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)

Experiments were conducted on rabbits with tetanus intoxication induced by the intravenous injection of a lethal dose of the toxin; a study was made of the therapeutic efficacy of the acetylcholinesterase reactivators--dipyroxim and isonitrosine, and also of the central cholinolytics--amizyl and diphacyl. In dose of 25 mg/kg dipyroxim produced no therapeutic effect, and in doses of 30--40 mg/kg caused the animal death. Amizyl and diphacil in a dose of 3--4 mg/kg caused elimination of tonic convulsions for 1 1/2--2 hours. As to isonitrosin--it produced the same effect for 4--5 hours. In case of combined administration of reactivators and cholinolytics convulsions were eliminated for 4--5 hours.
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PMID:[Use of acetylcholinesterase reactivators and central cholinolytics in the treatment of experimental tetanus poisoning]. 2 62

Characteristics of neuromuscular block produced by polymyxin B (PXB) were examined in 12 anesthetized cats, using sciatic nervetibialis anticus muscle preparations. The ED50 was 6.7 (+/- 1.4, SD) PXB base/kg body weight. The ED95 was 10.8 (+/- 2.4) mg/kg. Spontaneous recovery from 25 percent of control to 75 percent of control required 72 (+/- 16) minutes. During a 50 percent block, train-of-four twitches elicited at 2 Hz faded with a train-of-four ratio of 0.42 (+/- 0.13), but the tetanus did not fade. Edrophonium Cl, neostigmine methylsulfate, and pyridostigmine Br at sub-clinical dosages weakly antagonized the block but enhanced the block at anti-curare dosages. All 3 cholinesterase inhibitors were short acting, lasting 10 to 15 minutes, and noncumulative on repeated injection. The potency ratio was approximately 20:10:1 in the order of edrophonium, neostigmine, and pyridostigmine on a weight-for-weight basis. Calcium partially antagonized the block. The authors conclude that neuromuscular blocks produced by various antibiotics differ from each other and from that produced by other groups of neuromuscular blocking agents, including curare.
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PMID:Neuromuscular block by antibiotics: polymyxin B. 19 5

This paper describes the correlation between serum cholinesterase levels and the severity and course of tetanus in a young patient. The diagnostic and prognostic value and significance of this enzyme as well as the therapeutic value of cholinesterase-restoring agents in tetanus are discussed.
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PMID:Serum cholinesterase in tetanus. 33 69

Mouse sternomastoid muscles were incubated with diisopropylfluorophosphate (DFP) in vivo, and the time course of recovery was studied using histochemistry, EM autoradiography and physiology. We found that: (1) the ability of the muscle to sustain tetanus in response to nerve stimulation is eliminated when the esterases at the neuromuscular junctions are saturated with DFP. This ability is regained partially when less than 10% of the DFP-binding sites have recovered. (2) There is a positive correlation between the frequency of stimulation at which the tetanic response can be maintained and the extent of acetylcholinesterase (AChE) recovery. (3) Tetanic responses at fusion frequency (about 100 Hz) appear indistinguishable from controls with only about 25% of normal AChE. (4) Butyrylcholinesterase (BuChE) possibly of Schwann cell origin recovers more rapidly than does AChE. (5) The muscle shows fine structural changes involving Z band dissolution and the breakdown of sarcoplasmic reticulum within hours after esterase inactivation. (6) This myopathy reaches a peak at three days after esterase inactivation and is almost fully recovered by two weeks. (7) It can be eliminated if, at the time of esterase inactivation, the nerve is cut or the acetylcholine receptors at the endplate are inactivated by alpha-bungarotoxin. We suggest that the myopathy, seen after DFP, is mediated by Ca2+ fluxes due to prolonged action of acetylcholine (ACh) in the absence of esterases.
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PMID:Endplates after esterase inactivation in vivo: correlation between esterase concentration, functional response and fine structure. 43 72

1 Rat isolated diaphragm preparations were stimulated indirectly either intermittently at 20, 50 or 100 Hz or continuously at 0.2 Hz.2 Addition of 1.8 muM paraoxon (which inhibits acetylcholinesterase by forming a phosphorylated enzyme which undergoes slow spontaneous reactivation) for 5 min to the organ bath produced a failure of the muscle to maintain tetanic tension (tetanic fade, Wedensky inhibition) and potentiated the neuromuscular blocking activity of exogenous acetylcholine. The rates of recovery from both these effects were recorded.3 In a series of experiments with dyflos (which inhibits acetylcholinesterase by forming a phosphorylated enzyme which does not undergo spontaneous reactivation) the relationship between functional acetylcholinesterase activity and neuromuscular blocking activity of exogenous acetylcholine was also determined.4 From the data obtained, the relationship between functional acetylcholinesterase activity and tetanic fade was calculated. These calculations show that (i) a considerable reduction in functional acetylcholinesterase activity is required before the diaphragm loses its ability to respond with a sustained tetanus to indirect stimulation at higher frequencies, (ii) the minimum (critical) level of functional acetylcholinesterase activity required for a normal tetanic response is directly related to the frequency of stimulation and (iii) once functional acetylcholinesterase activity has been reduced to the critical level, a very small further reduction leads to a complete tetanic fade.5 The meaning of functional acetylcholinesterase assays and of conclusions which can be drawn from them, is discussed.
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PMID:Relationship between inhibition of acetylcholinesterase and response of the rat phrenic nerve-diaphragm preparation to indirect stimulation at higher frequencies. 46 87

The influence of lowering the temperature, by 10 degrees C increments, from 37 decrees C to 17 degrees C on the twitch )Pt) and tetanic (Po) tension during direct and indirect stimulation, on presynaptic acetylcholine (ACh) release and on muscle acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activity were investigated in vitro on the rat's phrenic-nerve-hemidiaphragm preparation. Decreasing the temperature from 37 degrees C to 17 decrees C caused a progressive increase of the isometric Pt to 195.8 +/- 9.6 (S.E. of mean) and 169.6 +/- 2.9% of control with direct and indirect stimulation respectively. This change in temperature also increased twitch duration and time to peak Pt by factors of about 4 and 6 respectively with both direct and indirect stimulation. The Po/Pt ratio did not change significantly between 37 degrees C and 27 degrees C, but dropped sharply between 27 degrees C and 17 degrees C. With direct stimulation tetanus was only maintained in 50% of the experiments at 37 degrees C and in none at 27 degrees C or 17 degrees C. With indirect stimulation tetanus was maintained in all experiments at 37 degrees C and 27 degress C and in none at 17 degrees C. Post-tetanic facilitation was greater with indirect than direct stimulation and at higher than at lower temperatures. Post-tetanic exhaustion, with both direct and indirect stimulation, was only observed at 37 degrees C. Presynaptic ACh release (pmol . g-1 . min-1) at rest and with stimulation rates of 0.1 to 50 Hz decreased by more than 60% as temperature was lowered from 37 degrees C to 17 degrees C. Cooling from 37 degrees C to 17 degrees C caused a similar decrease in the volley output (pmol . g-1 . volley-1) of ACh. Muscle-AChE and BuChE activities decreased by 34 and 52% respectively when the temperature was lowered from 37 degrees C to 17 degrees C. The findings presented indicate that the site of the facilitating effect of cooling on Pt is the muscle fiber. The facilitation is caused by the delay of the relaxation of the contracted muscle, causing prolongation of the active state and increased tension development. The decreased speed of nerve conduction and ACh release caused by cooling adversely affects neuromuscular transmission. This, however, is partially counteracted by decreased muscle-ChE activity and increased sensitivity of the postjunctional membrane to ACh caused by cooling.
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PMID:The influence of temperature on neuromuscular performance. 69 Jun 33

It is compared the true cholinesterase inhibition exerced in vitro either by the tetanus toxin and by "parathion". Rabbit's brain homogenates are used as source of the ChE. 4000 MLD of tetanus toxin show the same inhibitory effect than mg 1 of "parathion", during 30 min of incubation at 37 degrees C.
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PMID:[Comparison of the anticholinesterase action in vitro of tetanus toxin and parathion]. 75 32

As tetanus toxin results inactivated when mixed with mammals brain homogenate (Wassermann-Takaki phenomenon), the same may be observed for the organophosphorus compounds. When the brain homogenates are mixed before with one of both poisons and subsequently, after incubation, with the other, this one keeps its typical toxic activity. This behavior seems to be interpreted as the result from the linkage between the true cholinesterase and one toxic (Wassermann-Takaki phenomenon both for the tetanus toxin and the "parathion"), with the following interference for the second toxic, when added, at the enzymatic level, so that the second toxic remains free.
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PMID:[Possible interference between tetanus toxin and organo-phosphorus esters in blocking of cholinesterase]. 75 35

In rabbits injected i.m. with 1 MLD of tetanus toxin, the levels of the serum cholinesterase and of the erythrocytic cholinesterase were determined twice every day, during the course of the intoxication, until the death of the animals. The levels of the serum cholinesterase were decreasing day by day, while these of the erythrocytic cholinesterase did not show any significant variation. These results are strictly comparable to those one may observe in organophosphorus poisoning.
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PMID:[Behavior of serum and erythrocyte cholinesterase in experimental tetanus in rabbits]. 75 34

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44


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