Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Behavioral effects of nicotine and cytisine, and the cholinesterase inhibitors physostigmine and 9-amino-1,2,3,4-tetrahydroacridine (THA), administered intrathecally (IT) at the lumbar level in the rat have been evaluated. Antinociceptive dose relationships were established using the tail immersion test. Total activity, locomotion and rearing were also measured in computerized test boxes. The nicotinic receptor antagonist, mecamylamine, and the muscarinic receptor antagonist, atropine, were used to study the selectivity of the effects. Physostigmine and THA significantly decreased total activity, locomotion and rearing as compared to control animals. The motor effects of physostigmine were completely antagonized only partly. Mecamylamine had no antagonistic effect. Nicotine did not affect any activity parameter. Cytisin reduced total activity and locomotion 1-6 min after dose. IT physostigmine, 15 micrograms, increased tail immersion latency for 30 min. No significant increase in response latency in this test was observed after the IT administration of nicotine or THA, whereas cytisine elicited a small increase. The IT administration of THA, nicotine and cytisine was also associated with gnawing, vocalization and hyperactivity and in the case of THA, diarrhoea. These effects were blocked by mecamylamine. Physostigmine antinociception as well as the behavioral effects including total activity, locomotion and rearing caused by physostigmine and by THA are most probably due to an action on spinal muscarinic receptors. Nicotinic receptors do not seem to be involved in spinal antinociception. Some aversive behavioral effects caused by the IT administration of nicotinic receptor agonists could, however, be attenuated by the spinal administration of the antagonist mecamylamine, which may indicate the involvement of nicotinic receptors in afferent sensory transmission.
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PMID:Behavioral effects after intrathecal administration of cholinergic receptor agonists in the rat. 232 Jul 7

Eight-month-old Jersey bull calves given ivermectin intravenously or subcutaneously showed signs of depression, ataxia, difficulty in breathing, tachycardia, salivation, diarrhoea, miosis, and an increase in pseudocholinesterase activity. The clinical signs were severe in calves given the drug intravenously. The findings suggest that the cholinergic nervous system may be involved in some of the adverse effects of ivermectin observed in calves.
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PMID:Clinical signs and biochemical changes in calves caused by injection of ivermectin. 271 47

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

Thirty-eight 7-week-old white leghorn chickens of two strains (high and low antibody response to sheep erythrocytes) were divided into groups for exposure to high and low levels of social stress. They were then challenged orally with a toxic dose of the organophosphate insecticide malathion (250 mg/kg body weight) and evaluated 60 min later for muscarinic signs (diarrhea, lacrimation, respiratory secretions), nicotinic signs (muscle weakness), plasma cholinesterase activity, and brain acetylcholinesterase activity. A significant correlation was shown between clinical and biochemical indices of organophosphate toxicity. The correlation between social stress and malathion toxicity was less well defined. Chickens with low antibody response preexposed to high social stress were most resistant to organophosphate toxicity.
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PMID:Effects of social stress on the toxicity of malathion in young chickens. 381 4

1. Daily i.p. administration, for eight days, of the cholinesterase inhibitor disulfoton to rats produced mild to moderate signs of intoxication (tremors, incontinence and diarrhoea) but no deaths.2. Segments of ileum taken from the treated rats were subsensitive to carbachol but the vas deferens and the uterus did not exhibit any change in sensitivity to carbachol.3. The sensitivity to acetylcholine was increased in the ileum and vas deferens but not in the uterus.4. Acetylcholinesterase activity was 60-70% inhibited in all three tissues.
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PMID:Response of the rat ileum, uterus and vas deferens to carbachol and acetylcholine following repeated daily administration of a cholinesterase inhibitor. 476 90

Extracts of Sesbania drummondii administered to chickens by oral intubation are lethal within several days. Effects are dose-dependent; a dose of 1% of body weight is uniformly lethal in 5 days. Signs of poisoning include weakness, depression (CNS), anorexia, diarrhea, ruffled feathers, cold feet, and rapid loss of body weight. Microscopic examination indicates damage to kidney glomeruli and leakage of protein into the kidney tubules. Packed cell volume and plasma glucose concentrations show no difference between controls and treated chickens; however, creatine kinase is increased and plasma cholinesterase and total plasma protein values are severely depressed in poisoned birds. Neither a specific toxin nor a mechanism of action for toxicity has yet been identified.
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PMID:Determination of the oral toxicity of Sesbania drummondii seeds in chickens. 673 32

28 cases of phallinic syndrome have been studied: 24 out of them were from amanita phalloides poisoning and 4 from amanita verna poisoning. After a lag phase lasting from 7 to 30 hours, symptomatology characterized by starting gastroenteric troubles as vomit, diarrhea, abdominal cramps, meteorism and pain following abdomen palpation. In one case the syndrome started with parasympathicomimetic crisis, probabily due to ingested amanita containing muscarinic type poison. Subsequent evolution of clinical picture included signs of hepatic and renal involvement. As far as laboratory diagnosis is concerned, high levels of serum aminotransferases were found and, less frequently, hyperbilirubinmia and high BUN levels occurred. In severe cases, in addition, lowered values for plasma prothrombine, fibrinogen and cholinesterase were found. Low therapeutic effect followed rehydration, equilibration of electrolytic unbalance and administration of thioctic acid, coagulants and so on. As a matter of fact 3 out or 28 patients, treated only with such therapy, died. On the contrary good therapeutic effect followed to peritoneal dialysis, in two cases coupled to exchange transfusion: 10 patients were treated in such a way and no one died but all of them quickly recovered. Forced diuresis also appeared greatly useful and practical in therapeutic treatment of phallinic syndrome: results compared favourably with those obtained by means of peritoneal dialysis. As a matter of fact 15 patients, 5 of them having ingested a great amount of amanita phalloides, were treated with forced diuresis and no one of them died. Finally, the need is stressed for a very quick therapeutic intervention (exchange transfusion; plasmapheresis; peritoneal dialysis; forced diuresis, and so on) in order to lower the plasma concentration of the toxins responsible for the phallinic syndrome. Only in such a way diffusion of toxins from blood to tissues is avoided.
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PMID:[Phallin syndrome. Reports on 28 cases]. 679 69

Prolonged exposure to organophosphates in low concentrations caused diarrhoea in 38 students, lecturers and other personnel at an agricultural college. The symptoms of those affected, plasma pseudocholinesterase levels, topography of the orchards and vegetable gardens, the various insecticides and quantities used, and the exposure due to prevailing winds have been studied. We conclude that safety and precautionary measures must be strictly enforced.
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PMID:Chronic organophosphate poisoning. 740 75

The present study assessed the safety and efficacy of the cholinesterase inhibitor, velnacrine, for treating the cognitive symptoms of Alzheimer's disease. Patients (N = 236) meeting NINCDS-ADRDA criteria for Alzheimer's disease entered a double-blind, placebo-controlled dose-ranging protocol (30, 75, 150, 225 mg/day each for one week) to identify velnacrine responders (> or = four point improvement on the cognitive subscale of the Alzheimer's Disease Assessment Scale [ADAScog]). After a two week drug washout, velnacrine responders were randomly assigned to their best velnacrine dose or placebo in a six week dose-replication protocol employing the ADAScog and the Clinical Global Improvement scale as primary outcome measures. During dose-replication, intent-to-treat analysis revealed that velnacrine patients scored significantly better than placebo patients on the ADAScog after two (p < 0.004), four (p < 0.025) and six (p < 0.001) weeks of treatment. No significant treatment effect on Clinical Global Improvement scores was observed. The primary adverse event was an asymptomatic elevation of liver transaminases found among 28% of the 236 treated patients. Cholinergic side effects including diarrhea (14%), nausea (11%) and vomiting (5%) were observed and 8% of patients experienced skin rash. The present study identified a subgroup of Alzheimer's patients who demonstrated a significant, but modest, improvement during velnacrine treatment on structured cognitive testing.
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PMID:Double-blind placebo-controlled study of velnacrine in Alzheimer's disease. 863 8

A 20-year-old Arab crossbred gelding was examined because it had apparently suffered an overstimulation of the parasympathetic nervous system for three hours. The clinical signs consisted of hypersalivation, profuse sweating, maximal miosis, fasciculation of the muscles and lateral recumbency in combination with continuous convulsions without diarrhoea. The horse's plasma pseudocholinesterase activity was approximately 10 per cent of normal. It responded well to 10 mg atropine and 50 mg diazepam administered intravenously.
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PMID:Inhibition of pseudocholinesterase activity in a 20-year-old gelding. 864 36


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