Chlormethiazole
A sedative and anticonvulsant often used in the treatment of alcohol withdrawal. Chlormethiazole has also been proposed as a neuroprotective agent. The mechanism of its therapeutic activity is not entirely clear, but it does potentiate GAMMA-AMINOBUTYRIC ACID receptors response and it may also affect glycine receptors.
3,4-Methylenedioxyamphetamine
p-Chloroamphetamine
Clonazepam
An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.
Flunitrazepam
Psychoses, Alcoholic
Pentobarbital
A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)
Designer Drugs
Drugs designed and synthesized, often for illegal street use, by modification of existing drug structures (e.g., amphetamines). Of special interest are MPTP (a reverse ester of meperidine), MDA (3,4-methylenedioxyamphetamine), and MDMA (3,4-methylenedioxymethamphetamine). Many drugs act on the aminergic system, the physiologically active biogenic amines.
GABA Modulators
Substances that do not act as agonists or antagonists but do affect the GAMMA-AMINOBUTYRIC ACID receptor-ionophore complex. GABA-A receptors (RECEPTORS, GABA-A) appear to have at least three allosteric sites at which modulators act: a site at which BENZODIAZEPINES act by increasing the opening frequency of GAMMA-AMINOBUTYRIC ACID-activated chloride channels; a site at which BARBITURATES act to prolong the duration of channel opening; and a site at which some steroids may act. GENERAL ANESTHETICS probably act at least partly by potentiating GABAergic responses, but they are not included here.
Fenfluramine
Muscimol
N-Methyl-3,4-methylenedioxyamphetamine
Kindling, Neurologic
Dizocilpine Maleate
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
Chlordiazepoxide
Electronic Mail
Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.
Office Automation
Anti-Anxiety Agents
Coproporphyria, Hereditary
An autosomal dominant porphyria that is due to a deficiency of COPROPORPHYRINOGEN OXIDASE in the LIVER, the sixth enzyme in the 8-enzyme biosynthetic pathway of HEME. Clinical features include both neurological symptoms and cutaneous lesions. Patients excrete increased levels of porphyrin precursors, 5-AMINOLEVULINATE and COPROPORPHYRINS.
Coproporphyrins
Coproporphyrinogen Oxidase
An enzyme that catalyzes the oxidative decarboxylation of coproporphyrinogen III to protoporphyrinogen IX by the conversion of two propionate groups to two vinyl groups. It is the sixth enzyme in the 8-enzyme biosynthetic pathway of HEME, and is encoded by CPO gene. Mutations of CPO gene result in HEREDITARY COPROPORPHYRIA.
Porphyrias, Hepatic
A group of metabolic diseases due to deficiency of one of a number of LIVER enzymes in the biosynthetic pathway of HEME. They are characterized by the accumulation and increased excretion of PORPHYRINS or its precursors. Clinical features include neurological symptoms (PORPHYRIA, ACUTE INTERMITTENT), cutaneous lesions due to photosensitivity (PORPHYRIA CUTANEA TARDA), or both (HEREDITARY COPROPORPHYRIA). Hepatic porphyrias can be hereditary or acquired as a result of toxicity to the hepatic tissues.
Porphyrias
A diverse group of metabolic diseases characterized by errors in the biosynthetic pathway of HEME in the LIVER, the BONE MARROW, or both. They are classified by the deficiency of specific enzymes, the tissue site of enzyme defect, or the clinical features that include neurological (acute) or cutaneous (skin lesions). Porphyrias can be hereditary or acquired as a result of toxicity to the hepatic or erythropoietic marrow tissues.
Porphyrins
A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.
Porphyrinogens
Encyclopedias as Topic
Hypnotics and Sedatives
Alcohol Withdrawal Delirium
An acute organic mental disorder induced by cessation or reduction in chronic alcohol consumption. Clinical characteristics include CONFUSION; DELUSIONS; vivid HALLUCINATIONS; TREMOR; agitation; insomnia; and signs of autonomic hyperactivity (e.g., elevated blood pressure and heart rate, dilated pupils, and diaphoresis). This condition may occasionally be fatal. It was formerly called delirium tremens. (From Adams et al., Principles of Neurology, 6th ed, p1175)
Alcohol Withdrawal Seizures
A condition where seizures occur in association with ethanol abuse (ALCOHOLISM) without other identifiable causes. Seizures usually occur within the first 6-48 hours after the cessation of alcohol intake, but may occur during periods of alcohol intoxication. Single generalized tonic-clonic motor seizures are the most common subtype, however, STATUS EPILEPTICUS may occur. (Adams et al., Principles of Neurology, 6th ed, p1174)
Substance Withdrawal Syndrome
Receptors, GABA-A
Search Engine
Genome, Human
Receptors, GABA
Cell-surface proteins that bind GAMMA-AMINOBUTYRIC ACID with high affinity and trigger changes that influence the behavior of cells. GABA-A receptors control chloride channels formed by the receptor complex itself. They are blocked by bicuculline and usually have modulatory sites sensitive to benzodiazepines and barbiturates. GABA-B receptors act through G-proteins on several effector systems, are insensitive to bicuculline, and have a high affinity for L-baclofen.
Antibodies
Acetaminophen
Glioma
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
Analgesics, Non-Narcotic
Drug-Induced Liver Injury
Apoptosis
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Protein-Serine-Threonine Kinases
Cell Death
Glutamic Acid
Bromcresol Purple
Glutamates
Cerebral Cortex
Middle Cerebral Artery
Ethyl glucuronide--a marker of alcohol consumption and a relapse marker with clinical and forensic implications. (1/58)
Ethyl glucuronide (EtG) is a non-volatile, water-soluble, direct metabolite of ethanol that can be detected in body fluids and hair. We investigated urine and serum samples from three patient groups: (1) 33 in-patients in acute alcohol withdrawal; (2) 30 detoxified in-patients (treated for at least 4 weeks) from a 'motivation station'; and (3) 43 neuro-rehabilitation patients (non-alcoholics; most of them suffering from stroke, traumatic brain injury, Parkinson's disease etc.) using gas chromatography/mass spectrometry (GC/MS) with deuterium-labelled EtG as the internal standard and additionally in the second group of patients using liquid chromatography (LC/MS-MS). We found no correlation between the concentration of EtG in urine at hospitalization and the blood-ethanol concentration (r = 0.17), the time frame of detection (r = 0.5) or the total amount of clomethiazole required for the treatment of withdrawal symptoms (r = 0.28). In four out of 30 in-patients from the 'motivation station'--where neither clinical impression nor routine laboratory findings gave indications of relapse--concentrations of EtG in urine ranged between 4.2 and 196.6 mg/l. EtG concentrations in urine of between 2.89 and 23.49 mg/l were found in seven out of 43 neuro-rehabilitation patients using GC/MS. The GC/MS and the LC/MS-MS results showed a correlation of 0.98 with Pearson's correlation test and 1.0 with Spearman's correlation test. We suggest that EtG is a marker of alcohol consumption that can be detected for an extended time period after the complete elimination of alcohol from the body. When used as a relapse marker with a specific time frame of detection intermediate between short- and long-term markers, EtG fills a clinically as well as forensically important gap. Its specificity and sensitivity exceed those of all other known ethanol markers. (+info)Mode of action of ICS 205,930, a novel type of potentiator of responses to glycine in rat spinal neurones. (2/58)
The effect of a novel potentiator of glycine responses, ICS 205,930, was studied by whole-cell recordings from spinal neurones, and compared with that of other known potentiators, in an attempt to differentiate their sites of action. The ability of ICS 205,930 (0.2 microM) to potentiate glycine responses persisted in the presence of concentrations of Zn2+ (5-10 microM) that were saturating for the potentiating effect of this ion. Preincubation with 10 microM Zn2+ before application of glycine plus Zn2+ had an inhibitory effect, which did not result from Zn2+ entry into the neurone, since it persisted with either 10 mM internal EGTA or 10 microM internal Zn2+. To test whether the potentiating effects of ICS 205,930 and Zn2+ interact, both compounds were applied without preincubation. The potentiating effect of ICS 205,930 was similar for responses to glycine and for responses to glycine plus Zn2+, provided the concentrations of agonist were adjusted so as to induce control responses of identical amplitudes. ICS 205,930 remained able to potentiate glycine responses in the presence of ethanol (200 mM). ICS 205,930 also retained its potentiating effect in the presence of the anaesthetic propofol (30 90 microM), which strongly potentiated glycine responses but, in contrast with ICS 205,930, also markedly increased the resting conductance. The anticonvulsant chlormethiazole (50-100 microM) neither potentiated glycine responses nor prevented the effect of ICS 205,930, even though it increased the resting conductance and potentiated GABA(A) responses. The mechanism of action of ICS 205,930 appears to be different from those by which Zn2+, propofol or ethanol potentiate glycine responses. (+info)Post-translational inhibition of cytochrome P-450 2E1 expression by chlomethiazole in Fao hepatoma cells. (3/58)
Chlomethiazole (CMZ) is a sedative and anticonvulsant drug that has been shown to be an efficient transcriptional inhibitor of expression of rat hepatic ethanol-inducible cytochrome P-450 2E1 (CYP2E1). Recent results have shown that human CYP2E1 expression in vivo is almost completely inhibited in control subjects and in alcoholic patients treated with CMZ. In the present investigation, we evaluated the mode of action of CMZ on CYP2E1 expression in Fao rat hepatoma cells. Transcriptional activity of the CYP2E1 gene was monitored using reverse transcription-polymerase chain reaction-based quantification of CYP2E1 heterologous nuclear RNA (hnRNA) against a mimic DNA standard, mRNA was detected by Northern blotting, enzyme protein was detected by Western blotting, and CYP2E1-dependent catalytic activity was detected by assay of chlorzoxazone-6-hydroxylation. Six hours after CMZ treatment, the levels of both CYP2E1 protein and catalytic activity were concomitantly reduced at an IC50 value of about 5 microM. Ethanol treatment of the cells caused a 2-fold induction of CYP2E1 protein levels, which was inhibited by CMZ. Change of medium unexpectedly caused an increase in CYP2E1 gene transcription 4 h later, as monitored by quantitative determination of CYP2E1 hnRNA. However, CMZ failed to influence the expression of CYP2E1 hnRNA or mRNA both constitutively and after medium change, indicating no effect on gene transcription or mRNA synthesis/stability. Cycloheximide treatment of the cells did not abolish the inhibitory action of CMZ, further indicating an action at the post-translational level; in addition, CMZ inhibited CYP2E1 expression in V79 cells with stably expressed CYP2E1 under the control of the SV40 promoter. The data indicate that the CYP2E1 gene is transcriptionally activated in response to medium change and that CMZ, apart from a transcriptional inhibitor of CYP2E1 expression, acts in addition as an efficient high-affinity post-translational inhibitor of CYP2E1, probably due to an allosteric destabilization of the enzyme. This indicates a very rapid and effective CMZ-mediated inhibition of CYP2E1 in vivo. (+info)Results in 95 hemorrhagic stroke patients included in CLASS, a controlled trial of clomethiazole versus placebo in acute stroke patients. (4/58)
BACKGROUND AND PURPOSE: Clomethiazole is a neuroprotective drug that enhances gamma-aminobutyrate type A (GABA(A)) receptor activity. Its efficacy and safety were tested in the CLomethiazole Acute Stroke Study (CLASS). The protocol allowed a CT scan to be done after randomization but within 7 days of stroke onset to minimize delays before start of treatment. Ninety-five of the 1360 patients randomized were diagnosed as having intracranial hemorrhage rather than ischemic stroke. Safety results for clomethiazole compared with placebo in this group are reported. METHODS: The study included patients with a clinical diagnosis of acute hemispheric cerebral infarction. Treatment was a 24-hour intravenous infusion of 75 mg/kg clomethiazole or placebo. Patients with intracranial hemorrhage discovered on a postrandomization CT were withdrawn from study treatment if treatment was ongoing, and all patients were followed up to 90 days. RESULTS: Ninety-four patients received treatment, 47 in each group. The hemorrhage was classified as intracerebral in 89 patients (94%). Mortality at 90 days was 19.1% in the clomethiazole group and 23.4% in the placebo group. Sedation was the most common adverse event, occurring at a higher incidence in clomethiazole-treated patients (clomethiazole 53%, placebo 17%), followed by rhinitis and coughing. The incidence and pattern of serious adverse events was similar between the treatment groups. The percentage of patients reaching relative functional independence on the Barthel Index (score >/=60) at 90 days was 59.6% in the clomethiazole group and 53.2% in the placebo group. CONCLUSIONS: Clomethiazole appears safe to administer to hemorrhagic stroke patients compared with placebo. These results would obviate the need for a CT scan before therapy is initiated in acute stroke. The safety of clomethiazole in hemorrhagic stroke patients will be further evaluated in a prospective study that is under way in North America. (+info)The metabolism of clomethiazole in gerbils and the neuroprotective and sedative activity of the metabolites. (5/58)
A single dose of clomethiazole (600 micromol kg(-1) i.p.) has previously been shown to be neuroprotective in the gerbil model of global ischaemia. In gerbils, clomethiazole (600 micromol kg(-1)) injection produced a rapid appearance (peak within 5 min) of drug in plasma and brain and similar clearance (plasma t(1/2): 40 min) from both tissues. The peak brain concentration (226+/-56 nmol g(-1)) was 40% higher than plasma. One major metabolite, 5-(1-hydroxyethyl-2-chloro)-4-methylthiazole (NLA-715) and two minor metabolites 5-(1-hydroxyethyl)-4-methylthiazole (NLA-272) and 5-acetyl-4-methylthiazole (NLA-511) were detected in plasma and brain. Evidence suggested that clomethiazole is metabolized directly to both NLA-715 and NLA-272. Injection of NLA-715, NLA-272 or NLA-511 (each at 600 micromol kg(-1)) produced brain concentrations respectively 2.2, 38 and 92 times greater than seen after clomethiazole (600 micromol kg(-1)). Clomethiazole (600 micromol kg(-1)) injected 60 min after a 5 min bilateral carotid artery occlusion in gerbils attenuated the ischaemia-induced degeneration of the hippocampus by approximately 70%. The metabolites were not neuroprotective at this dose. In mice, clomethiazole (600 micromol kg(-1)) produced peak plasma and brain concentrations approximately 100% higher than in gerbils, drug concentrations in several brain regions were similar but 35% higher than plasma. Clomethiazole (ED(50): 180 micromol kg(-1)) and NLA-715 (ED(50): 240 micromol kg(-1)) inhibited spontaneous locomotor activity. The other metabolites were not sedative (ED(50) >600 micromol kg(-1)). These data suggest that the neuroprotective action of clomethiazole results from an action of the parent compound and that NLA-715 contributes to the sedative activity of the drug. British Journal of Pharmacology (2000) 129, 95 - 100 (+info)On the regulation of ischaemia-induced glutamate efflux from rat cortex by GABA; in vitro studies with GABA, clomethiazole and pentobarbitone. (6/58)
Prisms of adult rat cortex were maintained in vitro in either aerobic conditions (control) or conditions simulating an acute ischaemic challenge (hypoxia with no added glucose). Endogenous glutamate efflux increased with time in ischaemic conditions, being 2.7 fold higher than control efflux at 45 min. Returning prisms to control solution after 20 min of simulated ischaemia resulted in glutamate efflux returning to near-control values. Endogenous GABA efflux in ischaemic conditions also increased, being 4.5 fold higher than control efflux at 45 min. Ischaemia-induced glutamate efflux was not accompanied by increased lactate dehydrogenase efflux and was unaltered by omitting calcium from the extra-cellular solution and adding EGTA (0.1 mM). Both GABA and the GABA-mimetic clomethiazole inhibited ischaemia-induced glutamate efflux, with IC(50) values of 26 and 24 microM respectively. The maximum inhibition by either drug was 60 - 70%. Bicuculline (10 microM) abolished the inhibitory effect of GABA (100 microM) but not clomethiazole (100 microM). Picrotoxin (100 microM) abolished the action of both GABA and clomethiazole. Pentobarbitone inhibited glutamate efflux at 100 - 300 microM (maximal inhibition: 39%). Bicuculline (10 microM) abolished this effect. These data suggest that ischaemia-induced glutamate efflux from rat cerebral cortex is calcium-independent and not due to cell damage up to 45 min. The inhibitory effect of GABA, clomethiazole and pentobarbitone on ischaemia-induced glutamate efflux appears to be mediated by GABA(A) receptors. The results suggest that clomethiazole, unlike pentobarbitone, is able to activate the GABAA receptor-linked chloride channel directly and not merely potentiate the effect of endogenous GABA. (+info)Neuroprotective agent chlomethiazole attenuates c-fos, c-jun, and AP-1 activation through inhibition of p38 MAP kinase. (7/58)
Recent evidence suggests that stress-activated protein kinases expressed in glial cells have very important roles during cerebral ischemia. The neuroprotective agent chlomethiazole, which is known to enhance the conductance at the GABA(A) receptor complex, is presently in clinical trials for the treatment of severe stroke. Here the authors suggested that chlormethiazole has anti-inflammatory properties because it potently and selectively inhibited p38 mitogen-activated protein (MAP) kinase in primary cortical glial cultures. The inhibition of p38 MAP kinase resulted in the attenuation of the induction of c-fos and c-jun mRNA and AP-1 DNA binding by lipopolysaccharide (LPS). In addition, chlomethiazole inhibited the activation of an AP-1-dependent luciferase reporter plasmid in SK-N-MC human neuroblastoma cells in response to glutamate. Chlomethiazole inhibited the p38 MAP kinase activity as revealed by the decrease in the LPS-induced phosphorylation of the substrates ATF-2 and hsp27, whereas the phosphorylation status of the p38 MAP kinase itself was unaffected. Interestingly, chlomethiazole exhibited an IC(50) of approximately 2 micromol/L for inhibition of c-fos mRNA expression, indicating 25 to 75 times higher potency than reported EC(50) values for enhancing GABA(A) chloride currents. The results indicated a novel mechanism of action of chlomethiazole, and provided support for a distinctive role of p38 MAP kinase in cerebral ischemia. (+info)Chlormethiazole: effectiveness against toxic effects of cocaine in mice. (8/58)
Chlormethiazole positively modulates the gamma-aminobutyric acid (GABA)(A) receptor complex and is primarily used to treat certain life-threatening neurological events (e.g., refractory seizures and ethanol withdrawal syndrome). On account of several experimental and clinical studies reporting effectiveness against the toxic effects of heroin and methamphetamine, chlormethiazole was systematically tested in the present study for its effectiveness against cocaine-induced seizures and lethality in mice. The protective effects of chlormethiazole were evaluated against single, submaximal convulsive (75 mg/kg) or lethal (110 mg/kg) doses of cocaine. Chlormethiazole also was tested against the expression (anticonvulsant effect) and development (antiepileptogenic effect) of cocaine-kindled seizures, and against fully developed kindled seizures. Cocaine-kindled seizures were produced by a total of five daily treatments with 60 mg/kg cocaine. The inverted-screen test was used to assess behavioral side effects of chlormethiazole. Chlormethiazole protected against acute cocaine-induced convulsions (ED(50) = 7.0 mg/kg) and lethality (ED(50)= 21.8 mg/kg) with a robust separation [protective index (PI) = TD(50)/ED(50) = 22.3 and 7.2, respectively] from doses producing behavioral side effects (TD(50) = 156 mg/kg). Chlormethiazole suppressed the behavioral expression of cocaine-kindled seizures and prevented the development of sensitization to the convulsant effects of cocaine. It was also effective in suppressing fully developed kindled seizures. Relative to cocaine seizures in naive mice, chlormethiazole was equieffective, less potent (ED(50) = 22.3 mg/kg), and had a reduced protective index (PI = 3.7) against cocaine-induced seizures in kindled mice. The protective profile and protective index of chlormethiazole were superior to those of the benzodiazepines clonazepam and diazepam, which were of limited efficacy and had low protective indices (PI = approximately 1). The results of this study predict the potential utility of chlormethiazole for the treatment of life-threatening complications of cocaine abuse for which no specific treatment has yet been identified. (+info)
Clomethiazole - Wikipedia
Population pharmacokinetics of clomethiazole and its effect on the natural course of sedation in acute stroke patients
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Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
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Pharmacovigilance in Gerontopsychiatric Patients - Full Text View - ClinicalTrials.gov
The purpose of this multicenter-study is to investigate safety of psychopharmacological treatment and rates of adverse drug reactions in gerontopsychiatric inpatients. Elderly people are at higher risk for developing side effects under pharmacological treatment due to an altered metabolic situation, higher comorbidity rates and often polypharmacy. Furthermore gerontopsychiatric patients can often not articulate their symptoms clearly, for example due to pronounced cognitive impairment.. The aim of the study is to gain valid data of possible adverse drug reaction rates, their potential risk factors and outcome, as well as medical prescription practises.. To assess these outcomes an intensive pharmacovigilance-monitoring will be conducted at the five participating study sites.. At Baseline demographic data, previous and present disorders, use of drugs, previous and present medication, quality of life, cognitive function, physical examination results, laboratory results and ECG will be ...
Plasma level of chlormethiazole and two metabolites after oral administration to young and aged human subjects<...
Plasma level of chlormethiazole and two metabolites after oral administration to young and aged human subjects. R. L. Nation, J ... Plasma level of chlormethiazole and two metabolites after oral administration to young and aged human subjects. / Nation, R. L. ... Absorption of chlormethiazole was rapid in the subjects of both groups as assessed by the time taken to reach the peak plasma ... Absorption of chlormethiazole was rapid in the subjects of both groups as assessed by the time taken to reach the peak plasma ...
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TProtective effect of chlormethiazole, a sedative, against acetaminophen-induced liver injury in mice | The Korean Journal of...
Recently, chlormethiazole a sedative drug, is reported to be an efficient inhibitor of CYP2E1 activity in human beings. In this ... Chlormethiazole (60 mg/kg) or 5% dextrose water was given 30 min before or 2 h after acetaminophen. Serum aminotransferase ... Chlormethiazole effectively reduces acetaminophen-induced liver injury in mice. Further studies are needed to assess its role ... Full text: Available Index: WPRIM (Western Pacific) Main subject: Female / Humans / Chlormethiazole / Analgesics, Non-Narcotic ...
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Hu Y, Mishin V, Johansson I, von Bahr C, Cross A, Ronis MJ, Badger TM, and Ingelman-Sundberg M (1994) Chlormethiazole as an ... Pretreatment with chlormethiazole, an inhibitor of ethanol-inducible CYP2E1, significantly lowered the CYP2E1 enzyme activity ... Chlormethiazole (CMZ) was kindly provided by Dr. Joong-Ick Yang at Dong-A Pharmaceutical Company, Seoul, Korea. ... chlormethiazole; PAGE, polyacrylamide gel electrophoresis; RT-PCR, reverse transcription-polymerase chain reaction; GAPDH, ...
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GLATT, M. M., GEORGE, H. R., and FRISCH, E. P. Controlled trial of chlormethiazole in treatment of the alcoholic withdrawal ... Drummond, L. M. and Chalmers, L. Prescribing chlormethiazole reducing regimes in an emergency clinic. Br J Addict. 1986;81:247- ... Palsson, A. The efficacy of early chlormethiazole medication in the prevention of delirium tremens. A retrospective study of ... Tubridy, P. Alprazolam versus chlormethiazole in acute alcohol withdrawal. Br J Addict. 1988;83:581-585. View abstract. ...
Thiamine (Vitamin B1): Uses, Side Effects, Interactions, Dosage, and Warning
Drummond, L. M. and Chalmers, L. Prescribing chlormethiazole reducing regimes in an emergency clinic. Br J Addict. 1986;81(2): ... Palsson, A. The efficacy of early chlormethiazole medication in the prevention of delirium tremens. A retrospective study of ... Tubridy, P. Alprazolam versus chlormethiazole in acute alcohol withdrawal. Br J Addict. 1988;83(5):581-585. View abstract. ...
On the regulation of ischaemia-induced glutamate efflux from rat cortex by GABA; in vitro studies with GABA, clomethiazole and...
CROSS, A.J., STIRLING, J.M., ROBINSON, T.N., BOWEN, D.M., FRANCIS, P.T. & GREEN, A.R. (1989). The modulation by chlormethiazole ... BALDWIN, H.A., WILLIAMS, J.L., SNARES, M., FERRIERA, T., CROSS, A.J. & GREEN, A.R. (1994). Attenuation by chlormethiazole of ... HALES, T.G. & LAMBERT, J.J. (1992). Modulation of GABAA and glycine receptors by chlormethiazole. Eur. J. Pharmacol., 210, 239- ... CROSS, A.J., JONES, J.A., BALDWIN, H.A. & GREEN, A.R. (1991). Neuroprotective activity of chlormethiazole following transient ...
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Index by author - October 01, 2000, 295 (1) | Journal of Pharmacology and Experimental Therapeutics
Chlormethiazole: Effectiveness against Toxic Effects of Cocaine in Mice Maciej Gasior, Jesse T. Ungard and Jeffrey M. Witkin ... Chlormethiazole: Effectiveness against Toxic Effects of Cocaine in Mice Maciej Gasior, Jesse T. Ungard and Jeffrey M. Witkin ... Chlormethiazole: Effectiveness against Toxic Effects of Cocaine in Mice Maciej Gasior, Jesse T. Ungard and Jeffrey M. Witkin ...
Clomethiazole2
- Clomethiazole (also called chlormethiazole) is a sedative and hypnotic originally developed by Hoffmann-La Roche in the 1930s. (wikipedia.org)
- Use clomethiazole (chlormethiazole) for alcohol withdrawal. (hscni.net)
Sedative1
- Recently, chlormethiazole a sedative drug , is reported to be an efficient inhibitor of CYP2E1 activity in human beings. (bvsalud.org)
Neuroprotective3
- CYP2A6 is also one of the major enzymes involved in human nicotine metabolism (see below) and the major enzyme responsible for the metabolism of the platelet-activating factor receptor antagonist SM-12502 [(+)- cis -3,5-dimethyl-2-(3-pyridyl)thiazolidin-4-one hydrochloride] and the neuroprotective drug chlormethiazole. (aspetjournals.org)
- Chlormethiazole has also been proposed as a neuroprotective agent. (bvsalud.org)
- Is chlormethiazole neuroprotective in experimental global cerebral ischemia? (termsreign.ga)
Inhibitor3
- Zonated expression of cytokines in rat liver: effect of chronic ethanol and the cytochrome P450 2E1 inhibitor, chlormethiazole. (semanticscholar.org)
- In this study we wished to evaluate whether chlormethiazole , an inhibitor of CYP2E1 , could prevent acetaminophen -induced liver injury in mice . (bvsalud.org)
- Pretreatment with chlormethiazole, an inhibitor of ethanol-inducible CYP2E1, significantly lowered the CYP2E1 enzyme activity and the rate of APAP-induced cell death while it prevented the reduction of p53 and p21 in C6 glioma cells. (aspetjournals.org)
Young and elderly subjects2
- A study of the psychometric effects of chlormethiazole in healthy young and elderly subjects. (thefreedictionary.com)
- The time course of the plasma concentration of chlormethiazole and metabolites showed wide inter-subject variation, particularly between the young and elderly subjects. (monash.edu)
Acetaminophen4
- Chlormethiazole (60 mg/kg) or 5% dextrose water was given 30 min before or 2 h after acetaminophen . (bvsalud.org)
- In mice receiving chlormethiazole 2 h after acetaminophen , the mean AST and ALT levels were also less elevated, reaching only 20% of the value of acetaminophen -only group. (bvsalud.org)
- Whereas more than 50% of mice died at 500 mg/kg of acetaminophen , all the mice pretreated with chlormethiazole survived at the same dose . (bvsalud.org)
- Chlormethiazole effectively reduces acetaminophen -induced liver injury in mice . (bvsalud.org)
Elderly4
- The mean peak plasma level of chlormethiazole was more than five times greater in the elderly (2.90±1.56 μg/ml) than in the young (0.55±0.58 μg/ml) subjects. (monash.edu)
- The distribution of chlormethiazole in whole blood from six young and six elderly human subjects was investigated in vitro. (monash.edu)
- The unbound fraction of chlormethiazole in plasma increased significantly from 0.308±0.035 in young subjects to 0.403±0.067 in the elderly. (monash.edu)
- A double-blind controlled study of chlormethiazole and triazolam as hypnotics in the elderly. (cf.ac.uk)
Hypnotic1
- Not surpris- hypnotic chlormethiazole. (coveringthecorridor.com)
Dose2
- The plasma concentration of chlormethiazole and two of its metabolites has been measured in three young and three aged human subjects following administration of a single oral dose of chlormethiazole. (monash.edu)
- The chlormethiazole labeling states that dose. (forumlogopedyczne.pl)
GABA2
- This review provides moderate-quality evidence that fails to support the use of GABA receptor agonists (chlormethiazole or diazepam) for the treatment of people with acute stroke. (cochrane.org)
- GABA receptor agonists (chlormethiazole or diazepam) appear not to be effective for the treatment of acute ischemic or hemorrhagic stroke. (essentialevidenceplus.com)
Significantly1
- Compared to chlormethiazole, thioridazine was significantly inferior when assessed on some items of the CAPE and the Crichton Geriatric Behavioural Rating Scales. (cochrane.org)
Adverse1
- Somnolence and rhinitis are frequent adverse events related to chlormethiazole. (cochrane.org)
Diazepam2
- This group of drugs, which includes diazepam and chlormethiazole, has been used as traditional sedatives for several decades, and have been found to be beneficial in stroke studies in animals. (cochrane.org)
- There was no significant difference between the chlormethiazole and placebo groups or between the diazepam and placebo groups. (cochrane.org)
Oral1
- Oral chlormethiazole in childhood epilepsy. (naver.com)
Liver1
- Inhibition of ethanol-induced liver disease in the intragastric feeding rat model by chlormethiazole," Experimental Biology and Medicine , vol. 224, no. 4, pp. 302-308, 2000. (hindawi.com)
Drugs1
- Thioridazine has minimal or no effect on global ratings, while other drugs such as chlormethiazole are superior to it on behavioural ratings. (cochrane.org)
Effect2
- Een groot probleem is echter dat rt-PA binnen de 4,5 uur na het begin van de beroerte moet toegediend worden om enig effect te hebben en dikwijls is niet bekend hoe lang de klonter het bloedvat afsluit. (scriptiebank.be)
- Afkoeling van het lichaam, en van de hersenen in het bijzonder, heeft een effect op een hele waaier aan stapjes in de ischemische cascade en kan dus op verschillende niveaus de uitkomst beïnvloeden. (scriptiebank.be)
Study1
- Chlormethiazole, amobarbital, lidocaine and PLT 101 in spasticity and rigidity: a study of clinical and EMG-Registrable effects on intravenous injection. (nih.gov)
Effects1
- The most frequent side effects caused by chlormethiazole were drowsiness and nasal irritation. (cochrane.org)
Higher1
- The plasma level of chlormethiazole was consistently higher in the aged subjects and this was reflected by the larger area under the plasma curve in aged (7.62±5.37 μg.h/ml) than in young (0.94±0.66 μg.h/ml) individuals. (monash.edu)
Groups1
- Absorption of chlormethiazole was rapid in the subjects of both groups as assessed by the time taken to reach the peak plasma concentration. (monash.edu)