Suxamethonium chloride

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Suxamethonium chloride
Suxamethonium-chloride-2D-skeletal.svg
Suxamethonium chloride ball-and-stick.png
Clinical data
Pronunciation /ˌsʌksɪnɪlˈkoʊliːn/
Trade names Quelicin, Anectine, others
AHFS/Drugs.com Monograph
License data
Pregnancy
category
  • AU:A
Routes of
administration 		Intravenous, intramuscular
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability NA
Metabolism By pseudocholinesterase, to succinylmonocholine and choline
Onset of action 30–60 sec (IV), 2–3 min (IM)
Duration of action < 10 min (IV), 10–30 min (IM)
Excretion Kidney (10%)
Identifiers
  • 2,2'-[(1,4-dioxobutane-1,4-diyl)bis(oxy)]bis
    (N,N,N-trimethylethanaminium)
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
Formula C14H30Cl2N2O4
Molar mass 361.30 g·mol−1
3D model (JSmol)
  • [Cl-].[Cl-].O=C(OCC[N+](C)(C)C)CCC(=O)OCC[N+](C)(C)C
  • InChI=1S/C14H30N2O4.2ClH/c1-15(2,3)9-11-19-13(17)7-8-14(18)20-12-10-16(4,5)6;;/h7-12H2,1-6H3;2*1H/q+2;;/p-2 Yes check.svgY
  • Key:YOEWQQVKRJEPAE-UHFFFAOYSA-L Yes check.svgY
 X mark.svgNYes check.svgY  (what is this?)    (verify)

Suxamethonium chloride (brand names Scoline and Sucostrin, among others), also known as suxamethonium or succinylcholine, or simply sux in medical abbreviation, [5] is a medication used to cause short-term paralysis as part of general anesthesia. [6] This is done to help with tracheal intubation or electroconvulsive therapy. [6] It is administered by injection, either into a vein or into a muscle. [7] When used in a vein, onset of action is generally within one minute and effects last for up to 10 minutes. [7]

Contents

Common side effects include low blood pressure, increased saliva production, muscle pain, and rash. [7] Serious side effects include malignant hyperthermia, hyperkalemia and allergic reactions. [8] [9] It is not recommended in people who are at risk of high blood potassium or a history of myopathy. [6] Use during pregnancy appears to be safe for the baby. [10]

Suxamethonium is in the neuromuscular blocker family of medications and is of the depolarizing type. [7] It works by blocking the action of acetylcholine on skeletal muscles. [7]

Suxamethonium was described as early as 1906 and came into medical use in 1951. [5] It is on the World Health Organization's List of Essential Medicines. [11] Suxamethonium is available as a generic medication. [7]

Medical uses

A vial of suxamethonium chloride Succhs.jpg
A vial of suxamethonium chloride

Succinylcholine chloride injection is indicated, in addition to general anesthesia, to facilitate tracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. [9]

Its medical uses are limited to short-term muscle relaxation in anesthesia and intensive care, usually for facilitation of endotracheal intubation. It is popular in emergency medicine due to its rapid onset and brief duration of action. The former is a major point of consideration in the context of trauma care, where endotracheal intubation may need to be completed very quickly. The latter means that, should attempts at endotracheal intubation fail and the person cannot be ventilated, there is a prospect for neuromuscular recovery and the onset of spontaneous breathing before low blood oxygen levels occurs. It may be better than rocuronium in people without contraindications due to its faster onset of action and shorter duration of action. [12]

Suxamethonium is also commonly used as the sole muscle relaxant during electroconvulsive therapy, favoured for its short duration of action. [13]

Suxamethonium is quickly degraded by plasma butyrylcholinesterase and the duration of effect is usually in the range of a few minutes. When plasma levels of butyrylcholinesterase are greatly diminished or an atypical form is present (an otherwise harmless inherited disorder), paralysis may last much longer, as is the case in liver failure or in neonates. [14]

The vials are usually stored at a temperature between 2–8 °C, but issues have been reported with lower storage temperatures. [15] The multi-dose vials are stable for up to 14 days at room temperature without significant loss of potency. [4] Unless otherwise indicated in the prescribing information, room temperature for storage of medications is 15–25 °C (59–77 °F). [16]

Side effects

Side effects include malignant hyperthermia, muscle pains, acute rhabdomyolysis with high blood levels of potassium, [14] transient ocular hypertension, constipation [17] and changes in cardiac rhythm, including slow heart rate, and cardiac arrest. In people with neuromuscular disease or burns, an injection of suxamethonium can lead to a large release of potassium from skeletal muscles, potentially resulting in cardiac arrest. Conditions having susceptibility to suxamethonium-induced high blood potassium are burns, closed head injury, acidosis, Guillain–Barré syndrome, cerebral stroke, drowning, severe intra-abdominal sepsis, massive trauma, myopathy, and tetanus.

Suxamethonium does not produce unconsciousness or anesthesia, and its effects may cause considerable psychological distress while simultaneously making it impossible for a patient to communicate. Therefore, administration of the drug to a conscious patient is contraindicated.[ medical citation needed ]

Hyperkalemia

The side effect of high blood potassium may occur because the acetylcholine receptor is propped open, allowing continued flow of potassium ions into the extracellular fluid. A typical increase of potassium ion serum concentration on administration of suxamethonium is 0.5  mmol per liter.The increase is transient in otherwise healthy patients. The normal range of potassium is 3.5 to 5 mEq per liter. High blood potassium does not generally result in adverse effects below a concentration of 6.5 to 7 mEq per liter. Therefore, the increase in serum potassium level is usually not catastrophic in otherwise healthy patients. Severely high blood levels of potassium can cause changes in cardiac electrophysiology, which, if severe, can result in arrhythmias and even cardiac arrest. [18] [19]

Malignant hyperthermia

Malignant hyperthermia (MH) from suxamethonium administration can result in a drastic and uncontrolled increase in skeletal muscle oxidative metabolism. This overwhelms the body's capacity to supply oxygen, remove carbon dioxide, and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly.

Susceptibility to malignant hyperthermia is often inherited as an autosomal dominant disorder, for which there are at least six genetic loci of interest, the most prominent being the ryanodine receptor gene (RYR1). MH susceptibility is phenotype and genetically related to central core disease (CCD), an autosomal dominant disorder characterized both by MH symptoms and by myopathy. MH is usually unmasked by anesthesia, or when a family member develops the symptoms. There is no simple, straightforward test to diagnose the condition. When MH develops during a procedure, treatment with dantrolene sodium is usually initiated; dantrolene and the avoidance of suxamethonium administration in susceptible people have markedly reduced the mortality from this condition.

Apnea

The normal short duration of action of suxamethonium is due to the rapid metabolism of the drug by non-specific plasma cholinesterases. However plasma cholinesterase activity is reduced in some people due to either genetic variation or acquired conditions, which results in a prolonged duration of neuromuscular block. Genetically, ninety six percent of the population have a normal (Eu:Eu) genotype and block duration; however, some people have atypical genes (Ea, Es, Ef) which can be found in varying combinations with the Eu gene, or other atypical genes (see Pseudocholinesterase deficiency). Such genes will result in a longer duration of action of the drug, ranging from 20 minutes up to several hours. Acquired factors that affect plasma cholinesterase activity include pregnancy, liver disease, kidney failure, heart failure, thyrotoxicosis, and cancer, as well as a number of other drugs. [20]

If unrecognized by a clinician it could lead to awareness if anesthesia is discontinued whilst still paralyzed or hypoxemia (and potentially fatal consequences) if artificial ventilation is not maintained. Normal treatment is to maintain sedation and ventilate the patient on an intensive care unit until muscle function has returned. Blood testing for cholinesterase function can be performed.[ medical citation needed ]

Mivacurium, a non-depolarizing neuromuscular blocking drug, is also metabolized via the same route with a similar clinical effect in patients deficient in plasma cholinesterase activity.[ medical citation needed ]

Deliberate induction of conscious apnea using this drug led to its use as a form of aversion therapy in the 1960s and 1970s in some prison and institutional settings. [21] [22] [23] This use was discontinued after negative publicity concerning the terrifying effects on subjects of this treatment and ethical questions about the punitive use of painful aversion.[ citation needed ]

Mechanism of action

There are two phases to the blocking effect of suxamethonium.

Phase 1 block

Phase 1 blocking has the principal paralytic effect. Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor's monovalent cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum. [24]

In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by acetylcholinesterase. The muscle cell is then ready for the next signal. [24]

Suxamethonium has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize. When acetylcholine binds to an already depolarized receptor, it cannot cause further depolarization. [24]

Calcium is removed from the muscle cell cytoplasm independent of repolarization (depolarization signaling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculations.[ citation needed ]

The results are membrane depolarization and transient fasciculations, followed by flaccid paralysis.

Phase 2 block

While this phase is not abnormal and is a part of its mechanism of action, it is undesirable during surgery[ citation needed ], due to the inability to depolarize the cell again. [24] Often, patients must be on a ventilator for hours if Phase 2 block occurs.[ citation needed ] It generally occurs when suxamethonium is administered multiple times, or during an infusion occurring over too much time, but can also occur during an initial bolus if the plasma cholinesterase is abnormal [24] Desensitization may occur at the nerve terminal causing the myocyte becomes less sensitive to acetylcholine, resulting in the membrane repolarizing and being unable be depolarized again for a period of time. [24]

Chemistry

Suxamethonium is an odorless, white crystalline substance. Aqueous solutions have a pH of about 4. The dihydrate melts at 160 °C, whereas the anhydrous melts at 190 °C. It is highly soluble in water (1 gram in about 1 mL), soluble in ethyl alcohol (1 gram in about 350 mL), slightly soluble in chloroform, and practically insoluble in ether. Suxamethonium is a hygroscopic compound. [25] The compound consists of two acetylcholine molecules that are linked by their acetyl groups. It can also be viewed as a central moiety of succinic acid with two choline moieties, one on each end.

History

Suxamethonium was first discovered in 1906 by Reid Hunt and René de M. Taveau. When studying the drug, animals were given curare and thus they missed the neuromuscular blocking properties of suxamethonium. Instead in 1949 an Italian group led by Daniel Bovet was first to describe succinylcholine induced paralysis. The clinical introduction of suxamethonium was described in 1951 by several groups. Papers published by Stephen Thesleff and Otto von Dardel in Sweden are important but also to be mentioned is work by Bruck, Mayrhofer and Hassfurther in Austria, Scurr and Bourne in UK, and Foldes in America. [26]

Abuse

Dubai authorities declared that the assassination of Mahmoud Al-Mabhouh, a Hamas operative, was carried out on their soil by Mossad agents with the use of suxamethonium chloride injection. Entering Dubai under false passports in 2010, the Mossad agents found al-Mabhouh at a hotel, immobilized him with the drug, electrocuted him, and suffocated him with a pillow. A high concentration of suxamethonium chloride was found in al-Mabhouh's body post-mortem. The incident triggered significant diplomatic crises in the Middle East, Europe, and Australia. [27] [28]

It was used by serial killer Efren Saldivar (1988–1998), and in the murder of Kathy Augustine (2006).

Brand names

It is available in German-speaking countries under the trade name Lysthenon among others. [29]

Use in animals

It is sometimes used in combination with pain medications and sedatives for euthanasia and immobilization of horses.[ citation needed ]

Related Research Articles

<span class="mw-page-title-main">Cholinesterase</span> Esterase that lyses choline-based esters

The enzyme cholinesterase (EC 3.1.1.8, choline esterase; systematic name acylcholine acylhydrolase) catalyses the hydrolysis of choline-based esters:

<span class="mw-page-title-main">Anesthetic</span> Drug that causes anesthesia

An anesthetic or anaesthetic is a drug used to induce anesthesia ⁠— ⁠in other words, to result in a temporary loss of sensation or awareness. They may be divided into two broad classes: general anesthetics, which result in a reversible loss of consciousness, and local anesthetics, which cause a reversible loss of sensation for a limited region of the body without necessarily affecting consciousness.

<span class="mw-page-title-main">Malignant hyperthermia</span> Medical condition

Malignant hyperthermia (MH) is a type of severe reaction that occurs in response to particular medications used during general anesthesia, among those who are susceptible. Symptoms include muscle rigidity, fever, and a fast heart rate. Complications can include muscle breakdown and high blood potassium. Most people who are susceptible to MH are generally unaffected when not exposed to triggering agents.

<span class="mw-page-title-main">Vecuronium bromide</span> Muscle relaxant

Vecuronium bromide, sold under the brand name Norcuron among others, is a medication used as part of general anesthesia to provide skeletal muscle relaxation during surgery or mechanical ventilation. It is also used to help with endotracheal intubation; however, agents such as suxamethonium (succinylcholine) or rocuronium are generally preferred if this needs to be done quickly. It is given by injection into a vein. Effects are greatest at about 4 minutes and last for up to an hour.

In anaesthesia and advanced airway management, rapid sequence induction (RSI) – also referred to as rapid sequence intubation or as rapid sequence induction and intubation (RSII) or as crash induction – is a special process for endotracheal intubation that is used where the patient is at a high risk of pulmonary aspiration. It differs from other techniques for inducing general anesthesia in that several extra precautions are taken to minimize the time between giving the induction drugs and securing the tube, during which period the patient's airway is essentially unprotected.

Pseudocholinesterase deficiency is an autosomal recessive inherited blood plasma enzyme abnormality in which the body's production of butyrylcholinesterase is impaired. People who have this abnormality may be sensitive to certain anesthetic drugs, including the muscle relaxants succinylcholine and mivacurium as well as other ester local anesthetics.

<span class="mw-page-title-main">Tubocurarine chloride</span> Obsolete muscle relaxant

Tubocurarine is a toxic benzylisoquinoline alkaloid historically known for its use as an arrow poison. In the mid-1900s, it was used in conjunction with an anesthetic to provide skeletal muscle relaxation during surgery or mechanical ventilation. Safer alternatives, such as cisatracurium and rocuronium, have largely replaced it as an adjunct for clinical anesthesia and it is now rarely used.

<span class="mw-page-title-main">Neuromuscular-blocking drug</span> Type of paralyzing anesthetic including lepto- and pachycurares

Neuromuscular-blocking drugs, or Neuromuscular blocking agents (NMBAs), block transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished via their action on the post-synaptic acetylcholine (Nm) receptors.

<span class="mw-page-title-main">Rocuronium bromide</span> Non-depolarizing neuromuscular blocker

Rocuronium bromide is an aminosteroid non-depolarizing neuromuscular blocker or muscle relaxant used in modern anaesthesia to facilitate tracheal intubation by providing skeletal muscle relaxation, most commonly required for surgery or mechanical ventilation. It is used for standard endotracheal intubation, as well as for rapid sequence induction (RSI).

<span class="mw-page-title-main">Atracurium besilate</span> Chemical compound

Atracurium besilate, also known as atracurium besylate, is a medication used in addition to other medications to provide skeletal muscle relaxation during surgery or mechanical ventilation. It can also be used to help with endotracheal intubation but suxamethonium (succinylcholine) is generally preferred if this needs to be done quickly. It is given by injection into a vein. Effects are greatest at about 4 minutes and last for up to an hour.

<span class="mw-page-title-main">Mivacurium chloride</span> Drug used in a hospital setting

Mivacurium chloride is a short-duration non-depolarizing neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.

<span class="mw-page-title-main">Sugammadex</span> Selective relaxant binding agent

Sugammadex, sold under the brand name Bridion, is a medication for the reversal of neuromuscular blockade induced by rocuronium and vecuronium in general anaesthesia. It is the first selective relaxant binding agent (SRBA). It is marketed by Merck.

<span class="mw-page-title-main">Doxacurium chloride</span> Pharmaceutical drug

Doxacurium chloride is a neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to provide skeletal muscle relaxation during surgery or mechanical ventilation. Unlike a number of other related skeletal muscle relaxants, it is rarely used adjunctively to facilitate endotracheal intubation.

<span class="mw-page-title-main">Butyrylcholinesterase</span> Mammalian protein found in humans

Butyrylcholinesterase, also known asBChE, BuChE, BuChase, pseudocholinesterase, or plasma (cholin)esterase, is a nonspecific cholinesterase enzyme that hydrolyses many different choline-based esters. In humans, it is made in the liver, found mainly in blood plasma, and encoded by the BCHE gene.

<span class="mw-page-title-main">Gantacurium chloride</span> Chemical compound

Gantacurium chloride is a new experimental neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Gantacurium is not yet available for widespread clinical use: it is currently undergoing Phase III clinical development.

<span class="mw-page-title-main">Candocuronium iodide</span> Chemical compound

Candocuronium iodide is a aminosteroid neuromuscular-blocking drug. Its use within anesthesia for endotracheal intubation and for providing skeletal muscle relaxation during surgery or mechanical ventilation was briefly evaluated in clinical studies in India, though further development was discontinued due to attendant cardiovascular effects, primarily tachycardia that was about the same as the clinically established pancuronium bromide. Candocuronium demonstrated a short duration in the body, but a rapid onset of action. It had little to no ganglion blocking activity, with a greater potency than pancuronium.

<span class="mw-page-title-main">BW-A444</span> Chemical compound

BW A444U was an experimental neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, intended to be used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. It was synthesized and developed in the early 1980s.

<span class="mw-page-title-main">Postoperative residual curarization</span> Medical condition

Postoperative residual curarization (PORC) or residual neuromuscular blockade (RNMB) is a residual paresis after emergence from general anesthesia that may occur with the use of neuromuscular-blocking drugs. Today residual neuromuscular blockade is defined as a train of four ratio of less than 0.9 when measuring the response to ulnar nerve stimulation at the adductor pollicis muscle using mechanomyography or electromyography. A meta-analysis reported that the incidence of residual neuromuscular paralysis was 41% in patients receiving intermediate neuromuscular blocking agents during anaesthesia. It is possible that > 100,000 patients annually in the USA alone, are at risk of adverse events associated with undetected residual neuromuscular blockade. Neuromuscular function monitoring and the use of the appropriate dosage of sugammadex to reverse blockade produced by rocuronium can reduce the incidence of postoperative residual curarization. In this study, with usual care group receiving reversal with neostigmine resulted in a residual blockade rate of 43%.

<span class="mw-page-title-main">Cholinergic blocking drug</span> Drug that block acetylcholine in synapses of cholinergic nervous system

Cholinergic blocking drugs are a group of drugs that block the action of acetylcholine (ACh), a neurotransmitter, in synapses of the cholinergic nervous system. They block acetylcholine from binding to cholinergic receptors, namely the nicotinic and muscarinic receptors.

<span class="mw-page-title-main">Neuromuscular drug</span>

Neuromuscular drugs are chemical agents that are used to alter the transmission of nerve impulses to muscles, causing effects such as temporary paralysis of targeted skeletal muscles. Most neuromuscular drugs are available as quaternary ammonium compounds which are derived from acetylcholine (ACh). This allows neuromuscular drugs to act on multiple sites at neuromuscular junctions, mainly as antagonists or agonists of post-junctional nicotinic receptors. Neuromuscular drugs are classified into four main groups, depolarizing neuromuscular blockers, non-depolarizing neuromuscular blockers, acetylcholinesterase inhibitors, and butyrylcholinesterase inhibitors.

References

  1. ↑ "Product monograph brand safety updates". Health Canada. February 2024. Retrieved 24 March 2024.
  2. ↑ "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". nctr-crs.fda.gov. FDA . Retrieved 22 Oct 2023.
  3. ↑ "Anectine- succinylcholine chloride injection, solution". DailyMed. U.S. National Library of Medicine. 17 September 2018. Retrieved 23 November 2020.
  4. 1 2 "Quelicin- succinylcholine chloride injection, solution". DailyMed. U.S. National Library of Medicine. 15 February 2019. Retrieved 23 November 2020.
  5. 1 2 Lee C, Katz RL (March 2009). "Clinical implications of new neuromuscular concepts and agents: so long, neostigmine! So long, sux!". Journal of Critical Care. 24 (1): 43–49. doi:10.1016/j.jcrc.2008.08.009. PMID   19272538.
  6. 1 2 3 World Health Organization (2009). Stuart MC, Kouimtzi M, Hill SR (eds.). WHO Model Formulary 2008. World Health Organization. pp. 426–8. hdl: 10665/44053 . ISBN   9789241547659.
  7. 1 2 3 4 5 6 "Succinylcholine Chloride". The American Society of Health-System Pharmacists. Archived from the original on 21 December 2016. Retrieved 8 December 2016.
  8. ↑ "Anectine Injection - Summary of Product Characteristics (SPC) - (eMC)". www.medicines.org.uk. 12 January 2016. Archived from the original on 20 December 2016. Retrieved 16 December 2016.
  9. 1 2 "Coronavirus (COVID-19) Update: December 22, 2020". U.S. Food and Drug Administration (Press release). 22 December 2020. Retrieved 23 December 2020.PD-icon.svg This article incorporates text from this source, which is in the public domain .
  10. ↑ "Prescribing medicines in pregnancy database". Therapeutic Goods Administration (TGA). 16 December 2016. Archived from the original on 20 December 2016. Retrieved 16 December 2016.
  11. ↑ World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. hdl: 10665/325771 . WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
  12. ↑ Tran DT, Newton EK, Mount VA, Lee JS, Wells GA, Perry JJ (October 2015). "Rocuronium versus succinylcholine for rapid sequence induction intubation". The Cochrane Database of Systematic Reviews. 2015 (10): CD002788. doi:10.1002/14651858.CD002788.pub3. PMC   7104695 . PMID   26512948.
  13. ↑ Lee C (March 2009). "Goodbye suxamethonium!". Anaesthesia. 64 (Suppl 1): 73–81. doi: 10.1111/j.1365-2044.2008.05873.x . PMID   19222434.
  14. 1 2 Rang HP, Dale MM, Ritter JM, Flower RJ, Henderson G (25 March 2011). Rang and Dale's Pharmacology (7th ed.). Elsevier Science Health Science Division. ISBN   978-0-7020-3471-8. Archived from the original on 10 September 2017.
  15. ↑ Dewachter P, Mouton-Faivre C (February 2016). "Frozen succinylcholine: the danger of being overzealous with its cold storage". Br J Anaesth. 116 (2): 299–300. doi: 10.1093/bja/aev465 . PMID   26787804.
  16. ↑ "Guidelines for the Storage of Essential Medicines and Other Health Commodities: 3. Maintaining the Quality of Your Products: Controlling temperature". apps.who.int. World Health Organization. Archived from the original on May 25, 2011. Retrieved 2020-03-10.
  17. ↑ DiPiro JT, Talbert RL, Yee GC (2005). Matzke Pharmacotherapy: A Pathophysiologicḣ Approach (6th ed.). McGraw-Hill. p. 685.
  18. ↑ Hager HH, Burns B (2022). "Succinylcholine Chloride". StatPearls. PMID   29763160.
  19. ↑ Martyn JA, Richtsfeld M (January 2006). "Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms". Anesthesiology. 104 (1): 158–169. doi: 10.1097/00000542-200601000-00022 . PMID   16394702. S2CID   4556150.
  20. ↑ Peck TE, Hill SA, Williams M (2003). Pharmacology for Anaesthesia and Intensive Care (2nd ed.). London, UK: Greenwich Medical Media Limited. ISBN   1-84110-166-4.
  21. ↑ Reimringer MJ, Morgan SW, Bramwell PF (1970). "Succinylcholine as a modifier of acting-out behavior". Clinical Medicine. 77 (7): 28.
  22. ↑ von Hoffman N (5 April 1972). "A Bit of 'Clockwork Orange,' California-Style". Washington Post.
  23. ↑ Sansweet RJ (1975). The Punishment Cure. New York: Mason/Charter. ISBN   0-88405-118-8.
  24. 1 2 3 4 5 6 Appiah-Ankam J, Hunter JM (February 2004). "Pharmacology of neuromuscular blocking drugs". Continuing Education in Anaesthesia Critical Care & Pain. 4 (1): 2–7. doi: 10.1093/bjaceaccp/mkh002 .
  25. ↑ Gennaro A (2000). The Science and Practice of Pharmacy (20th ed.). Remington: Lippincott Williams & Wilkins. p. 1336.
  26. ↑ Dorkins HR (April 1982). "Suxamethonium-the development of a modern drug from 1906 to the present day". Medical History. 26 (2): 145–168. doi:10.1017/S0025727300041132. PMC   1139149 . PMID   7047939.
  27. ↑ "Dubai Hit: Police Say They Know How Mahmoud al-Mabhouh Was Killed". ABC News.
  28. ↑ "Succinylcholine, A Perfect Poison, Makes Appearance in the Dubai Killing". Medgadget. 8 March 2010.
  29. ↑ Compendium.ch: LYSTHENON 2% Inj Lös 100 mg/5ml [ permanent dead link ](in German)
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