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1. |
Editorial |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 296-296
Arthur A. Ward,
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ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04970.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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2. |
Phenytoin Revisited |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 297-298
Arthur Raines,
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ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04971.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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3. |
The Influences of Phenytoin on the Fundamental Electrical Properties of Simple Neural Systems |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 299-307
G. F. Ayala,
Daniel Johnston,
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摘要:
SUMMARYThe effects of phenytoin on some neurophysiological properties of simple neuronal systems are reviewed. From all the available data phenytoin decreases or has no effect on post‐ tetanic hyperpolarization, which is interpreted as an expression of the electrogenic pump. Al‐ though in some neurons the membrane conduc‐ tance is increased, the resting membrane poten‐ tial is minimally affected. The effect on the action potential varies with different preparations and with different neurons of the same ganglion. If an effect is present, the overshoot is decreased or the falling phase is prolonged, or both. Post‐ synaptic potentials are also affected by pheny‐ toin. EPSPs are decreased in size, while the chloride‐dependent, GABA‐mediated IPSPs of the crayfish stretch receptor are prolonged. No effect was seen on chloride‐dependent, ACh‐ mediated IPSPs in the abdominal ganglion of the Aplysia. Finally, phenytoin arrests endogenous or pharmacologically induced bursting. Most of the described effects are consistent with the an‐ tiarrhythmic and antiepileptic p
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04972.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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4. |
The Role or Non‐Role of ATPase Activation by Phenytoin in the Stabilization of Excitable Membranes |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 309-315
Jean D. Deupree,
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摘要:
SUMMARYThe role or non‐role of NaK ATPase, Mg ATP‐ase, and CaMg ATPase involvement in stabilization of excitable membranes by phenytoin is critically evaluated. There is no substantial evidence to indicate that the membrane‐stabilizing effect of phenytoin is due to activation of the NaK ATPase. Previous reports of activation of the NaK ATPase at low potassium and high sodium are probably not due to phenytoin but to a potassium contamination in the phenytoin solution.In vitroexperiments do not provide any clear evidence of any alterations of NaK ATPase properties by phenytoin. However, one cannot rule out the possibility that phenytoin alters the efficiency of the sodium‐potassium pump. Likewise, the Ca ATPase is not inhibited by phenytoin. However, there is some evidence that the Mg ATPase in synaptic vesicles is substantially inhibited by phenytoin. There is substantial evidence indicating that phenytoin partially blocks passive diffusion of sodium into stimulated nerves. The mechanism by which phenytoin blocks sodium influx and the relationship of this effect to the drug's anticonvulsant action remain to be det
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04973.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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5. |
Phenytoin, Electric, Ionic, and Metabolic Responses in Cortex and Spinal Cord |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 317-329
J. LaManna,
E. Lothman,
M. Rosenthal,
G. Somjen,
W. Younts,
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摘要:
SUMMARYPost‐tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug‐free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion‐selective microelectrodes. The post‐stimulation clearing of [K+]0was not accelerated by phenytoin, and frequently it was slowed. Post‐stimulus under‐ shooting of [K+]0was diminished. Oxidation of NADH in cortex and of cytochromea,a3in spinal cord were measured by optical methods. Stimulus‐evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+‐K+‐activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of “resting” redox levels of respiratory enzymes. The local regulation of blood flow re‐ mained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus‐evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04974.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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6. |
Phenytoin: Effects on Calcium Flux and Cyclic Nucleotides |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 331-336
James A. Ferrendelli,
Dorothy A. Kinscherf,
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摘要:
SUMMARYPrevious studies have demonstrated that phenytoin alters calcium conductance in isolated presynaptic nerve endings (synaptosomes) from rat or rabbit brain. Drug concentrations of 0.08 ITIM (20 μg/ml) or higher inhibit stimulated calcium influx into synaptosomes depolarized by high concentrations of potassium (69 min) by 7–58%. Calcium transport into undepolarized synaptosomes is only inhibited by 0.4 min or greater concentrations of phenytoin. Recent investigations show that in mouse brain slices, phenytoin inhibited elevations of cyclic GMP and cyclic AMP produced by ouabain or verat‐ridine. In contrast, elevations of the two cyclic nucleotides produced by high concentrations of potassium were not inhibited by phenytoin, suggesting that the anticonvulsant suppresses depolarization‐induced elevation of cyclic nucleotide levels in brain slices by inhibiting influx of sodium into cells. These data indicate that phenytoin inhibits both sodium and calcium influx into cells during cellular depolarization and alters regulation of brain cyclic nucleotide levels. Both of these actions may be important for the antiepileptic effect of phe
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04975.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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7. |
Effects of Phenytoin on the Cyclic Nucleotide System in the Motor Nerve Terminal |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 337-348
Kenneth L. Dretchen,
Frank G. Standaert,
Arthur Raines,
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摘要:
SUMMARYThe effects of phenytoin on the motor nerve terminal were evaluated on thein vivocat soleus nerve muscle preparation. Phenytoin, 10 mg/kg, reduced the repetitive aftercharges in motor nerve endings due to tetanic conditioning. It also reduced the repetitive activity due to adenylate cyclase activation with NaF, or to exogeneous dibutyryl cyclic AMP. These effects of phenytoin could be reversed by administering theophylline, a phosphodiesterase inhibitor, or by increasing the extracellular concentration of calcium. The effects of phenytoin could also be reversed by 3‐aminopyridine, but not by tetraethylammonium chloride. Verapamil, a calcium current antagonist, produced effects that were identical to phenytoin. It is concluded that phenytoin blocks a cyclic nucleotide‐mediated calcium influx that is associated with transmitter release. This calcium flux also appears to control a slow potassium current that is responsible for post‐tetanic hyperpolariz
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04976.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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8. |
Effects of Phenytoin on the Release of14C‐Adenine Derivatives |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 349-355
Edward Lewin,
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摘要:
SUMMARYThe release of14C‐containing compounds from rat cortical slices prelabeled with14C‐adenine consisted largely of adenosine (6—7%), inosine (13‐ 18%), and hypoxanthine (70–74%), with small amounts of nucleotides including cyclic AMP and adenine. This efflux was increased by both ouabain (0.1 mM) and veratridine (0.05 mM), the increment in released radioactivity consisting almost entirely of these three compounds. However, relatively more inosine than adenosine output was evoked by ouabain while the reverse was true with veratridine. Phenytoin partially reversed the effect of both depolarizing agents. After prelabeling, the efflux from astrocytoma cell cultures contained predominantly inosine (74%) and hypoxanthine (23%) with little adenosine. Ouabain increased the release of14C‐adenine derivatives, and this increase was diminished by phenytoin. Preliminary studies with neuroblastoma cell cultures have shown considerable variability in the composition of the effluent, with hypoxanthine the prevalent compound and almost no adenosine. Ouabain enhanced the efflux from these cells, and this effect was apparently reversed b
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04977.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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9. |
Possible Role of Calcium‐Dependent Protein Phosphorylation in Mediating Neurotransmitter Release and Anticonvulsant Action |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 357-365
Robert J. Lorenzo,
Steven D. Freedman,
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摘要:
SUMMARYThe results demonstrate that calcium and phenytoin have antagonistic actions on the net level of endogenous phosphorylation of specific rat brain proteins. These specific phosphoproteins were shown to be present in synaptosome preparations, and evidence is presented for the localization of these phosphoproteins within the presynaptic nerve terminal. The data are compatible with the hypothesis that the antagonistic actions of calcium and phenytoin on the phosphorylation of synaptosome proteins may be the underlying molecular mechanism mediating the opposing actions of these agents on the release of neurotransmitter from the presynaptic nerve terminal.
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04978.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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10. |
Evaluation of a New Immunoassay for Determination of Phenytoin and Phenobarbital: Results of a European Collaborative Control Study |
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Epilepsia,
Volume 18,
Issue 3,
1977,
Page 367-374
D. Schmidt,
V. Goldberg,
P. J. M. Guelen,
S. Johannessen,
E. v. d. Kleijn,
J. W. A. Meijer,
H. Meinardi,
A. Richens,
H. Schneider,
Y. Stein‐Lavie,
N. Symann‐Louette,
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摘要:
SUMMARYThe performance of a new enzyme multiplied immunoassay technique (EMIT) was compared with other current methods, namely gas‐liquid chromatography and thin‐layer chromatography, for the determination of phenytoin and phenobarbital in serum. Forty‐three serum samples were sent as unknowns to the participating laboratories for determination.The precision of repeated determinations was very similar for EMIT and chromatography. There was good agreement among gas chromatography, thin‐layer chromatography, and EMIT results. Interlaboratory variability was lower for EMIT determinations of both an‐tiepileptic drugs. The rapid analysis of small samples, made possible by the EMIT system, could have beneficial effects on the treatment of epilepsies.RESUMENSe han determinado los niveles en suero de di‐fenilhidantoina y fenobarbital mediante una nueva técnica de medición de enzimas con immunoensayo mul‐tiplicado (EMIT) y los resultados se han comparado con otrós mdtodos actuates y fundamentalmente con cromatografia de gas‐liquido y cromatografia de capa fina. Se enviaron 43 muestras sin codificar a los laboratorios participantes. La precisión de las deter‐minaciones repetidas fué muy semejante entre la EMIT y la cromatografía con una buena correlatión entre las diversas teacnicas. La variabilidad entre los laboratorios fué menor, utilizando la EMIT. La rapidez del análisis y las mínimas dosis utilizadas pueden contribuir beneficiosamente en el tratamiento de las epilepsías.ZUSAMMENFASSUNGEine neue enzymatische Immunoassaytechnik (EMIT) wurde mit anderen gangigen Methoden z.B. der Gaschromatographie und der Dünnschichtchro‐matographie zur Bestimmung von Diphenylhydantoin und Phenobarbital im Serum verglichen. 43 Serum‐proben wurden ungekennzeichnet den teilnehmenden Labors zur Bestimmung ilbersandt. Die Genauigkeit von wiederholten Bestimmungen war für die EMIT und die chromatographische Methode sehr ahnlich. Es bestand eine gute Übereinstimmung der Resultate, die durch Gaschromatographie, Dünnschichtchroma‐tographie und die EMIT‐Methode erzielt wurden. Die Unterschiede zwischen den Labors waren geringer für die EMIT‐Bestimmungen beider Antiepileptika. Die schnelle Analyse kleiner Mengen, die das EMIT‐System erlaubt, konnte sich vort
ISSN:0013-9580
DOI:10.1111/j.1528-1157.1977.tb04979.x
出版商:Blackwell Publishing Ltd
年代:1977
数据来源: WILEY
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