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diphenylhydantoin/инсулт
Линкът е запазен в клипборда
6 резултата
Paroxysmal "nightmares". Sequel of a stroke responsive to diphenylhydantoin.
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A 65-year-old man had nightmares a few weeks after a right temporal lobe infarction. Electroencephalography showed no epileptic activity. Therapy with diphenylhydantoin produced complete remission of his symptoms. On the bases of their acute onset, their association with sleep, their occasional
[Comparative studies on the contractile and hemodynamic effects of antiarrhythmic agents (lidocaine, diphenylhydantoin, ajmaline) (author's transl)].
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The contractile and hemodynamic effects of lidocaine, diphenylhydantoin and ajmaline were compared in isolated ventricular myocardium and in patients during diagnostic cardiac catheterization. The animal experiments show that diphenylhdantoin is 3-5 times more potent as a contractility inhibitor
Diphenylhydantoin attenuates hypoxia-induced release of [3H]glutamate from rat hippocampal slices.
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The ability of diphenylhydantoin (DPH) to prevent hypoxia-induced [3H]glutamate release was examined in perfused rat hippocampal slices. Hypoxia (25 min; 95% N2/5% CO2) caused a prolonged release of [3H]glutamate, which was reduced significantly if DPH (20 microM) was present from the beginning of
Diphenylhydantoin protects against hypoxia-induced impairment of hippocampal synaptic transmission.
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The ability of diphenylhydantoin (DPH) to protect against hypoxia-induced neuronal damage was examined using electrophysiological recordings of extracellular evoked potentials from CA1 pyramidal neurons of rat hippocampal slices in vitro. In normal medium, a 15-min hypoxic insult (95% N2/5% CO2)
Phenytoin protects against hypoxia-induced death of cultured hippocampal neurons.
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The neuroprotective actions of the anticonvulsant phenytoin (diphenylhydantoin, PHT) were evaluated using 3 week old primary hippocampal cultures derived from 19 day embryonic rat. When added to the culture medium prior to a hypoxic insult, PHT increased neuronal viability two-fold. Doubling
Altered Na(+)-channel function as an in vitro model of the ischemic penumbra: action of lubeluzole and other neuroprotective drugs.
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Veratridine blocks Na(+)-channel inactivation and causes a persistant Na(+)-influx. Exposure of hippocampal slices to 10 microM veratridine led to a failure of synaptic transmission, repetitive spreading depression (SD)-like depolarizations of increasing duration, loss of Ca(+)-homeostasis, a large
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