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At least 19 recordsLinked to original sources
PubMedDate not supplied

Binding of organic compounds to rat liver and lung.

The binding of various radioisotopically labeled organic compounds to rat liver and lung was investigated in vitro. Pieces of rat lung and slices of rat liver were incubated at 37 degrees C under a nitrogen atmosphere in a modified Krebs-Ringer phosphate solution (pH 7.4) CONTAININg the compound to be studied. Of the neutral compounds investigated, digitoxin, digoxin and dexamethasone were highly bound to both liver and lung tissue, whereas the degree of binding of amitrole, erythritol, and ouabain was 20% or less. The weak acids which were bound to the greatest extent in both liver and lung were phenobarbital, pentobarbital, and diphenylhydantoin. Barbital was poorly bound, and there was no evidence for the binding of 5,5-dimethyloxazolidine-2,4-dione or p-aminohippuric acid in either tissue. Binding of the cardiac glycosides and the barbiturates directly paralleled their lipid solubilities. The degree of binding of neutral compounds and weak acids to lung and liver tissue did not vary greatly with concentration, even though broad concentration ranges were studied. This was also true of the weak base morphine. On the other hand, the binding to liver and lung of the organic bases nicotine, pilocarpine, d-amphetamine, lidocaine, erythromycin, and chloroquine, did vary with concentration. The quaternary ammonium compound decamethonium was bound only to liver, and this binding also varied with concentration. Two additional quaternary ammonium compounds, tetraethylammonium and N1-methylnicotinamide, were not significantly bound to either tissue. Comparisons on the basis of equal content of solids revealed that the binding of diverse organic compounds in liver is greater than or equal to that in lung.

Amitrole↗
PubMed1975

Cholinomimetic teratogens. II. Interaction with inorganic ions.

Treatment of chicken embryos after 96 h of incubation showed that the teratogenic activity of the cholinomimetic compounds carbachol, neostigmine, decamethonium, and tetramethylammonium is reduced in the presence of calcium acetate. Similarly, supplementation with potassium acetate reduced the teratogenicity of carbachol and tetramethylammonium.

Abnormalities, Drug-Induced↗
PubMed1975

Cholinomimetic teratogens: studies with chicken embryos.

The cholinomimetic compounds carbachol, decamethonium, neostigmine, succinylcholine, trimethylphenylammonium, and others were tested for their interference with normal chick development. All these compounds led to abnormalities of the cervical vertebrae; at higher dosage interference with normal morphogenesis involved the whole vertebral column. Hypoplasia of the leg muscles occurred with lower incidence. Responses, tested with carbachol, rose from 24 to 72 and 96 h, then declined to 120 h of incubation. Two of the cholinometic compounds used in combined treatment produced a high degree of synergism. Gallamine, benzoquinomium, butyrylcholine, and bethanechol had protective effects. Acetylcholine, at high dosage, caused defects different from the above. It is suggested that the cholinomimetic teratogens interfere with normal development by displacing acetylcholine from its receptors or by forming complexes with it.

Acetylcholine↗
PubMed1976

Characteristics and mechanism of neuromuscular block in myasthenia gravis.

The neuromuscular block of myasthenia gravis has the characteristics of an antidepolarizing (competitive block), similar to that produced by d-tubocurarine in normal subjects: progressive decrease in muscle action potentials evoked by two or more nerve stimuli, posttetanic facilitation, posttetanic fatigue, inhibition of the depolarizing action of acetylcholine (ACh) or anticholinesterase compounds, and reversal of the block by ACh or anticholinesterase compounds. In myasthenic patients spontaneously recurring negative discharges were more difficult to locate in the end-plate zone than in normal subjects, suggesting that the number or density of functioning end plates may be reduced. The threshold dose of intra-arterial ACh that increased electrical activity was higher than in normal subjects; the duration of the increased electrical activity was briefer, and was followed by more depression of negative discharges than in normal subjects and by a greater increase in the threshold dose of ACh. These results indicate that the end-plate zone of myasthenic patients is less responsive than that of normal subjects to the excitatory action of ACh, and may be more readily desensitized by ACh. In both myasthenic patients and normal subjects the intra-arterial injection of ACh produced a prompt transient decrease in evoked potentials, attributable to depolarization of the end plates, followed by recovery (and in myasthenic patients by repair), and then by a more prolonged late decrease in evoked potentials, attributable to desensitization of the end plates to transmitter. This prompt depressant effect of ACh on evoked potentials was less in myasthenic patients than in normal subjects, and the late depressant effect of ACh was greater. In myasthenic patients the late block produced by ACh had the characteristics of an antidepolarizing (competitive) type of block, including inhibition of the depolarizing action of ACh and reversibility by ACh or neostigmine, while in normal subjects the characteristics were those of a depolarizing (noncompetitive) type of block, including little or no inhibition of the depolarizing action of ACh and lack of reversal by ACh or neostigmine. The differences between the late depressant action of ACh in myasthenic patients and normal subjects resembled differences in the effect of other depolarizing compounds, such as choline, succinylcholine, and decamethonium, and are best explained by differences in behavior of the postsynaptic receptor. The disease appears to be due to the presence of abnormal forms of receptor or to abnormal responses of receptor to the transmitter. The predominance of one or other form of receptor may determine the clinical state of the myasthenic patient and his response to anticholinesterase medication.

Acetylcholine↗
PubMed1985

The action of cholinomimetic and cholinolytic agents, hemicholinium-3 and alpha- and beta-bungarotoxin on the body wall muscle of the earthworm, Lumbricus terrestris.

Strips of muscle, approximately 12 segments in length, were prepared from the body wall of the earthworm, Lumbricus terrestris, from which the nerve cord and viscera had been removed. Contractions to electrical stimulation and acetylcholine agonists were recorded using an isometric transducer. A range of nicotinic and muscarinic agonists and antagonists were tested on this preparation and the results indicate that the acetylcholine receptor on this muscle cannot be classified as either nicotinic or muscarinic. Hemicholinium-3 abolished electrically induced muscle twitches at concentrations which had no effect on the acetylcholine response. Alpha-Bungarotoxin blocked the responses to both electrical stimulation and acetylcholine while beta-bungarotoxin blocked the contractions induced by electrical stimulation but potentiated the acetylcholine contraction.

Acetylcholine↗
PubMed1992

[Resistance of hospital strains of microorganisms to antibiotics and antiseptics].

The development of resistance of collection and freshly isolated S. aureus and C. albicans strains to the antiseptic decamethoxim and an original diarylcyclohexane derivative was studied comparatively in vitro. It was shown that the rate of the resistance development was low. After 20 subcultures in the presence of increasing concentrations of decamethoxin, its sensitivity of S. aureus and C. albicans decreased 16-32 and 16-fold respectively. After 20 subcultures in the presence of increasing doses of the diarylcyclohexane derivative, its sensitivity S. aureus and C. albicans decreased 4- and 4-8-fold, respectively. It was found that in the hospital strains of S. aureus and C. albicans, the antibiotic resistance and sensitivity to decamethoxin and the diarylcyclohexane remained high, which indicated that there was no cross resistance to these compounds in the strains studied.

Anti-Infective Agents, Local↗
PubMed1986

Rotifer neuropharmacology--II. Synergistic effect of acetylcholine on local anesthetic activity in Brachionus calyciflorus (Rotifera, Aschelminthes).

A number of compounds showing general anesthetic action in the rotifer Brachionus calyciflorus were investigated in the presence of acetylcholine. Non-ionizing anesthetics, including tricaine, showed no interaction with acetylcholine. However, highly ionized compounds like the local anesthetics procaine and lidocaine, the muscarinic blocker and local anesthetic atropine, and the beta-adrenergic blocker propranolol showed a synergistic effect with acetylcholine. ACh increased the general anesthetic effect of these compounds in a statistically highly significant dose-dependent fashion. To account for the mechanism of this unusual and novel effect it is proposed that these compounds interact with the anesthetic binding site of the rotifer cholinoceptor ionophore in the open state. It is also proposed that non-ionizing compounds have a general membrane effect only. In addition to anesthesia, atropine and propranolol cause foot paralysis in B. calyciflorus. This other novel effect is also enhanced by acetylcholine as well as decamethonium, a neuromuscular blocker.

Acetylcholine↗
PubMed1979

Isolation and determination of quaternary ammonium compounds by means of amberlite XAD-columns and thin layer chromatography.

The potentials of XAD-columns for the isolation of quaternary ammonium compounds from aqueous media have been investigated. When adequate amounts of counter ions (perchlorate, chloride, phosphate, nitrate) were added to the aqueous sample, to the column pretreatment fluid and to the aqueous washing fluid, most quaternary compounds investigated were retained on the column and could be recovered by elution with methanol. This approach proved also suitable for urine. Quantitation of quaternaries isolated in this way from urine samples could be performed on silicagel thin layer plates through visualization with iodine, followed by densitometric evaluation. For decamethonium detection limits were 0.1 micrograms/ml. Recoveries at the 1 micrograms/ml level were between 80--90% with variation coefficients of less than 10%.

Chromatography, Ion Exchange↗
PubMed1989

[Mass-spectrometric analysis of an anti-microbial preparation decamethoxine].

I. I. Mechnikov Kharkov Research Institute of Microbiology, Vaccines and Sera, Ministry of Public Health of the Ukrainian SSR. The results of mass spectrometric investigation of decamethoxine++, an antimicrobial chemotherapeutic drug, are presented. It was shown that desorption-field mass spectrometry provided recording decamethoxine++ intensive quasimolecular ions [M.Cl]+ and [M]++ forming under conditions of high electric intensity only from the intact parent molecule. Hence, the presence of the peaks in the desorption field mass spectra made it possible to definitively determine decamethoxine++ in the samples. Therefore, the procedure of desorption-field mass spectrometry proved reliable in identification of bisquaternary ammonium compounds. Ways for thermal decomposition and mass spectrometric fragmentation of the decamethoxine++ molecule under various ionization conditions are also discussed.

Anti-Infective Agents↗
PubMed1988

Pharmacologic blockade of ionic channels in lens membranes.

Channel blockers are compounds that disrupt the flow of current through ionic channels in membranes. We use the patch clamp technique to characterize the interactions of blocking particles with individual lens membrane channels. The mean current amplitude at many voltages is determined. The ratios of blocked to unblocked currents at several blocker concentrations are compared to a one binding site model to determine the kd and electrical distance of the site. When channel flickers are too fast to be resolved, the calculation of the power spectral density of the open channel current is useful. It is suggested that channel blockers might be useful therapeutically in some types of cataracts.

Animals↗
PubMed1978

The mode of action of antagonists of the excitatory response to acetylcholine in Aplysia neurones.

1. The mode of action of various antagonists of acetylcholine (ACh) excitatory effects on Aplysia neurones was studied under voltage clamp. ACh was applied by iontophoresis whereas antagonists were applied in the bath. Tubocurarine and hexamethonium were the most thoroughly studied compounds. 2. The 'elementary current', calculated as the ratio of the variance of the ACh noise to the mean ACh induced current, was not modified by any of the antagonists tested. 3. The evolution of the ACh induced current after a voltage jump, which is normally described by a single exponential, was modified by all the antagonists tested. A common feature of the modified relaxations was the appearance, over a certain concentration range of the antagonist, of two successive and opposite exponential components. 4. The characteristics of the composite relaxations depend on the antagonist. For a given antagonist they vary with membrane potential, ACh concentration, and antagonist concentration. 5. The noise power spectra of the ACh induced current showed changes consistent with those of the relaxations. 6. In the absence of antagonists, the current induced by a steady application of ACh increases linearly with hyperpolarization. In the presence of antagonists, the I-V curve shows a marked curvature, indicating a proportionally larger reduction of the ACh response at more negative membrane potentials. 7. The voltage sensitivity of the blocking action of hexamethonium and decamethonium is noticeably stronger than that of monovalent antagonists. 8. A model is proposed which accounts for the observed effects. It assumes that the antagonists studied bind perferentially to the 'activated' ACh-receptor complex, and convert it to a non-conducting state. Kinetic constants can be calculated for this reaction; e.g. for curare, at 12 degrees C and -80 mV, the dissociation and association constants were estimated at 0.1 sec-1 and 4 X 10(5) M-1 sec-1. 9. Partial replacement of the extracellular Na by Tris modifies the relaxations observed in the presence of hexamethonium. Hexamethonium appears less effective in the presence of Tris, which supports the hypothesis that the binding site of the antagonists is linked to the ionic channel.

Acetylcholine↗
PubMedDate not supplied

[The effect of dexamethoxin on the integrity of cytoplasmic membrane in gram-positive and gram-negative microorganisms].

Decamethoxin is shown to be able to increase membrane permeability of Pseudomonas aeruginosa, Escherichia coli and Micrococcus lysodeikticus, that is confirmed by a loss of compounds with the absorption maximum at 260 nm by cells. Parallel with this the number of viable individuals has fallen and activity of dehydrogenases has been inhibited. The aspartate and alanine aminotransferase activity was not inhibited by decamethoxin and even increased. Decamethoxin lysed the protoplasts of the tested microorganisms. At high decamethoxin concentrations (over 500 micrograms/ml for P. aeruginosa and over 200 mu/ml--for E. coli) the outflow of components from the cells of gram-negative bacteria ceased, that may be associated with the coagulation changes in the cytoplasm. A loss of the low-molecular components by M. lysodeikticus cells and lysis of protoplasts proceeded less intensely than the same processes in the gram-negative microorganisms, that is explained by a less resistance of M. lysodeikticus to decamethoxin and earlier coagulation of the cytoplasm preventing lysis.

Anti-Bacterial Agents↗
PubMed1975

A simple, single-injection method for inducing long-term paralysis in embryonic chicks, and preliminary observations on growth of the tibia.

A method for inducing paralysis in embryonic chicks is described. This involves single injections of the neuromuscular blocking agents, D-tubocurrarine Chloride or decamethonium iodide, into 10-day embryos. The dose which optimises survival and paralysis is determined along with the effect of the drugs on embryonic growth. Decamethonium iodide at a dose of 1 mg per embryo gave maximum survival and paralysis to 18 days of incubation. Paralysis was assessed by observation of treated embryos in ovo and by examination of embryos removed from their shells between 11 and 18 days of incubation. Embryos were completely paralysed 24 hours post-injection and remained paralysed until 18 days of incubation. Paralysed embryos failed to hatch. Development of the leg musculature was severely retarded in paralysed embryos. This method of inducing paralysis has considerable advantages over previous continuous infusion methods. The growth and collagen content of the tibia in the paralysed embryos was reduced and these results, and other applications of the method, are discussed.

Acetylcholinesterase↗
PubMed1992

Substrate inhibition of acetylcholinesterase: residues affecting signal transduction from the surface to the catalytic center.

Amino acids located within and around the 'active site gorge' of human acetylcholinesterase (AChE) were substituted. Replacement of W86 yielded inactive enzyme molecules, consistent with its proposed involvement in binding of the choline moiety in the active center. A decrease in affinity to propidium and a concomitant loss of substrate inhibition was observed in D74G, D74N, D74K and W286A mutants, supporting the idea that the site for substrate inhibition and the peripheral anionic site overlap. Mutations of amino acids neighboring the active center (E202, Y337 and F338) resulted in a decrease in the catalytic and the apparent bimolecular rate constants. A decrease in affinity to edrophonium was observed in D74, E202, Y337 and to a lesser extent in F338 and Y341 mutants. E202, Y337 and Y341 mutants were not inhibited efficiently by high substrate concentrations. We propose that binding of acetylcholine, on the surface of AChE, may trigger sequence of conformational changes extending from the peripheral anionic site through W286 to D74, at the entrance of the 'gorge', and down to the catalytic center (through Y341 to F338 and Y337). These changes, especially in Y337, could block the entrance/exit of the catalytic center and reduce the catalytic efficiency of AChE.

Acetylcholinesterase↗
PubMed1990

Paralysis and growth of the musculoskeletal system in the embryonic chick.

Avian embryos can be completely paralyzed by injection of neuromuscular-blocking agents. We used a single injection of decamethonium iodide to paralyze embryos at 7, 8, or 10 days of incubation and analyzed the growth of individual bones (clavicle, mandible, ulna, femur, tibia, humerus) and of individual muscles that act upon some of those bones (clavicular and sternal heads of m. pectoralis, and mm. biceps brachii, depressor mandibulae, pseudotemporalis, and adductor externus). Growth of the bones is not equally affected by paralysis. Only 27% of clavicular growth (by mass) but 77% of mandibular growth occurred in paralyzed embryos, whereas the four long bones exhibited 52-63% of their normal growth. Analysis of muscle weight, fiber length and physiological cross-sectional area (weight/fiber length) indicate that there was greater reduction of the muscles acting on the limbs than of those acting on the mandible, i.e., diminished growth of the skeleton is correlated with reduced muscular activity. Specific retardation of clavicular growth is due to fusion of sternal rudiments and collapse of the thorax, as well as virtual absence of the musculature that normally attaches to the clavicle. We discuss these results in the light of intrinsic and extrinsic factors governing growth of the embryonic skeleton. Paralysis reduces skeletal growth by reducing both the movements taking place in ovo, and the loads imposed on the bones by muscle contraction, changes that represent alterations in the mechanical environment of the skeleton.

Animals↗
PubMedDate not supplied

Myasthenia gravis: a personal view of pathogenesis and mechanism, part 2.

A review of our current knowledge of the etiology and pathogenesis of myasthenia gravis is presented, with particular emphasis on the immunological aspects of the disease. Part 1, published in the January/February issue of MUSCLE & NERVE, dealt with the clinical and genetic features of myasthenia gravis which led to the autoimmune theory of the etiology of the disease. Part 2, which appears in this issue, provides a review of the dysfunction of physiology, pharmacology, and structure of the neuromuscular junction in myasthenia gravis, and the part played by the autoimmune process.

Autoimmune Diseases↗