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At least 865 records · Page 48Linked to original sources
PubMed1984

[Heterogeneity of antibodies blocking the binding of bungarotoxin to the acetylcholine receptor in myasthenia].

Inhibitory effect of myasthenic patients antibodies on alpha-bungarotoxin binding to the human acetylcholine receptor has been demonstrated by radioimmunoassay. By using decamethonium, an acetylcholine agonist, we have shown the existence of two antibody sub-groups reacting with the toxin-binding site: one sub-group is represented by antibodies which block the binding directly, the other by antibodies that inhibit the binding, only in the presence of decamethonium.

Antibodies↗
PubMed1983

The role of movements in the development of sutural and diarthrodial joints tested by long-term paralysis of chick embryos.

Chick embryos were paralysed in ovo with a neuromuscular blocking agent between 8 and 20 days of incubation. To evaluate the rôle of muscular activity in the development of sutural articulations, sutures of the cranial vault of control and paralysed embryos were studied histologically and the findings compared with the effect of the agent on the development of the ankle joint and some synovial joints of the jaws. Paralysed embryos showed a consistent lack of development of joint cavities in synovial joints. In most embryos, fusion of opposing cartilaginous elements had occurred. In contrast to synovial joints, sutural articulation showed a micromorphology comparable to that of controls. The findings indicate that different embryonic factors regulate the development of sutural and synovial articulations. Movements of neuromuscular origin play no essential role in the morphogenetic development of sutures, but are a prerequisite for the formation of joint cavities and other specialised structures of synovial joints.

Animals↗
PubMed1983

Erythrocyte membrane stabilization by decamethonium and succinylcholine.

The effects of decamethonium and succinylcholine on hypotonic haemolysis of erythrocytes were studied. These drugs at concentrations of 5 X 10(-8) M to 10(-4) M caused a dose-dependent inhibition of haemolysis of erythrocytes in 0.45% NaCl but lysis occurred when the drug concentrations were increased to 10(-3) M. These results indicate that decamethonium and succinylcholine may have a membrane stabilization-lysis effect on erythrocytes.

Decamethonium Compounds↗
PubMed1983

[Inhibition of cholinesterases by aziridinium derivatives of polymethylene bischloroethylamines].

Cyclization of polymethylene bischloroethylamines, differing in the methylene chain-length (n = 6 or 10) and the N-substituents (R = CH3 or CH2C6H5), was carried out and the respective aziridinium derivatives were obtained. These derivatives of hexamethonium and decamethonium manifested reversible inhibition (Ki approximately 100-1 microM) and irreversible alkylating activity (kII approximately 10(2) M-1 . min-1) towards acetylcholinesterase from human erythrocytes and horse serum butyrylcholinesterase. Upon varying n and R, the alkylation biomolecular rate constants changed symbately with changes in the reversible inhibition constants. The most potent alkylating agent with respect to acetylcholinesterase (kII 7,8 x 10(2) M-1 . min-1) and butyrylcholinesterase (kII 4,2 . 10(2) M-1 . min-1) was found to be the aziridinium analog of hexamethonium with R = CH2C6H5. Based on the kinetic data, the problem of alkylation of anionic sites in the catalytic and allosteric centers of the two cholinesterases is discussed.

Acetylcholinesterase↗
PubMed1983

Interaction of cholinergic ligands with the purified acetylcholine receptor protein. I. Equilibrium binding studies.

We have studied the binding equilibria of two fluorescent ligands and several nonfluorescent cholinergic ligands with the purified acetylcholine receptor from Electrophorus electricus. The assay was based on the specifically cholinergic and reversible quenching of fluorescence observed upon complex formation between the receptor protein and N-7-(4-nitrobenzo-2-oxa-1,3-diazole)-5-aminopentanoic acid beta-(N-trimethylammonium) ethyl ester. This way, a large body of accurate, true equilibrium data was obtained. We find 1) all ligands studied compete for the same number of binding sites at the receptor; 2) agonists compete for half of these sites with high affinity and for the other half of these sites with significantly lower affinity; 3) antagonists compete for all of these sites with one affinity; and 4) in the presence of disulfide reducing agents, the binding patterns of some agonists and antagonists are changed in accordance with the electrophysiological changes observed under the same conditions with Rana pipiens Sartorius muscle fibers. Our studies indicate that the mechanism of ligand recognition is still functional at equilibrium and is not subject to the presence of an intact membrane environment. Furthermore, the existence of two types of agonist sites at every receptor molecule excludes most of the presently discussed two-state models as the basis for a mechanism of receptor-ligand interaction. To explain sigmoidal dose-response curves, a two-site model is already sufficient.

4-Chloro-7-nitrobenzofurazan↗
PubMed1978

Transport interaction phenomena between monoquaternary and polymethylene-bisquaternary amines in mouse kidney cortex slices.

The polymethylene-bisquaternary amine 14C-decamethonium accumulates in mouse kidney cortex slices incubated in Krebs-Ringer bicarbonate buffer (37 degrees C, pH 7.4) aerated with O2-CO2 95:5 v/v%. The accumulation rate was enhanced in the presence of monoquaternary amines which on the other hand depressed maximum accumulation ratio of decamethonium in the tissue. The stimulation phenomenon was apparently related to the intracellular concentration of monoquaternary amine since tissue preloaded with a monoquaternary amine took up decamethonium at an increased rate. This effect was due to an accelerated influx of decamethonium and not to inhibition of efflux since no decamethonium efflux was shown to occur in wash-out experiments. Flux stimulation may represent an interaction phenomenon of accelerative exchange diffusion type. Furthermore, various amines inhibited accumulation of decamethonium in a competitive manner. The study supports the idea that common steps are involved in cellular transport of monoquaternary and polymethylene-bisquaternary amines in the kidney.

Animals↗
PubMed1978

Ionic and metabolic requirements for decamethonium transport in mouse kidney cortex slices.

Decamethonium accumulates in mouse kidney cortex slices incubated in Krebs-Ringer bicarbonate buffer (37 degrees C, pH 7.4) aerated with O2-CO2 95:5 v/v%. Maximum tissue-medium accumulation ratio decreased with increasing external decamethonium concentration. Decamethonium was released from the tissue at a slow rate. The metabolic inhibitor cyanide inhibited accumulation of decamethonium but did not produce release of decamethonium already accumulated in the tissue. Substitution of external Na+ by other cations depressed decamethonium uptake. However, this cannot be ascribed to absence of Na+ since no inhibition occurred when Na+ was substituted by isoosmotic sucrose. Decamethonium uptake is inhibited when active Na+-transport is impaired (omission of K+ or addition of ouabain). The slow onset of this inhibition is compatible with the idea that it may be secondary to changes in the intracellular electrolyte concentrations. Furthermore, decamethonium uptake was depressed in absence of external Ca2+.

Animals↗
PubMedDate not supplied

[Effect of decamethoxin, decamine and levorin on the carbohydrate-protein component content in the liver connective tissue of white rats].

It has been shown in rat experiments that decamethoxin increases the level of acid glycosaminoglycans, glyco- and mucoproteins, whereas decamin lowers the content of total glycoproteids at the expense of changes in the content of glyco- and mucoproteins. Levorin has been demonstrated to bring down the content of total glycoproteins and oxyproline in the liver.

Animals↗