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laudanosine/seizures
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Interactions between laudanosine, GABA, and opioid subtype receptors: implication for laudanosine seizure activity.
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We examined the interactions of D,L-laudanosine, a potentially epileptogenic metabolite of the neuromuscular relaxant atracurium besylate, with gamma-aminobutyric acid (GABA) and opioid binding sites, all of which have been implicated in seizure activity. Laudanosine was almost ineffective at
Cardiovascular and neurological effects of laudanosine. Studies in mice and rats, and in conscious and anaesthetized dogs.
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The effects of laudanosine, a metabolite of atracurium, on the behaviour of conscious mice, rats and dogs, and on cardiovascular function in conscious and anaesthetized dogs have been evaluated: EEG studies were performed in anaesthetized dogs. In mice and rats, i.v. bolus doses of laudanosine 10-20
Laudanosine, an atracurium and cisatracurium metabolite.
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Laudanosine is a metabolite of the neuromuscular-blocking drugs atracurium and cisatracurium with potentially toxic systemic effects. It crosses the blood-brain barrier and may cause excitement and seizure activity. Its interest in recent years has increased because of the recognized interaction
Modulation of rat brain synaptosomal plasma membrane achieved by atracurium and its metabolite laudanosine.
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OBJECTIVE
Atracurium besylate and laudanosine cause excitement and seizures when introduced into the central nervous system of laboratory animals. We examined the modulation of lipid-protein interaction in the lipid environment of rat brain synaptosomal plasma membrane (SPM)-bound enzymes as a
Modification by drugs used in anaesthesia of CNS stimulation induced in mice by laudanosine and strychnine.
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We have investigated in mice the effects of several drugs which may be administered as part of an anaesthetic technique on the convulsive threshold to laudanosine and to strychnine, which is reported to have a similar mechanism of action. I.v. administered propofol, thiopentone and midazolam
Pharmacology of laudanosine in dogs.
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The authors determined the pharmacokinetics (including transfer into cerebrospinal fluid [CSF]) and the cardiovascular and central nervous system (CNS) effects of laudanosine, a metabolite of atracurium. Eight dogs were anesthetized with halothane; blood pressure and a fronto-occipital
Convulsive effects and pharmacokinetics of laudanosine in the rat.
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Laudanosine, which is a degradation product of atracurium, is a convulsant drug in the rat. Laudanosine plasma concentrations were measured by high performance liquid chromatography after administration of both laudanosine and atracurium; protein binding and renal excretion of laudanosine were also
Laudanosine and atracurium concentrations in a patient receiving long-term atracurium infusion.
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OBJECTIVE
Atracurium is sometimes used for muscle relaxation in patients undergoing mechanical ventilation. Use of atracurium in high doses or for a long period of time has raised the possibility of the accumulation of laudanosine, a breakdown product known to cause seizure activity in animals. The
Electroencephalographic effects of laudanosine in an animal model of epilepsy.
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We examined the effects of laudanosine, one of the principal metabolites of atracurium, on the electroencephalogram (EEG) in an animal model of induced epilepsy. Fourteen rabbits were anaesthetized with 4% halothane in oxygen, the trachea intubated and the lungs ventilated mechanically with 30%
Laudanosine does not displace receptor-specific ligands from the benzodiazepinergic or muscarinic receptors.
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The present study was designed to investigate whether D,L-laudanosine (a breakdown product of the neuromuscular relaxant atracurium besylate) interacts with benzodiazepinergic receptors or muscarinic receptors, both of which are involved in epilepsy and other types of seizures. The ability of
Blockade and activation of the human neuronal nicotinic acetylcholine receptors by atracurium and laudanosine.
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BACKGROUND
Curaremimetic nondepolarizing muscle relaxants are widely used in clinical practice to prevent muscle contraction either during surgery or during intensive care. Although primarily acting at the neuromuscular junction, these compounds can cause adverse effects, including modification of
Pharmacodynamics and atracurium and laudanosine concentrations during a fixed continuous infusion of atracurium in mechanically ventilated patients with acute respiratory distress syndrome.
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The present study was designed to assess the pharmacodynamics and the plasma levels of atracurium and laudanosine found during a 72-hour fixed rate infusion of atracurium in acute respiratory distress syndrome patients without renal or liver failure. Nine sedated and mechanically ventilated acute
Effects of atracurium, vecuronium or pancuronium pretreatment on lignocaine seizure thresholds in cats.
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Among the non-depolarizing neuromuscular blocking drugs, atracurium appears to be unique in its ability to produce cerebral stimulation in lightly anaesthetized animals. This effect is attributed to the atracurium metabolite, laudanosine. The following studies were performed to determine if
Laudanosine has no effects on respiratory activity but induces non-respiratory excitement activity in isolated brainstem-spinal cord preparation of neonatal rats.
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Laudanosine, a degradation of neuomuscular blocking agent atracurium, crosses the blood-brain barrier and is indicted to trigger seizures at high concentration. In Xenopus Oocytes expressing nicotinic acetylcholine receptors (nAChRs), laudanosine has activating and inhibiting effects on nAChRs
The pharmacokinetics of cisatracurium in patients with acute respiratory distress syndrome.
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Continuous neuromuscular blockade is often necessary in patients being treated for acute respiratory distress syndrome (ARDS) to optimize oxygenation. In this study, neuromuscular blockade (no response to two responses at the train-of-four stimulation at the orbicularis oculi muscle) was achieved in
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