Neuromuscular-blocking drugs

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Global view of a neuromuscular junction:
1. Axon
2. Motor end-plate
3. Muscle fiber
4. Myofibril
Detailed view of a neuromuscular junction:
1. Presynaptic terminal
2. Sarcolemma
3. Synaptic vesicle
4. Nicotinic acetylcholine receptor
5. Mitochondrion

Neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished either by acting presynaptically via the inhibition of acetylcholine (ACh) synthesis or release, or by acting postsynaptically at the acetylcholine receptor. While there are drugs that act presynaptically (such as botulin toxin and tetrodotoxin), the clinically-relevant drugs work postsynaptically.

Clinically, neuromuscular block is used as an adjunct to anesthesia to induce paralysis, so that surgery, especially intra-abdominal and intra-thoracic surgeries, can be carried out with fewer complications. Because neuromuscular block may paralyze muscles required for breathing, mechanical ventilation should be available to maintain adequate respiration.

Patients are still aware of pain even after full conduction block has occurred; hence, general anesthetics and/or analgesics must be given to prevent anesthesia awareness.


These drugs fall into two groups:

  • Non-depolarizing blocking agents: These agents constitute the majority of the clinically-relevant neuromuscular blockers. They act by blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.[1]
  • Depolarizing blocking agents: These agents act by depolarizing the plasma membrane of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.

Non-depolarizing blocking agents

All of these agents act as competitive antagonists against acetylcholine at the site of postsynaptic acetylcholine receptors.

Tubocurarine, found in curare of the South American plant genus Strychnos, is the prototypical non-depolarizing neuromuscular blocker. It has a slow onset (>5 min) and a long duration of action (1-2 hours). Side effects include hypotension, which is partially explained by its effect of increasing histamine release, a vasodilator,[2] as well as its effect of blocking autonomic ganglia.[3] It is excreted in the urine.

This drug needs to block about 70-80% of the Ach receptors for neuromuscular conduction to fail, and hence, for effective blockade to occur. At this stage, end-plate potentials (EPPs) can still be detected, but are too small the reach the threshold potential needed for activation of muscle fiber contraction.

Examples of these drugs used clinically include:

Ultra short-acting:


  • Onset: 90 seconds, Duration: 12-18 minutes
  • Benzyl-Isoquinolinium agent: needs to be refrigerated, and causes release of histamine
  • No longer manufactured secondary to marketing, manufacturing, financial concerns


  • Onset: 90 seconds, Duration: 60-80 minutes
  • Benzyl-Isoquinolinium agent: needs to be refrigerated, and causes release of histamine
  • Racemic mixture
  • Toxic metabolite called laudanosine, greater accumulation in individuals with renal failure
  • Laudanosine decreases seizure threshold
  • Onset: 90 seconds, Duration: 60-80 minutes
  • Benzyl-Isoquinolinium agent: needs to be refrigerated, and causes release of histamine
  • Stereospecific enantiomer
  • -Non-organ elimination via Hoffmann elimination (pH & temperature specific)
  • Onset: 60 seconds, Duration: 70-120 minutes
  • Aminosteroid: non-refrigerated, and may promote muscarinic block
  • Onset: 75 seconds, Duration: 45-70 minutes
  • Aminosteroid: non-refrigerated, and may promote muscarinic block


  • Onset: 90 seconds, Duration: >180 minutes
  • Aminosteroid: non-refrigerated, and may promote muscarinic block

Depolarizing blocking agents

Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. However, these agents are more resistant to degradation by acetylcholinesterase, the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers. This differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle.

There are two phases to the depolarizing block. During phase I (depolarizing phase), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually, after sufficient depolarization has occurred, phase II (desensitizing phase) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. At this point, full neuromuscular block has been achieved.

The prototypical depolarizing blocking drug is succinylcholine (suxamethonium). It is the only such drug used clinically. It has a rapid onset (30 seconds) but very short duration of action (5-10 minutes) because of hydrolysis by various cholinesterases. Succinylcholine was originally known as diacetylcholine because structurally it is composed of two acetylcholine molecules joined with a methyl group. Decamethonium is sometimes, but rarely, used in clinical practice.

Inhibition of acetylcholinesterase may be used to cause the same effect as a depolarizing neuromuscular block.

Comparison of drugs

The main difference is in the reversal of these two types of neuromuscular-blocking drugs.

  • Non-depolarizing blockers are reversed by acetylcholinesterase inhibitor drugs. Since they are competitive antagonists at the ACh receptor so can be reversed by increases in ACh.
  • The depolarizing blockers already have ACh-like actions, so these agents will have prolonged effect under the influence of acetylcholinesterase inhibitors. The administration of depolarizing blockers will initially exhibit fasciculations (a sudden twitch just before paralysis occurs). This is due to the depolarization of the muscle. Also, post-operative pain is associated with depolarizing blockers.

The tetanic fade is the failure of muscles to maintain a fused tetany at sufficiently-high frequencies of electrical stimulation.

  • Non-depolarizing blockers will have this effect on patients.
  • Depolarizing blockers will not.

Adverse effects

Since these drugs may cause paralysis of the diaphragm, mechanical ventilation should be at hand to provide respiration.

Additionally, these drugs may exhibit cardiovascular effects, since they are not fully selective for the nicotinic receptor and hence may have effects on muscarinic receptors.[3] If nicotonic receptors of the autonomic ganglia or adrenal medulla are blocked, these drugs may cause autonomic symptoms. Additionally, neuromuscular blockers may facilitate histamine release, which causes hypotension, flushing, and tachycardia.

In depolarizing the musculature, suxamethonium may trigger a transient release of large amounts of potassium from muscle fibers. This puts the patient at risk for life-threatening complications, such as hyperkalemia and cardiac arrhythmias.


  1. Bufler J, Wilhelm R, Parnas H, Franke C, Dudel J (1996). "Open channel and competitive block of the embryonic form of the nicotinic receptor of mouse myotubes by (+)-tubocurarine". J. Physiol. (Lond.). 495 ( Pt 1): 83–95. PMID 8866353.
  2. Inada E, Philbin DM, Machaj V; et al. (1986). "Histamine antagonists and d-tubocurarine-induced hypotension in cardiac surgical patients". Clin. Pharmacol. Ther. 40 (5): 575–80. PMID 2429800.
  3. 3.0 3.1 Ostergaard D, Engbaek J, Viby-Mogensen J (1989). "Adverse reactions and interactions of the neuromuscular blocking drugs". Medical toxicology and adverse drug experience. 4 (5): 351–68. PMID 2682131.

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