Muscle relaxation is useful in a variety of surgeries including laparoscopic cases such as this. When used during induction, muscle relaxants help provide optimal intubating conditions by inhibiting contraction of the muscles attached to the vocal cords, allowing for ease of passage of the endotracheal tube. Additionally, neuromuscular blockers can improve surgical conditions in many instances, facilitating the safe and efficient completion of the surgery.

Neuromuscular blockers act at the acetylcholine receptor, located largely in the neuromuscular junction. The receptors are composed of five subunits—two alpha subunits, one beta, one delta, and one epsilon. Acetylcholine binds to the alpha subunits, as do most neuromuscular blocking medications. There are two classes of acetylcholine receptors—nicotinic and muscarinic. Nicotinic receptors are located on skeletal muscle and autonomic ganglia and are the site of action of neuromuscular blocking medications. Muscarinic acetylcholine receptors are found throughout the body in smooth muscle, the SA and AV node in the heart and in the secretory glands.

The transmission of a signal begins with an action potential moving down a nerve causing calcium influx through voltage gated calcium channels. The sudden increase in intracellular calcium leads to the movement of acetylcholine-containing storage vesicles from the cytoplasm to the cell membrane. At the cell membrane, the vesicles fuse and release acetylcholine into the neuromuscular junction. The acetylcholine molecules cross the junction and bind to nicotinic acetylcholine receptors at the motor end plate. In order for a conformational change to occur in the nicotinic acetylcholine receptor, both alpha subunits making up the receptor must have an acetylcholine molecule bound to them. Once two acetylcholine molecules are bound, the receptor conformational change opens an ion channel, allowing sodium and calcium to move into the cell and for potassium to move out. The movement of these ions causes a change in potential across the cellular membrane. When enough receptors are triggered and a large enough potential difference exists across the perijunctional membrane, depolarization occurs. This leads to opening of sodium channels on the muscle cell membrane, causing calcium to leave the sarcoplasmic reticulum. This sudden increase in intracellular calcium allows actin and myosin to interact and cause muscle contraction.

The immature acetylcholine receptor is found in fetal muscle and contains a gamma instead of epsilon subunit. Immature acetylcholine receptors are also called extrajunctional receptors because they can also be located outside of the neuromuscular junction when found in adults.

As acetylcholine molecules diffuse away from the nicotinic receptors on the motor end plate, the molecules are rapidly broken down in the neuromuscular junction by the enzyme acetylcholinesterase into choline and acetate. The choline can then be taken up by the presynaptic membrane and converted back into acetylcholine. Acetylcholinesterase is located at the motor end plate adjacent to the acetylcholine receptors.

The two classes are depolarizing and nondepolarizing muscle relaxants. Succinylcholine is the only depolarizing neuromuscular blocking drug in clinical use. There are several different nondepolarizing muscle relaxants, examples of which include rocuronium, vecuronium, cisatracurium, and pancuronium.

Structurally similar to acetylcholine, depolarizing neuromuscular blockers (succinylcholine) bind at the acetylcholine binding site (alpha subunits) and cause propagation of an action potential. Unlike acetylcholine, however, depolarizing muscle relaxants are not broken down by acetylcholinesterase. This results in longer binding, leading to which increases the time until the motor end plate can repolarize and causes a short period of muscle relaxation. Thus, they are competitive agonists at the acetylcholine receptor.

When administered to a patient, the majority of a dose of succinylcholine is metabolized before ever reaching the neuromuscular junction. It is broken down quickly and efficiently by plasma pseudocholinesterase (also known as butyrylcholinesterase). The fraction that does reach the neuromuscular junction can then bind the acetylcholine receptor and cause its clinical effects. Subsequently, succinylcholine will redistributes from the neuromuscular junction and is rapidly broken down.

The normal onset of succinylcholine is 30–90 s and the duration of action is 3–5 min. However, this can be significantly lengthened in a variety of situations. Pseudocholinesterase deficiency decreases the amount of enzyme available to break down succinylcholine. For patients who are heterozygous for an atypical pseudocholinesterase gene, the duration of succinylcholine can be 20–30 min. For homozygous patients, a single dose of succinylcholine can cause paralysis for several hours.