Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hour after suicidal ingestion of about 20 mL of a 38% solution of bromofosmethyl, CAS: 2104-96-3 (bromophos), a 52 year-old female was admitted to the hospital with extreme miosis, hypersalivation, hyperperistalsis and muscular fibrillation. Gastric lavage was performed and activated charcoal administered. Cholinergic symptoms were antagonized by repeated doses of 0.5 mg atropine. Because of the high dose of bromophos, hemoperfusion was performed with amberlite XAD4. The bromophos clearance during hemoperfusion was 95 mL/min (flow 200 mL/min). The patient received two doses of 500 mg obidoxime for recurrent muscular fibrillation. The further clinical course was uneventful. On day 4, the patient was transferred to a psychiatric ward because of persistent suicidality. In contrast to poisoning by most organophosphates, red blood cell acetyl cholinesterase was only minimally depressed but the plasma butyryl cholinesterase was initially decreased and normalized within a few days. The records of 25 patients reported to our Poison Control Center with ingestion of more than 1 g bromophos were also evaluated. The most frequent symptoms were miosis, hyperperistalsis, hypersalivation, agitation, nausea/vomiting and convulsions. Nine of the patients had no symptoms. Bromophos is relatively less toxic than its phosphate derivative, parathion.
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PMID:Acute poisoning with bromofosmethyl (bromophos). 205 7

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Critical tests were done on 24 naturally parasitized horses to compare the antiparasitic activity of an oral paste preparation of mebendazole and trichlorfon with that of the marketed powder formulation. Each formulation was administered at the recommended dosages of 8.8 mg of mebendazole and 40 mg of trichlorfon/kg of body weight. Efficacy of the paste formulation ranged from 97.7% to 100% against 2nd- and 3rd-stage Gasterophilus spp, adult Strongylus vulgaris, S edentatus, Parascaris equorum, small strongyles; and larval and adult forms of Oxyuris equi. Adverse effects were generally limited to slight softening of the feces. Mild and transient restlessness or sweating were also observed in 2 of 12 horses treated with the paste formulation. The toxic effects of the paste, administered at 2.2 times the therapeutic dose, were examined in 6 horses and compared with the effects of a nonmedicated paste, administered in similar volumes to 6 other horses. Drug-related changes were not detected in clinical chemical analyses, hematologic values, or liver function tests. Transient clinical signs of organophosphate toxicosis (primarily the passage of loose feces) and prolonged inhibition of erythrocyte cholinesterase activity were evident within 1 hour after drug treatment. These effects were similar to those reported for the 2.2 X dose of marketed powder formulation.
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PMID:Critical test and safety evaluations of an oral paste preparation of mebendazole and trichlorfon in horses. 352 28

Male and female F344/N rats and B6C3F1 mice were exposed to lethal and sublethal concentrations of methyl isocyanate by inhalation. Mortality, clinical signs, body and organ weights, and changes in clinical pathology and hematology were monitored immediately after 2-hr exposures and during the ensuing 3 months. Additional studies investigated the possible involvement of cyanide in the toxicity of methyl isocyanate. During exposures, signs of restlessness, lacrimation, and a reddish discharge from the nose and mouth were evident in rats and mice. Following exposures, rats and mice were dyspneic and weak. Deaths of rats and mice exposed to lethal concentrations (20 to 30 ppm) began within 15-18 hr, with males more prone to early death than females. A second wave of deaths occurred after 8 to 10 days, affecting primarily female rats and mice exposed to 20 to 30 ppm of methyl isocyanate, and male and female rats exposed to 10 ppm. Most deaths occurred during the first month following the exposures and were preceded by periods of severe respiratory distress. Body weights decreased in proportion to dose early, but then weight gain resumed in survivors at control rates. The only organ with a consistent, dose-related weight change was the lung, which was heavier throughout the studies in animals exposed to high concentrations of methyl isocyanate. No significant clinical pathology, or hematologic changes were observed in exposed rats. Blood and brain cholinesterase were not inhibited. Studies attempting to measure cyanide in the blood of methyl isocyanate-exposed rats, and attempting to affect lethality with a cyanide antidote (sodium nitrite and sodium thiosulfate) gave negative results.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicity of inhaled methyl isocyanate in F344/N rats and B6C3F1 mice. I. Acute exposure and recovery studies. 362 44

Healthy camels were experimentally infected with Trypanosoma evansi and then treated with isometamidium chloride (samorin) at single intravenous doses of 0.5 or 1.0 mg/kg. Five to 10 min after the drug administration, the camels at both dosages showed lacrimation, salivation, trembling, restlessness, frequent urination and defecation, followed by diarrhea. Moreover, the camels at the higher dose showed an unsteady gait for about an hour with hindleg weakness and walking backward. The animals fell to the ground, laid on their sides, and bent their necks into an "S" shaped curve. Three hours after the drug administration all the animals stood up and remained quiet. The treatment increased the concentration of plasma ammonia and total protein. No significant change was found in the plasma bilirubin concentration. Two hours after treatment, the activity of plasma cholinesterase was significantly reduced. The enzyme activity recovered 24 h after drug administration, but was still significantly below the control value. The treatment did not produce statistically significant changes in the hemogram of the infected camels. The results suggest that the drug should not be used clinically against T evansi infection due to its low margin of safety. If the drug is to be used at all in camels, pretreatment with an anticholinergic agent might be considered.
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PMID:Some observations on the toxicosis of isometamidium chloride (samorin) in camels. 377 85

Agitation or psychosis or both occur in half or more of patients with dementia at some point during the course of illness. The treatment of these signs and symptoms ideally entails identification and alteration of physical, environmental, social, and psychiatric factors. Environmental modification, education of caregivers, and therapeutic activity programs are nonpharmacologic approaches that can effectively reduce some signs and symptoms of this nature. For those that remain, empirical administration of pharmacologic agents may be appropriate. One approach is to inventory the specific behaviors and develop a "therapeutic metaphor," i.e., subtype the agitated behaviors according to the presence of target symptoms likely to respond to specific classes of medication. Available evidence is reviewed regarding the efficacy and safety of somatic therapies for agitation, including antipsychotics, antidepressants, anticonvulsants, benzodiazepines, and cholinesterase inhibitors.
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PMID:Treatment strategies for agitation and psychosis in dementia. 902 33

On the day of the disaster, 641 victims were seen at St. Luke's International Hospital. Among those, five victims arrived with cardiopulmonary or respiratory arrest with marked miosis and extremely low serum cholinesterase values; two died and three recovered completely. In addition to these five critical patients, 106 patients, including four pregnant women, were hospitalized with symptoms of mild to moderate exposure. Other victims had only mild symptoms and were released after 6 hours of observation. Major signs and symptoms in victims were miosis, headache, dyspnea, nausea, ocular pain, blurred vision, vomiting, coughing, muscle weakness, and agitation. Almost all patients showed miosis and related symptoms such as headache, blurred vision, or visual darkness. Although these physical signs and symptoms disappeared within a few weeks, psychologic problems associated with posttraumatic stress disorder persisted longer. Also, secondary contamination of the house staff occurred, with some sort of physical abnormality in more than 20%.
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PMID:Sarin poisoning on Tokyo subway. 919 33

Systemic and localised adverse effects of local anaesthetic drugs usually occur because of excessive dosage, rapid absorption or inadvertent intravascular injection. Small children are more prone than adults to methaemoglobinaemia, and the combination of sulfonamides and prilocaine, even when correctly administered, should be avoided in this age group. The incidence of true allergy to local anaesthetics is rare. All local anaesthetics can cause CNS toxicity and cardiovascular toxicity if their plasma concentrations are increased by accidental intravenous injection or an absolute overdose. Excitation of the CNS may be manifested by numbness of the tongue and perioral area, and restlessness, which may progress to seizures, respiratory failure and coma. Bupivacaine is the local anaesthetic most frequently associated with seizures. Treatment of CNS toxicity includes maintaining adequate ventilation and oxygenation, and controlling seizures with the administration of thiopental sodium or benzodiazepines. Cardiovascular toxicity generally begins after signs of CNS toxicity have occurred. Bupivacaine and etidocaine appear to be more cardiotoxic than most other commonly used local anaesthetics. Sudden onset of profound bradycardia and asystole during neuraxial blockade is of great concern and the mechanism(s) remains largely unknown. Treatment of cardiovascular toxicity depends on the severity of effects. Cardiac arrest caused by local anaesthetics should be treated with cardiopulmonary resuscitation procedures, but bupivacaine-induced dysrhythmias may be refractory to treatment. Many recent reports of permanent neurological complications involved patients who had received continuous spinal anaesthesia through a microcatheter. Injection of local anaesthetic through microcatheters and possibly small-gauge spinal needles results in poor CSF mixing and accumulation of high concentrations of local anaesthetic in the areas of the lumbosacral nerve roots. In contrast to bupivacaine, the hyperbaric lidocaine (lignocaine) formulation carries a substantial risk of neurotoxicity when given intrathecally. Drugs altering plasma cholinesterase activity have the potential to decrease hydrolysis of ester-type local anaesthetics. Drugs inhibiting hepatic microsomal enzymes, such as cimetidine, may allow the accumulation of unexpectedly high (possibly toxic) blood concentrations of lidocaine. Reduction of hepatic blood flow by drugs or hypotension will decrease the hepatic clearance of amide local anaesthetics. Special caution must be exercised in patients taking digoxin, calcium antagonists and/or beta-blockers.
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PMID:Adverse effects and drug interactions associated with local and regional anaesthesia. 956 36

Alzheimer's disease (AD) is characterized by a gradual decline in 3 domains: cognition, behavior, and function. Ideally, an effective treatment would target all 3 types of impairment. However, available treatments for AD diminish only certain symptoms and cannot halt the dementing process. Most pharmacologic agents currently available or in development target a specific symptom cluster (e.g., cognitive loss), and are based on the known neurobiology of the disease (e.g., neurotransmitter deficit) or hypothesized antidementia approaches (e.g., anti-inflammation, antioxidation). Two currently available cholinesterase inhibitors improve memory and other aspects of cognition during short-term treatment. Additional cholinergic agents will soon become available. Other promising agents under study for cognitive enhancement or protection include vitamin E, selegiline, estrogen, and nonsteroidal anti-inflammatory drugs. As scientists uncover the basic pathogenetic mechanisms of AD, additional treatments will likely emerge. Therapies for behaviors associated with dementia (e.g., depression, agitation, anxiety) are sometimes effective. Choices of specific medications, including antidepressants, antipsychotics, and anxiolytics, depend on specific side-effect profiles. Psychotherapies aimed at enhancing cognition are ineffective for dementia but nonpharmacologic interventions may minimize depression and agitation and may improve quality of life.
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PMID:Treatment of Alzheimer's disease: current approaches and promising developments. 961 51

Disruptive agitation and psychotic symptoms are important problems in the management of Alzheimer's disease and are major determinants of nursing home placement. This article reviews interpretable, placebo-controlled studies of psychopharmacologic approaches to the treatment of these "noncognitive" psychiatric and behavioral problems. Clinical trials of antipsychotic drugs demonstrate modest efficacy for psychosis and agitation, but adverse effects are common. Trials of serotonin selective reuptake inhibitors suggest they may be effective for emotional disturbances complicating Alzheimer's disease. Trials of drugs that enhance central cholinergic activity (certain cholinesterase inhibitors and selective M1 muscarinic cholinergic agonists) demonstrate positive effects on both cognitive deficits and noncognitive psychiatric and behavioral problems. Further clinical studies are needed to provide guidelines for the management of noncognitive psychiatric and behavioral problems in Alzheimer's disease.
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PMID:Psychopharmacology of noncognitive abnormal behaviors in Alzheimer's disease. 972 Apr 84


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