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anticholinergic/epileptični krč
Povezava se shrani v odložišče
Stran 1 iz 314 rezultatov
Anticonvulsant treatment of nerve agent seizures: anticholinergics versus diazepam in soman-intoxicated guinea pigs.
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A total of eight anticholinergic drugs (aprophen, atropine, azaprophen, benactyzine, biperiden, procyclidine, scopolamine, trihexyphenidyl) were tested in parallel with diazepam for the ability to terminate seizure activity induced by the nerve agent soman. Guinea pigs, implanted with electrodes to
Anticholinergics induce eclamptic seizures.
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Severe preeclampsia is a pathophysiological disorder specific to pregnancy and characterized by vasoconstriction and hypercoagulability. Eclampsia (convulsion associated with preeclampsia) and hemolysis, elevated liver enzymes, and low platelet count associated with preeclampsia (HELLP syndrome) are
Pilocarpine-induced convulsions in rats: evidence for muscarinic receptor-mediated activation of locus coeruleus and norepinephrine release in cholinolytic seizure development.
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We recently reported that systemic administration of the anticholinesterase, soman, caused rapid depletion of forebrain norepinephrine (NE) in convulsive but not in nonconvulsive rats. As neurons in nucleus locus coeruleus (LC) provide the bulk of NE innervation to most of the forebrain and the sole
Combined treatment with muscarinic and nicotinic cholinergic antagonists slows development of kindled seizures.
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Rats were given daily injections of atropine, mecamylamine or both drugs in combination, 1 h prior to daily electrical amygdaloid kindling stimulation. Neither drug was effective alone, but the two drugs in combination significantly increased the latency to develop stage 5 kindled seizures.
The anticholinergic and antiglutamatergic drug caramiphen reduces seizure duration in soman-exposed rats: synergism with the benzodiazepine diazepam.
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Therapy of seizure activity following exposure to the nerve agent soman (GD) includes treatment with the anticonvulsant diazepam (DZP), an allosteric modulator of γ-aminobutyric acid A (GABA(A)) receptors. However, seizure activity itself causes the endocytosis of GABA(A) receptors and diminishes
[Effect of some cholinolytic and tranquilizing agents on the duration of convulsions produced with nicotine and arecoline in rabbits].
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Epileptic seizures exacerbated by anticholinergic drugs.
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[Prevention of arecolinic and nicotinic convulsions in rabbits with cholinolytic substances].
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Transdermal anticholinergic treatment of reflex anoxic seizures.
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On certain correlations between the cholinolytics, the convulsive reactivity of the central nervous system, and the anticonvulsive activity of the anticonvulsants. II. Communication: cholinolytics upon corazol, strychnine, and thiosemicarbazide convulsions.
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Gastric mucosal damage induced by arecoline seizure in rats.
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In an attempt to know the relation of seizure and gastric mucosal damage, we challenged arecoline (ACL) centrally to induce seizure and investigated gastric hemorrhagic injury in acid-irrigated stomachs of rats. The protective effects of several drugs also were evaluated. After deprivation of food
In Vivo Evaluation of A1 Adenosine Agonists as Novel Anticonvulsant Medical Countermeasures to Nerve Agent Intoxication in a Rat Soman Seizure Model.
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Organophosphorus nerve agents (NAs) irreversibly inhibit acetylcholinesterase, which results in the accumulation of acetylcholine and widespread excitotoxic seizure activity. Because current medical countermeasures (anticholinergics, AChE reactivators, and benzodiazepines) lack sufficient
Anti-nicotinic properties of anticholinergic antiparkinson drugs.
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The nature of the antagonism by anticholinergic compounds of nicotine-induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to brain tissue in-vitro, these compounds are thought to be non-competitive antagonists in the brain,
[Antagonism of the novel cholinolytic tricyclopinate on nicotinic and muscarinic cholinergic receptors].
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Tricyclopinate hydrochloride(TCPN.HCl) and methiodide(TCPN.CH3I) have been identified as new chemical entities. The effects of these two compounds on central and peripheral nicotinic and muscarinic cholinergic receptor activities were investigated. Excitation of the central nicotinic receptors by
The involvement of the NMDA receptor complex in the protective effect of anticholinergic drugs against soman poisoning.
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Organophosphate poisoning is associated with adverse effects on the central nervous system such as seizure/convulsive activity and long term changes in neuronal networks. This study reports on investigations designed to assess the consequences of soman exposure on excitatory amino acids receptors in
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