PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Decamethonium Compounds”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

Cardiac vagolytic action of some neuromuscular blockers.

Cardiac vagolytic effect of four commonly used neuromuscular blockers, (viz. D-tubocurarine, decamethonium, pancuronium and gallamine) was compared in midcollicular decerebrate rats. The intravenous doses of neuromuscular blockers used (d-tubocurarine: 0.1 mg/kg; decamethonium: 2 mg/kg; pancuronium: 0.1 mg/kg; gallamine: 20 mg/kg) were sufficient to produce the paralysis of respiratory muscles. Bradycardia was induced by electrical stimulation of the vagus or by injecting dimethyl-phenyl-piperazinium (DMPP; a ganglionic stimulant). It was observed that d-tubocurarine and decamethonium were devoid of cardiac vagolytic action. On the other hand, pancuronium and gallamine inhibited significantly the bradycardia induced by electrical stimulation of the vagus or injection of DMPP; gallamine was found to have greater vagolytic action. The pressor responses to DMPP were not attenuated by pancuronium and gallamine indicating that in the dose administered, these agents did not block the ganglia. Bradycardia induced by the administration of acetylcholine in the left atrium was also attenuated by pancuronium and gallamine suggesting that the drugs produce cardiac vagolytic action by acting on the post-synaptic cholinergic receptors of the heart.

Acetylcholine↗

Interactive responses to stimulation of the amygdaloid central nucleus and baroreceptor afferent activation in the rabbit.

Recent evidence suggests that the amygdaloid central nucleus (ACE) may contribute to the regulation of arterial baroreceptor-vagal reflex sensitivity. To obtain additional data relevant to this suggestion, interactions between stimulation of the ACE and arterial baroreceptor afferent activation were examined. New Zealand rabbits were anesthetized with alpha-chloralose and a stimulating electrode was implanted stereotaxically in the ACE. In the first series of experiments, cardiovascular responses to stimulation of the ACE were assessed during periods in which blood pressure was decreased using sodium nitroprusside or increased in the rostral arterial compartment by inflating the tip of a Swan-Ganz catheter positioned in the descending aorta. It was found that the magnitude of bradycardia to stimulation of the ACE was correlated with the level of arterial blood pressure at the onset of stimulation, such that higher blood pressures were associated with larger bradycardic responses. These data suggest that arterial baroreceptor afferent activity may be an important factor in the elicitation of bradycardia from the ACE. In the second series of experiments, the aortic nerve was isolated, and cardiovascular responses to stimulation of the aortic nerve and to low frequency (5 Hz) stimulation of the ACE were assessed both alone and in combination. Stimulation of the aortic nerve during low frequency stimulation of the ACE was found to produce bradycardia of a significantly larger magnitude than the sum of the responses produced by each stimulus presented alone. These data demonstrate that bradycardia to stimulation of baroreceptor afferent fibers is augmented significantly during low frequency stimulation of the ACE. Taken together, these results are consistent with the notion that the ACE may contribute to the sensitivity of the arterial baroreceptor-vagal reflex.

Afferent Pathways↗

Properties and affinity purification of the mixed-type putative acetylcholine receptor from wild and a mutant strain of hose flies.

Binding of decamethonium to a soluble preparation from house fly head (either wild or a mutant strain) showed a single kind of binding with values for wild strain of Kd = 0.095 micrometers and Bmax = 0.22 nmol/mg protein. The mutant had a four-fold greater affinity and a seven-fold lesser amount. The binding was blocked by both nicotinic and muscarinic drugs. The decamethonium binding migrated in sucrose gradients as a single peak, with sedimentation coefficient s20,w = 12.5 S and therefore a molecular weight of 342 000. Purification by affinity chromatography was achieved with only partial loss of activity, andthe purified material demonstrated a single band on analytical disc gel electrophoresis. Electrophoresis in sodium dodecyl sulphate gels showed two subunits of molecular wegiths 94 000 and 64 000. Both subunits had an isoelectric point of 4.8.

Animals↗

Substrate-ligand interactions with acetylcholinesterase and energetics of binding.

Ester hydrolysis by acetylcholinesterase (from electric eel, Electrophorus electricus) increased in the presence of low concentrations (ca 10(-7) M) of edrophonium, propidium, d-tubocurarine, gallamine, decamethonium or bis-N-methylacridinium, and decreased at higher concentrations. The overall sensitivity of the substrates to inhibition by the ligands was acetylcholine (Ach) greater than phenylacetate (PA) greater than indophenylacetate (IPA). Complete (saturable) inhibition was unattainable with edrophonium or gallamine for IPA and, to a lesser degree, with propidium for PA. Reaction heats between the enzyme and the ligands (edrophonium, propidium and decamethonium) measured directly in a microcalorimeter revealed binding sites that are different from each other in their interaction energetics.

Acetylcholinesterase↗