Skeletal muscle relaxation can be produced by deep inhalational anesthesia, regional nerve block, or neuromuscular junction blocking agents ( commonly called musclar relaxants). in 1942 Harorld publized the result of syudy using a refined axtract of curare during anesthesi.
MECHANISM OF ACTION
Neuromuscular blocking agents are devided into two classes : depolarizing and nondeporarizing, this division ferlects distinc differences in :
1. mechanism of action
2. resonse to peripheral nerve stimulation and
3. reversal of block
mechanism of action
depolarizing muscle relaxants physically resemble ACh and therefore bind to ACh reseptor, generating a muscle action potensial, however, unlike ACh these drugs are not metabolized by acetylcholinesterase, thus their consentration in the synaptic cleft doest not fall as rapidly, resulting in a prolonged deporarization of the muscle endplate.
Continuous endplate depolarization causes muscle relaxation in the following way. As has been explained, an endplate potensial of sufficient strength will result in generation of an action potential in the neighboring perijuctional muscle membrane. However, the subequent opening of perijunctional sodium chanels is time-limeted. After initial-axcitation and opening, these ion chanels close. furthermore, these sodium chanels cannot reopen until the endplate repolarizes, which is not possible as long as a depolarizer continues to bind to ACh reseptors. once the perijunctional chanels close, the action potensial disappears and the membrane downstream return to its resting state, resulting in muscle relaxation, tihs is a phase i block.
Nondepolarizing muscle relaxants aso bind to ACh reseptor but are incapable of inducing the conformational change necessary for ion chanel opening since ACh is precluded from binding to its reseptors no endplate potensial develops.
