Хуудас 1 -аас 598 үр дүн
A case is reported where atropine sulphate eye drops increased the frequency of fits in a child suffering regular akinetic seizures. This increase was marked and observed during two separate courses of eye drops. This is discussed with reference to previous reports of central nervous toxicity after
The ability of relatively low doses of atropine, NBQX and TCP administered in combination to prevent or stop seizures induced by soman, was studied in rats. While these drugs injected together early after soman prevented the onset of seizures, their delayed concomitant administration after 5 or 30
Two guinea pig models were used to study the anticonvulsant potency of diazepam, midazolam, and scopolamine against seizures induced by the nerve agents tabun, sarin, soman, cyclosarin, O-ethyl S-(2-(diisopropylamino)ethyl)methylphosphonothioate (VX), and O-isobutyl S-(2-diethylamino)ethyl)-methyl
Fasted rodents treated with antimuscarinics develop convulsions after refeeding. Food deprivation for 48 hr produces changes in [3H]glutamate binding suggesting glutamatergic contribution to the underlying mechanism of the seizures that are somewhat unresponsive to antiepileptics. In 7 children with unusually severe or frequent reflex anoxic seizures atropine treatment, which was well tolerated, reduced seizure frequency by a mean value of 98%. Treatment withdrawal (five patients) was followed by an increase in seizure frequency and reintroduction (three patients) by
Effects of local administration of atropine into the medial septal nucleus (MSN) and dorsal septal nucleus (DSN) were tested in laboratory rats. Atropine administration led to the development of a spike/wave activity in the hippocampus as well as amygdala within 10 minutes. The frequency of spikes
This study evaluated the effects of different doses of atropine and new antiepileptics, levetiracetam and topiramate, on the development of convulsions triggered by food intake in antimuscarinic-treated fasted animals. Mice deprived of food for 24 h and treated i.p. with atropine at a dose of 2.4 or
BACKGROUND
Electrocardiogram abnormalities have been reported during electroconvulsive therapy (ECT). A corrected QT interval (QTc) prolongation indicates delayed ventricular repolarization, which can trigger ventricular arrhythmias such as torsade de pointes (TdP). We examined the QTc changes
Male rats were forced to drink a barbital solution as their only drinking fluid for 33 weeks. During the last part of the treatment the average dose of barbital was around 200 mg/kg/day. In the abstinence period after barbital treatment, tolerance was recorded with a hexobarbital anaesthesia
The present study describes the effects of pyridostigmine (PYR; 0.2 mg/kg) and atropine sulphate (AS; 5 mg/kg) on guinea-pigs intoxicated by a high dose (2xLD50) of the organophosphate compound, soman, an irreversible inhibitor of acetylcholinesterase. The medication was shown to counteract the
The present study demonstrates that dose combinations of atropine sulfate and 2-pyridine aldoxime methylchloride (2-PAM), which do not produce any overt toxic effects on the behavior of mice or guinea pigs in a stable environment, elicit clonic-tonic convulsions and death when the animals are
Effects of atropine or diazepam pretreatment on soman-induced convulsions and brain phosphoinositide (PI) metabolism, as assessed by brain regional inositol-1-phosphate (IP1) levels, were studied in saline and LiCl-pretreated rats. IP1, an intermediate in PI turnover, was measured in cortex,
The ability of five organophosphorus nerve agents (tabun, sarin, soman, GF, and VX) to produce brain seizures and the effectiveness of atropine as an anticonvulsant treatment against these nerve agents were studied in two different animal models--the rat and guinea pig. All animals were implanted