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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of pentobarbital and phenytoin on the high-affinity uptake of the putative neurotransmitters gamma-aminobutyric acid (GABA), glutamate, and norepinephrine was examined in synaptosomes prepared from rat brain. Both pentobarbital and phenytoin inhibited the uptake of norepinephrine. Pentobarbital increased the uptake of GABA twofold and only slightly increased the uptake of glutamate. Phenytoin facilitated GABA uptake to a lesser extent than did pentobarbital, but also increased the uptake of glutamate. This suggests that these drugs may limit the propagation of seizures through the balance of excitatory glutamate pathways and inhibitory GABA and norepinephrine pathways. The contrasting effects of these drugs on GABA and glutamate uptake may be related to the hypnotic properties of pentobarbital not present in phenytoin.
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PMID:Mechanism of action of anticonvulsants. Role of the differential effects on the active uptake of putative neurotransmitters. 0 91

The protective effects of pentobarbitone, hydroxydione and diazepam against acute and chronic toxicity of high-pressure oxygen (HPO) were studied in rats. During exposure to hyperbaric oxygen body temperature was measured and ECG as well as EMG tracings from the diaphragm were obtained. Long term observations of animals after the exposure to HPO were conducted. Pentobarbitone and hydroxydione reduced the manifestations of acute toxicity but increased those of chronic toxicity. Diazepam reduced the manifestations of acute toxicity and seemed to counteract those of chronic toxicity. Lowering of body temperature of the animals which occurred during exposure to HPO was probably connected with manifestations of chronic toxicity. Observation of the cardiorespiratory functions suggested a possible connection between their disturbances and an onset of seizures and development of oxygen-induced paralysis.
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PMID:The protective action of certain anaesthetics and tranquilizers against the effects of hyperbaric oxygen. 1 48

Six barbiturates with diverse time-action characteristics--thiopental, pentobarbital, butabarbital, phenobarbital, diphenylbarbiturate, and barbital--were evaluated for "anticonvulsant" and "neurotoxic" effects. For the former, the MES test, clonic seizures induced by pentylenetetrazol, 90 mg/kg, s.c., and maximal seizures produced by pentylenetetrazol, 200 mg/kg, s.c., were employed. For the latter, we used a rotorod technique. Time to peak activity in the MES test was employed as the time for other tests. Pentobarbital required at least neurotoxic doses to produce substantial "anticonvulsant" activity, its protective index ranging from 0.79 to 0.98 in the three tests. Among the drugs tested, phenobarbital and diphenylbarbiturate exhibited the most favorable protective indices, ranging from 2.71 to 3.41 for phenobarbital and from 3.85 to 5.0 for diphenylbarbiturate. Barbital, another drug with a prolonged duration of action, exhibited a range from 0.84 to 2.81. Although a prolonged duration of action is an important characteristic for antiepileptic activity, this property does not confer per se a favorable protective index.
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PMID:Differential selectivity of several barbiturates on experimental seizures and neurotoxicity in the mouse. 3 70

With systemic (60-150 mg/kg) and topical application, Aldactone exhibited strong convulsant action on the cat cerebral cortex. The most common abnormal interictal features of the surface ECoG pattern were sequences of fast waves and slow negative waves associated with positive sharp waves, negative field potentials and burst-like neuronal activation in the extracellular microelectrode record. Another abnormal pattern was a period of ECoG and neuronal inactivity subsequent to the negative transients. These series of sharp and slow waves and of inactivity were interrupted by tonic and clonic ECoG seizures characterized by regular surface positive spikes. Development of seizures, but not of interictal phenomena, could be prevented by intravenous application of Diazepam (1 mg), Nembutal (30 mg/kg) and--less effectively--by Phenhydane (20 mg/kg).
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PMID:The effects of a spirolactone derivative on EEG and cortical single unit activity in the cat. 5 40

We have compared the sleep-producing effects of thalidomide and pentobarbital. In a dose range that did not produce ataxia, thalidomide increased slow wave sleep and rapid eye movement sleep in cats (2-8 mg/kg p.o.) and rats (16 mg/kg p.o.). Pentobarbital had hypnotic activity in the same dose range but produced ataxia also at these doses. Thalidomide reduced spontaneous activity of both mice and rats. This occurred over a dose range of 8 to 1000 mg/kg p.o., but plateaued at a level of activity well above the complete inactivity of anesthesia that occurred with pentobarbital at well above the complete inactivity of anesthesia that occurred with pentobarbital at doses (greater than or equal to 32 mg/kg p.o.) above the hypnotic range. Several simple screens for thalidomide-like activity have been described which, together, could facilitate the search for thalidomide-like hypnotics. Pentobarbital, at doses 3 to 10 times the hypnotic range, prevented audiogenic seizures in physically dependent rats withdrawn from sodium barbital but thalidomide did not substitute for barbiturates even at doses 30 times those that increased sleep. Thalidomide, but not pentobarbital, enhanced the sleep-producing effect of electrical stimulation of basal forebrain in cats. The latter two findings suggest that thalidomide probably has a mechanism of action different from that of pentobarbital and that this may involve the activation of a sleep center in the forebrain.
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PMID:A comparison of thalidomide and pentobarbital - new methods for identifying novel hypnotic drugs. 56 42

Continuous monitoring of regional cerebral blood flow (rCBF) of the hippocampus was made during limbic seizure status in cats by means of a heat clearance method with a calibration method by an electrolytic hydrogen clearance method. A stereotaxic operation was made under Nembutal anesthesia. Local anesthetics were applied to the painful area. Femoral artery and vein were cannulated and served for arterial blood pressure monitoring and drug injection, respectively. Tracheostomy was made and ventilated artificially. A double cannula was inserted to the amygdala and fixed to the skull with a dental cement. Electrodes for heat clearance method, electrolytic hydrogen clearance method and EEG recording were inserted to the dorsal hippocampus. Limbic seizure status was induced by kainic acid microinjection (2 ug) into amygdala via implanted cannula. Baseline rCBF was measured in each cats. Continuous monitoring of rCBF was made before and after intravenous administration of anticonvulsants such as zonisamide (ZNS), valproic acid (VPA), diazepam (DZP), phenobarbital (PB) and phenitoin (PHT). Physiological saline (PHS) was injected for controls. Injection of DZP resulted in strong seizure suppression with decrease of arterial blood pressure and hippocampal rCBF. Intravenous PB demonstrated analogous action with DZP with a mild anticonvulsant effect. Intravenous ZNS or VPA resulted in inhibition of seizure propagation from limbic system to cortex. However, these drugs augmented rCBF of the hippocampus more than 2 hours after administration. PHT and PHS demonstrated no anticonvulsant effect nor rCBF change in the present study.
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PMID:[Effect of anticonvulsants upon experimental limbic seizure status and regional cerebral blood flow in the hippocampus]. 159 Nov

1. The effects of BRL 34915 (cromakalim), a potassium channel opener, have been tested on the epileptiform activity elicited by high dose/concentrations of some calcium antagonists in in vivo (diltiazem) and in vitro (diltiazem and verapamil) experiments in rats. 2. Diltiazem (150-300 mg kg-1, i.p.) induced behavioural and electroencephalographic (EEG) seizures that were completely prevented by cromakalim (10 nmol/10 microliters, i.c.v.). Whereas, pentobarbitone (5-10 mg kg-1, i.p.) only prevented the behavioural component of the seizures. 3. In hippocampal slices, verapamil (1.5-2.0 mM) produced, within 30-60 min of perfusion, a CA1 epileptiform bursting in 80% of the experiments. This epileptiform activity was prevented by the cromakalim concentration (50 microM) that did not affect the control CA1 synaptic transmission per se. Pentobarbitone also prevented verapamil-induced epileptiform bursting only at the concentration (100 microM) that also reduced control CA1 synaptic transmission. 4. Diltiazem (1.5 mM) produced a biphasic excitatory-depressant effect within 60 min of perfusion. A CA1 epileptiform bursting appeared in 100% of the experiments within 30 min of perfusion. These excitatory effects were followed by a depression phase, characterized by a reduction of the magnitude of CA1 excitatory postsynaptic potentials (e.p.s.ps) and population spike. 5. The diltiazem-induced epileptiform bursting was prevented by cromakalim at a concentration (50 microM) that did not affect the control CA1 synaptic transmission per se. Pentobarbitone also prevented the diltiazem-induced epileptiform bursting only at a concentration (100 microM) that also reduced the control CA1 synaptic transmission. Both cromakalim (50 microM) and pentobarbitone (100 microM) failed to affect the depressant effects of diltiazem on CA1 hippocampal area. On the contrary, high (3.3mM) calcium solutions prevented both the excitatory and the depressant effects of 1.5 mm diltiazem within 60 min.6. These data indicate an involvement of potassium currents in the epileptiform activity elicited by high doses of diltiazem and verapamil.
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PMID:Cromakalim (BRL 34915) counteracts the epileptiform activity elicited by diltiazem and verapamil in rats. 166 91

A model for the development of pentobarbital tolerance and dependence was characterized and correlated with changes in radioligand binding to the GABAA-benzodiazepine receptor chloride channel complex. While one day of pentobarbital exposure decreased the duration of loss of righting reflex, tolerance to the hypothermic effects of thiopental and barbital took 7 days to develop, indicating that pharmacokinetic and pharmacodynamic tolerance are separable. Increased sensitivity to pentylenetetrazol-induced seizures was first observed after 3 days of pentobarbital exposure, suggesting brain areas involved in seizure control develop tolerance to, and dependence on pentobarbital faster than those involved in temperature regulation. Acute exposure to pentobarbital in vivo did not affect cortical binding of [3H]muscimol in vitro, while tolerance caused a decrease in binding due to an increase in the low-affinity site KD. Pentobarbital tolerance also caused a decrease in the cortical binding of the benzodiazepine, [3H]flunitrazepam. These observations suggest that the acute effects of barbiturates on the GABAA receptor complex are reversible, while tolerance causes receptor modifications which may be related to the development of physical dependence.
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PMID:Pentobarbital tolerance and withdrawal: correlation with effects on the GABAA receptor. 196 22

High pressure and anaesthetic agents are mutual antagonists in intact animals, but antagonism is not observed in isolated nerve cells. In order to test the hypothesis that a neural network might display pressure-anaesthetic antagonism not found in simpler systems, we have examined the effects of pentobarbitone at normal pressure and at 10.1 MPa helium pressure on the rhythmic activity of medullary respiratory centres of isolated brainstem and spinal cord from 0-3 day old rats. Pentobarbitone 5-80 mumol litre-1 depressed the frequency, amplitude and area of spontaneous bursts recorded from C5, reduced respiratory drive, and altered the response to trigeminal nerve root stimulation. Compression to 10.1 MPa decreased ventilatory frequency and respiratory drive, and either did not interact with or enhanced the depressant effects of pentobarbitone. Pentobarbitone and helium pressure altered the response to trigeminal nerve root stimulation in the same manner. The results are consistent with additive rather than antagonistic effects of pressure and a barbiturate on the determinants of output from the respiratory centre-motor neurone pathway. Pressure-anaesthetic antagonism may be a property unique to the neural circuitry which underlies awake behaviour and pressure-induced seizures, rather than reflecting a fundamental molecular-level antagonism.
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PMID:Barbiturate alteration of respiratory rhythm and drive in isolated brainstem-spinal cord of newborn rat: studies at normal and hyperbaric pressure. 199 65

Status epilepticus developed in four dogs, 2 to 3 days after ligation of an extrahepatic portosystemic shunt. Pentobarbital or phenobarbital intravenously was required to control seizure activity. Two dogs treated with phenobarbital recovered. Exacerbation of hepatic encephalopathy secondary to metabolic changes after surgery may be a cause of this syndrome. A treatment protocol for status epilepticus after ligation of a portosystemic shunt is proposed.
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PMID:Status epilepticus after ligation of portosystemic shunts. 226 77


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