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Biomedical subjects

J Faff

Publications and source records attributed to J Faff.

35 records · Page 2Linked to original sources
PubMedDate not supplied

Adaptation of neuromuscular junction to transmission of impulses after inactivation of acetylcholinesterase.

Adaptation of neuromuscular junction to transmission of impulses after inactivation of acetylcholinesterase. Acta Physiol. Pol., 1977, 28 (1): 23-30. Isolated preparation of rat diaphragm with phrenic nerve was incubated in paraoxon solutions which caused complete inactivation of acetylcholinesterase. This inactivation was associated with disturbances of neuromuscular transmission in the form of blockade of the tetanic response, post-tetanic inhibition of twitch responses and a decreased amplitude of the second response after the first one when two stimuli at a short interval were used. These disturbances were withdrawn somewhat during further incubation of the preparation, although it was kept in paraoxon solution which maintained complete inactivation of acetylcholinesterase. It is suggested that the observed recession of transmission disturbances may be caused by partial adaptation of blockade of the tetanic response, post-tetanic inhibition of twitch blockade of enzymatic hydrolysis of acetylcholine.

Acetylcholinesterase↗
PubMedDate not supplied

Fluostigmine effect on glycogen level in the skeletal muscle.

Fluostigmine in a dose not producing evident toxicity reduced the glycogen content in the gastrocnemius muscle in rats, with a consequent decrease of glycogen utilization during contractions of the muscle induced with direct tetanic stimuli. Administration of atropine or atropine with obidoxime failed to change this effect of fluostigmine. The authors suggest that the effect is not due to disturbances of the cholinergic system function.

Animals↗
PubMedDate not supplied

The effect of certain electrolytes on neuromuscular transmission disturbances evoked by direct action of phospholine on synaptic structures.

In an isolated preparation of rat diaphragm stimulated indirectly (12 impulses per minute) after total inactivation of acetylcholinesterase phospholine reduced the amplitude of the response proportional to its concentration. The rise in the concentration of potassium, magnesium or calcium in the incubation fluid failed to alleviate the disturbances produced by phospholine. Phospholine increased significantly reduction of response amplitude caused by increased calcium and magnesium concentration and increased to a small extent response depression caused by raised potassium concentration. The obtained results, point out that phospholine exerts a direction on the neuromuscular junction which is connected with the postsynaptic action of this agent.

Animals↗
PubMedDate not supplied

Protective effects of a series of new pyridinium derivatives against inhibition of acetylcholinesterase by fluostigmine.

The protective effects of a series of new pyridinium derivatives against inhibition of acetylcholinesterase (AChE) by fluostigmine was studied in vitro on human erythrocytes. It was stated that some of these compounds exhibit protective action for AChE against inhibition by fluostigmine. The best protective index had N-methyl-4-[gamma-pyridyl]-pyridinium iodide.

Acetylcholinesterase↗
PubMedDate not supplied

Neuromuscular function in fluostigmine intoxication.

In experiments with isolated nerve-diaphragm preparation and intact anterior tibial muscle of the rat, it was found that repeated administration of fluostigmine (1 to 30 days) caused a decrease of the indirectly elicited tetanic response and post-tetanic depression of twitch response. Impairment of neuromuscular transmission increased during the first days of treatment. In the following period marked recovery occurred in spite of further fluostigmine administration. The recovery of neuromuscular function was much more pronounced in diaphragm preparation than in the anterior tibial muscle. It was not associated with any recovery in the activity of inhibited acetylcholinesterase. The sensitivity of the neuromuscular junction to carbachol increased during the first days of treatment and then decreased in the later stage. The sensitivity to d-tubocurarine in the diaphragm preparation decreased on the tenth day of treatment and returned to normal value after 30 days. In the anterior tibial muscle the sensitivity to d-tubocurarine slightly decreased on the fifth day, and after 20 to 30 days, was markedly increased. The underlying mechanisms are discussed.

Acetylcholinesterase↗