Curare neuromuscular blockade

Neuromuscular blockade Neurotoxicity can occur. Aminoglycosides may aggravate muscle weakness because of a potential curare-like effect on the neuromuscular junction. 

In very high doses, aminoglycosides can produce a curare-like effect with neuromuscular blockade that results in respiratory paralysis. This paralysis is usually reversible by calcium gluconate (given promptly) or neostigmine. Hypersensitivity occurs infrequently. 

The sudden absorption of postoperatively instilled kanamycin from the peritoneal cavity (3-5 g) has resulted in curare-like neuromuscular blockade and respiratory arrest. Calcium gluconate and neostigmine can act as antidotes. 

Protein components of the venom of the banded krait (Bungarus multicinctus). Two major components a- and (3-bungarotoxins. ct-Bungarotoxin binds irreversibly to ACh receptor causing neuromuscular blockade and muscle paralysis similar to effects of curare, p-Bungarotoxin contains several components prevents ACh release at skeletal neuromuscular junction. Crude venom LD50 SC mouse, 0.16 mg/kg bw. 

Historically, Bernard (1851, 1856) demonstrated that curare (from arrow poisons used by South American Indians) blocked nerve impulse transmission at the junction of the nerve and skeletal muscle. It was later shown that many alkaloids, such as morphine, atropine, nicotine, and even strychnine and brucine (the latter two normally causing convulsions), will become muscle relaxants when quaternized by methylation. It soon became apparent that a great many quaternary ammonium compounds qualitatively share the ability to produce neuromuscular blockade. In fact, the onium ion need not be a nitrogen atom. Thus sulfonium (/ 3S+), phosphonium (/ 3P+), and arsonium (/ 3As+) ions have been shown to be curariform , although of lesser activity than ammonium ions. 

Edrophonium is an anticholinesterase muscle stimulant that facihtates myoneural junction impulse transmission by inhibiting acetylcholine destmction by cholinesterase. It is indicated in differential diagnosis of myasthenia gravis as an adjunct in evaluating treatment of myasthenia gravis in evaluation of aner-gency treatment of myasthenic aises in reversal of neuromuscular blockade by curare gallamine or tubo-curarine and in treatment of respiratory depression caused by curare overdose. 

Neuromuscular blockade Though rare, a curare-like block may occur at high doses of aminoglycosides and may result in respiratory paralysis. It is usually reversible by treatment with calcium and neostigmine, but ventilatory support may be required. 

The effects of curare develop rapidly after it enters the body. Victims develop rapid weakness of voluntary muscles followed by paralysis, respiratory failure, and death. The cause is a blockade of nicotinic cholinergic receptors at the neuromuscular junctions in skeletal muscle. Unlike botulinum toxin, release of acetylcholine by the cholinergic nerve terminals is not affected. When curare is present, however, the acetylcholine that is released cannot bind to the receptors because they are reversibly occupied by the curare. As a consequence, nerve-muscle communication fails and paralysis ensues. 

Penicillins G and V (119) have been reported to cause neuromuscular block in animal preparations, but only at exceptionally high doses. Calcium is effective in reversal. The acylaminopenicillins augment vecuronium-induced blockade (120). Possible re-curarization with piperacillin was successfully reversed by neostigmine (121). 

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