960s, an increasing number of synthetic analeptics agents such as nikethamide, pentylenetetrazol, bemegride, amphetamine, and methylphenidate were enthusiastically recommended as barbiturate antidotes, often at very high doses. Unfortunately, utilizing generous amounts of multiple convulsants was not without its share of complications. Using this analeptic strategy the mortality rate after moderate to severe barbiturate overdose remained as high as 45%. Beginning in the mid-1940s a group of Scandinavian physicians pioneered a revolutionary approach to sedativehypnotic overdose that rejected the use of analeptics and relied on respiratory ventilation and supportive care. CONCLUSIONS: Although barbiturate overdose mortality decreased to less than 1% using this strategy, it would take another 20 years before this technique was universally adapted. While analeptic therapies for the treatment of drug overdose have now been abandoned, one of these analeptics, methylphenidate, currently enjoys wide use in the treatment of attention deficit hyperactivity disorder.

Barbiturates↗
PubMed1975

Simple, highly selective screening method for barbiturates in urine.

I present a new, simple colorimetric method for detecting and estimating barbiturates in urine. After the barbiturates are extracted with ether, an aliquot of the washed ether phase is added to the color reagent (a bivalent mercury/dithizone chelate in chloroform). On addition of diluted pyridine and shaking, a pinkish-violet color appears if a barbiturate is present. The overall sensitivity of the above method was evaluated by probit analysis in the case of sodium phenobarbital. The concentration of sodium phenobarbital in urine detectable at least 99% of the time was 6.72 mg/liter, with 95% confidence limits of 5.37 to 10.36 mg/liter. Sodium phenobarbital, 10 mg/liter, can be detected in the presence of phenytoin (50 mg/liter), glutethimide (100 mg/liter), or bemegride (100 mg/liter). The whole procedure requires less than 10 min. An excretion study illustrates application of the procedure.

Amobarbital↗
PubMed2002

[Prooxidant-antioxidant condition under increased convulsive activity].

During the clinical-biochemical research it was found that the trand's manner of epileptic disease in general is determined by the oxidative-antioxidant balance condition in the sick organism. The experimental research, made on rats, which were under bemegrid kindling confirmed the supposition that the pro-antioxidant brain balance disruption is one of the major factors in the increased convulsive activity development and probably plays the key role in the genesis and clinical revelation of epilepsy.

Animals↗