Succinylcholine is the only therapeutic depolarizing blockingdrug. Although it’s similar to the nondepolarizing blockers in its therapeutic effect, its mechanism of action differs. Succinyl-choline acts like acetylcholine, but it isn’t inactivated by cholinesterase. It’s the drug of choice when short-term muscle re-laxation is needed.
Because succinylcholine is absorbed poorly from the GI tract, the preferred administration route is I.V.; the I.M. route can be used, if necessary.
Succinylcholine is hydrolyzed in the liver and plasma by the en-zyme pseudocholinesterase, producing a metabolite with a nonde-polarizing blocking action. Succinylcholine is excreted by the kid-neys, with a small amount excreted unchanged.
After administration, succinylcholine is rapidly metabolized, but at a slower rate than acetylcholine. As a result, succinylcholine re-mains attached to receptor sites on the skeletal muscle membrane for a longer period of time. This prevents repolarization of the mo-tor end plate and results in muscle paralysis.
Succinylcholine is the drug of choice for short-term muscle relax-ation, such as during intubation and ECT.
The action of succinylcholine is potentiated by a number of anes-thetics and antibiotics. In contrast to their interaction with nonde-polarizing blockers, anticholinesterases increase succinylcholine blockade. (See Adverse reactions to succinylcholine.)