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Cycrimine on rat diaphragm
Archives Internationales De Pharmacodynamie Et De Therapie
|January 1, 1976
Summary
Cycrimine hydrochloride, an anti-Parkinson drug, causes neuromuscular blockade by directly affecting the muscle, not nerve transmission. This action is independent of other neuromuscular agents.
Area of Science:
- Pharmacology
- Neuroscience
- Muscle Physiology
Background:
- Cycrimine hydrochloride is an anti-Parkinson drug with central cholinolytic properties.
- Its effects on neuromuscular function require further elucidation.
Purpose of the Study:
- To investigate the mechanism of neuromuscular blockade induced by cycrimine hydrochloride.
- To determine the site of action of cycrimine at the neuromuscular junction.
Main Methods:
- Isolated rat diaphragm preparation.
- Administration of cycrimine hydrochloride, neostigmine, tetraethylammonium, and d-tubocurarine.
- Pharmacological denervation of the rat diaphragm.
- Retrograde intravenous injection of acetylcholine.
Main Results:
- Cycrimine hydrochloride induced neuromuscular blockade in the rat diaphragm.
- The blockade was unaffected by neostigmine and tetraethylammonium.
- Low concentrations of cycrimine potentiated d-tubocurarine-induced paralysis.
- Cycrimine caused paralysis in pharmacologically denervated preparations.
- Acetylcholine responses were inhibited by cycrimine.
Conclusions:
- Cycrimine hydrochloride produces neuromuscular blockade through a direct postsynaptic effect on the muscle.
- The drug's action is not mediated by altering nerve impulse transmission or by affecting acetylcholine release.