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

---

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

In a survey of 21 patients with myasthenia gravis receiving regular acetylcholinesterase inhibitor therapy, 8 were found to have air-flow limitation associated with their antimyasthenic therapy. In 6 of these subjects, detailed assessments were made of the effect of antimyasthenic therapy on airways function. Pyridostigmine was given together with either placebo or the anticholinergic bronchodilator ipratropium bromide (72 micrograms) by inhalation administered double blind on 2 consecutive days. Airways resistance (Raw) increased significantly after pyridostigmine and placebo inhaler (0.49 +/- 0.13 kPa/L/s basal versus 0.60 +/- 0.13 kPa/L/s at 2 h; mean +/- SEM, p less than 0.05), whereas a significant decrease in Raw followed the combination of pyridostigmine with ipratropium bromide (0.57 +/- 0.08 kPa/L/s basal versus 0.41 +/- 0.07 kPa/L/s at 2 h, p less than 0.05). Thus, acetylcholinesterase inhibitor therapy in subjects with myasthenia gravis with airflow limitation led to significant increase in airways resistance that could be completely reversed by the inhalation of the muscarinic receptor blocker ipratropium bromide.
...
PMID:Air-flow limitation in myasthenia gravis. The effect of acetylcholinesterase inhibitor therapy on air-flow limitation. 622 24

Antagonism of neuromuscular block using cholinesterase inhibitors and atropine is charged with several risks, which are at least partly caused by pharmacological characteristics of the anticholinergic drugs, e.g. short duration of action causing secondary bradycardia. Compared to atropine, ipratropium bromide, a new anticholinergic drug, is--due to its quarternary ammonium compound--characterized by longer duration of action. In contrast to atropine, this substance does not penetrate the blood-brain and placental barrier. Our present study was designed to compare the haemodynamic effects of both substances, using invasive monitoring, during antagonism of neuromuscular block with pyridostigmine. In contrast to atropine, ipratropium bromide induced a higher degree of initial tachycardia but did not allow secondary reduction of heart rate by rebound vagal stimulation. While cardiac output was almost constant, ipratropium bromide caused changes in stroke volume, which were due to alterations in heart rate. There were no clinically relevant changes of the other haemodynamic parameters. Cardiac arrhythmia were observed more often after administration of atropine and were of longer duration. In conclusion, ipratropium bromide is a useful alternative to atropine in patients with pre existing low heart rate and bradyarrhythmia.
...
PMID:[Hemodynamic effects in antagonism of neuromuscular blockage: atropine-pyridostigmine versus ipratropium bromide-pyridostigmine]. 623 62

In experiments on cats it has been shown that 2 beta, 16 beta-bis (4'-dimethyl-1'-piperazino)-3 alpha, 17 beta-diacetoxy-5 alpha-androstane dibromide (pipecurium bromide, RGH-1106, Arduan), is a non-depolarizing muscular blocker. The order of myorelaxation evoked by this agent is characteristic: first the chewing and limb muscles, then abdominal muscles and diaphragm and at the end intercostal muscles are relaxed. Pipercurium bromide has no cardiotropic, atropine-like, or ganglion-blocking activity. It fails to influence the coronary blood-supply or myocardial oxygen consumption. No acetylcholinesterase inhibiting action of the compound was seen. It does not affect the central nervous system.
...
PMID:On some properties of a new steroid curare-like compound pipecurium bromide. 624 77

The acetylcholinesterase (AchE) inhibitory effect of a muscle relaxant 2 beta,16 beta-bis-(4'-dimethyl-1'-piperazino)-3 alpha,17 beta-diacetoxy-5 alpha-androstane dibromide (pipecurium bromide, RGH-1106, Arduan), was studied in vitro. The inhibition of AchE activity of human red blood cells, expressed as pI50, was 3.99, whereas that of serum cholinesterase (ChE) was 4.33. The AchE inhibitor action was reversible. The inhibition was not influenced by the combined administration of promethazine or atropine. The combined effect of pipecurium bromide and of some other diamino-azasteroid agent proved to be additive. Pipecurium bromide showed mixed-type inhibitory effect both on AchE and ChE.
...
PMID:The effect of the steroid muscle relaxant pipecurium bromide on the acetylcholinesterase activity of red blood cells in vitro. 624 79

In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) or the cholinergic muscarinic receptor agonist oxotremorine (0.25 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Complete suppression of the GH-releasing effect of eserine and oxotremorine was induced by blockade of cholinergic muscarinic receptors by atropine (80 or 20 micrograms/kg, 30 min before) but not by scopolamine-N-butyl bromide (0.8 mg/dog, 30 min before), an anticholinergic drug which does not cross the blood brain barrier (BBB). In contrast, activation of cholinergic nicotinic receptors by nicotine (6 mg) failed to alter resting cGH concentrations, and pre-treatment with the nicotinic receptor blocker mecamylamine (5 mg, 30 min before) did not counteract the GH-releasing effect of eserine. Other cholinomimetic drugs, e.g. pilocarpine, 4-aminopyridine, carbachol and bethanechol failed to induce a rise in plasma cGH concentrations. These data indicate that: 1) cholinergic muscarinic but not nicotinic receptors located in the central nervous system (CNS) inside the BBB play a facilitatory role in tonic cGH release; 2) pharmacologically distinct muscarinic receptors may exist in the CNS.
...
PMID:Effect of agonists and antagonists of cholinergic neurotransmission on growth hormone release in the dog. 630 74

The effect of chemical modification on the acetylcholinesterase and the aryl acylamidase activities of purified acetylcholinesterase from electric eel and basal ganglia was investigated in the presence and absence of acetylcholine, the substrate of acetylcholinesterase, and 1,5-bis[4-(allyldimethylammonium)phenyl]pentan-3-one dibromide (BW284C51), a reversible competitive inhibitor of acetylcholinesterase. Trinitrobenzenesulfonic acid, pyridoxal phosphate, acetic anhydride, diethyl pyrocarbonate, and 2-hydroxy-5-nitrobenzyl bromide under specified conditions inactivated both acetylcholinesterase and aryl acylamidase in the absence of acetylcholine and BW284C51. Chemical modifications in the presence of acetylcholine and BW284C51 by all the above except diethyl pyrocarbonate selectively prevented the loss of acetylcholinesterase but not aryl acylamidase activity; modification by diethyl pyrocarbonate in the presence of acetylcholine and BW284C51 prevented the loss of both acetylcholinesterase and aryl acylamidase activities. Treatment with N-acetylimidazole resulted in the inactivation of acetylcholinesterase and the activation of aryl acylamidase. These changes in both the activities could be prevented by acetylcholine and BW284C51. Modification by phenylglyoxal, 2,4-pentanedione, or N-ethylmaleimide did not affect the enzyme activities. Indophenylacetate hydrolase activity followed a pattern similar to that of acetylcholinesterase in all the above modification studies. The results suggested essential lysine, tyrosine, tryptophan, and histidine residues for the active center of acetylcholinesterase and essential lysine, histidine, and tryptophan residues for the active center of aryl acylamidase.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Chemical modification of acetylcholinesterase from eel and basal ganglia: effect on the acetylcholinesterase and aryl acylamidase activities. 638 42

A modified method of Ellman's reaction with a continuous flow was used to study the cerebral cholinesterase activity in its biological environment with rat brain slices including the striatum. Comparative studies were performed under various conditions of flow and substrate concentrations (acetylthiocholine bromide) and with or without formaldehyde fixation. We could thus measure either the inhibition rate of cerebral ChE by paraoxon or MPT or the reactivation rate by some oximes in the presence of substrate and after removing excess inhibitor.
...
PMID:In vitro study of organophosphorus inactivators of membrane acetylcholinesterase and of reactivating pyridinium-oximes using rat brain slices. 641 4

In this study we investigated the effects of a series of phosphonium salts and phosphoranes on the catalytic activity of acetylcholinesterase and on the viability of the various life stages of Schistosoma mansoni worms. All the tested compounds showed an inhibitory effect towards the S. mansoni acetylcholinesterase (AChE) activity. The most effective compound, p-xylylene bis(triphenylphosphonium) dibromide (No. 16) displayed approximately 100% inhibition at concentration of 10(-5)-10(-6)M. No significant difference was found in the sensitivity of the enzyme obtained from the various stages of the parasite life cycle to the effect of the drugs. Each compound was also tested for its toxicity towards 3 h old schistosomula and 7-9 week adult worms under in vitro culture conditions. In the case of the larvae, after 2 days in culture, only three compounds (Nos. 4, 11 and 12) out of sixteen tested exhibited efficient killing of the schistosomula while the others had a very slight toxic activity or no toxicity at all. On the other hand, all the compounds showed a significant toxicity towards the adult worms and the most effective one, allytriphenylphosphonium bromide (No. 11), retained its toxic effect even at an extremely high dilution (10(-8)M). However, the cumulative results in this paper do not demonstrate a significant correlation between the inhibitory effect of the phosphonium salts and phosphoranes on the AChE activity of the schistosomes and their toxicity towards the worms. The LD50 value (i.v.) of the compound which showed the highest toxic effect in vitro (No. 11) was found to be 30 +/- 1.7 mg/kg in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effect of phosphonium salts and phosphoranes on the acetylcholinesterase activity and on the viability of Schistosoma mansoni parasites. 651 Nov 45

A correlation was found among the degree of memory loss, intellectual impairment, the quantity of senile plaques, and a decrease in choline acetyltransferase and acetylcholinesterase activity in patients affected by senile dementia of the Alzheimer type. In this study, patients were subjected to a series of computerized electroencephalographic (EEG) recordings and neuropsychological evaluations after acute administration of the following drugs: placebo; the cholinergic drugs physostigmine, pyridostigmine bromide, and edrophonium chloride; and the anticholinergic drugs scopolamine and orphenadrine. The results obtained show that the acute administration of some cholinergic drugs improved memory and attention performances, whereas the anticholinergic drugs induced opposite effects. The cholinergic drugs exhibited a tendency to shift the EEG spectrum analysis into more normal patterns compatible with the patient's age. This study supports the view that the cholinergic system plays an important role in memory and attention disturbances found in senile dementia of the Alzheimer type.
...
PMID:Effect of cholinergic and anticholinergic drugs on short-term memory in Alzheimer's dementia: a neuropsychological and computerized electroencephalographic study. 666 30

The effects of spinal cord transection and acidosis on succinylcholine (SCC)-induced hyperkalemia were studied in Sprague-Dawley rats. The effectiveness of pretreatment with subparalyzing doses ("self-taming") of SCC or with the cholinesterase inhibitor hexafluorenium bromide in preventing hyperkalemia was also studied. The increase in plasma potassium after administration of SCC (1 mg/kg) was found to be significantly increased 10 days after spinal cord transection. This potassium increase could not be prevented by pretreatment with either hexafluorenium (0.3 mg/kg) or subparalyzing doses (0.15 mg/kg) of SCC. Respiratory acidosis caused an increase in plasma K+ in both normal and in spinal cord transected rats. Acidosis had a synergistic effect on succinylcholine-induced hyperkalemia. These findings support the clinical practice of not using succinylcholine in patients at risk of having a pathological sensitivity to SCC. Furthermore, SCC may be especially dangerous when administered to patients who are acidotic.
...
PMID:Synergistic effect of acidosis and succinylcholine-induced hyperkalemia in spinal cord transected rats. 671 Dec 67


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---