Neuromuscular blocking agents skeletal muscle effects

The cholinesterase inhibitors have important therapeutic and toxic effects at the skeletal muscle neuromuscular junction. Low (therapeutic) concentrations moderately prolong and intensify the actions of physiologically released acetylcholine. This increases the strength of contraction, especially in muscles weakened by curare-like neuromuscular blocking agents... 

Leuwer M, Motsch P 1996 Neuromuscular blocking agents and skeletal muscle relaxants. In Dukes M N G (ed), Meyler s side-effects of drugs. Elsevier, Amsterdam, pp. 298-346... 

Succinylcholine, a depolarizing neuromuscular blocking agent (0.3 to 1.1 mg/kg IV over 10 to 30 seconds), is used to induce skeletal muscle relaxation to facilitate intubation, ventilation, or orthopedic manipulations and to lessen muscular contraction in convulsions induced by physicians. A peripheral nerve stimulator may be used to monitor effects and degree of blockade. 

Muscle Isoflurane produces some relaxation of skeletal muscle via its central effects. It also enhances the effects of depolarizing and nondepolarizing muscle relaxants. Isoflurane is more potent than halothane in its potentiation of neuromuscular blocking agents. The drug relaxes uterine smooth muscle and is not recommended for analgesia or anesthesia for labor and vaginal delivery. 

De urane produces direct skeletal muscle relaxation and enhances the effects of nondepolarizing and depolarizing neuromuscular blocking agents. Consistent with its minimal metabolism, desflurane has no reported nephrotoxicity or hepatotoxicity. 

Muscle Sevoflurane produces skeletal muscle relaxation and enhances the effects of nondepolarizing and depolarizing neuromuscular blocking agents. 

Other tissues The effects of these drugs on the heart are discussed in Chapter 14 (see class I antianhythmic agents). Most local anesthetics also have weak blocking effects on skeletal muscle neuromuscular transmission, but these actions have no clinical application. The mood elevation induced by cocaine probably reflects actions on dopamine or other amine-mediated synaptic transmission in the CNS rather than a local anesthetic action on membranes. 

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