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Neuromuscular blockers - Tubocurarine Atracurium Cisatracurium Mivacurium Rocuronium Pancuronium Vecuronium Succinylcholine AchE inhibitors - Neostigmine Edrophonium Muscarinic Antagonists - Glycopyrrolate Spasmolytics - Dantrolene Diazepam Baclofen Tizanidine Gabapentin Progabide Glycine Idrocilamide Riluzole Dantrolene Botulinum toxin Cyclobenzaprine Neuromuscular blockers. - Used during surgical procedures and in intensive care units to cause paralysis. NONDEPOLARIZING BLOCKERS - • They are competitive antagonists. In small clinical doses they act predominantly at the nicotinic receptor site by competing with acetylcholine. Their action can be overcome by increasing the concentration of acetylcholine in the synaptic cleft; this can be achieved, for example, by administration of acetylcholinesterase inhibitors such as neostigmine or edrophonium. Anaesthesiologists use this strategy to shorten the duration of the neuromuscular blockade. • In larger doses, nondepolarizing blockers also enter the pore of the ion channel to cause a more intense motor blockade. This further weakens neuromuscular transmission and diminishes the ability of acetylcholinesterase inhibitors to antagonize the action of nondepolarizing blockers. • Nondepolarizing blockers may also block prejunctional sodium channels. As a result, they reduce the release of acetylcholine at the nerve ending. • During anesthesia, the IV administration of a nondepolarizing blocker first causes motor weakness; ultimately, skeletal muscles become totally flaccid and inexcitable to stimulation. Larger muscles (e.g. those of the trunk) are more resistant to block and recover more rapidly than smaller ones (e.g. muscles of the hand).