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A general anaesthetic (or anesthetic, see spelling differences) drug is an anaesthetic drug that brings about a reversible loss of consciousness. These drugs are generally administered by an anaesthesia provider in order to induce or maintain general anaesthesia to facilitate surgery. The biological mechanism(s) of action of general anesthetics are not well understood.

Contents

Mode of administration

Drugs given to induce or maintain general anaesthesia are either given as:

Most commonly these two forms are combined, with an injection given to induce anaesthesia and a gas used to maintain it, although it is possible to deliver anaesthesia solely by inhalation or injection.

Inhalation

Inhalational anaesthetic substances are either volatile liquids or gases and are usually delivered using an anaesthesia machine. An anaesthesia machine allows composing a mixture of oxygen, anaesthetics and ambient air, delivering it to the patient and monitoring patient and machine parameters. Liquid anaesthetics are vaporized in the machine.

Many compounds have been used for inhalation anaesthesia, but only a few are still in widespread use. Desflurane, isoflurane and sevoflurane are the most widely used volatile anaesthetics today. They are often combined with nitrous oxide. Older, less popular, volatile anaesthetics, include halothane, enflurane, and methoxyflurane. Researchers are also actively exploring the use of xenon as an anaesthetic.

Injection

Injection anaesthetics are used for induction and maintenance of a state of unconsciousness. Anaesthetists prefer to use intravenous injections as they are faster, generally less painful and more reliable than intramuscular or subcutaneous injections. Among the most widely used drugs are:

The volatile anaesthetics are a class of general anaesthetic drugs composed of gasses and liquids which evaporate easily for administration by inhalation. All of these agents share the property of being quite hydrophobic (i.e., as liquids, they are not freely miscible with in water, and as gases they dissolve in oils better than in water).

Method of Action

Lipid theory

Overton and Meyer postulated that general anaesthetics exert their action by acting on the plasma membrane. This is supported by evidence that the potency of the drug has a direct, positive correlation with the lipid solubility of the blood. [1]

The mechanism of action was proposed to be increased fluidity of the membrane. The interpretation of the Overton and Meyer finding has been challenged and discredited.[2]

Ion Channels

General anaesthetics inhibit excitatory functions of some CNS receptors, such as neuronal nACh [3], glutamate, or 5-HT3 receptors. Some general anaesthetics also excite inhibitory receptors, notably GABAA receptors and TREK. GABAA is a major target of the IV anaesthetics thiopental and propofol.

General anaesthetics may decrease transmitter release pre-synaptically or decrease excitability of post-synaptic neuron.

Pharmacokinetics

Induction

Elimination

Volatile anaesthetics are eliminated in the terminal phase via the lungs. A low blood:gas coefficient is therefore necessary for quick removal of anaesthetic. When oil:water coefficient is high, there will be little anaesthetic in the blood, so elimination will be slow, giving a prolonged hangover effect:

Some drugs are metabolised by the liver, and so consequently their metabolites are often toxic (e.g. chloroform)

See also

Notes

  • Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. (2007). Rang & Dale's pharmacology (6th ed.). Edinburgh: Churchill Livingstone. ISBN 0-443-06911-5. 
  1. ^ "Mechanism of action of inhaled anaesthetic agents". Anesthesia UK. 2005. http://www.frca.co.uk/article.aspx?articleid=100341. 
  2. ^ Ueda I (January 1999). "The window that is opened by optical isomers". Anesthesiology 90 (1): 336. PMID 9915358. 
  3. ^ Weber M, Motin L, Gaul S, Beker F, Fink RH, Adams DJ (January 2005). "Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons". Br. J. Pharmacol. 144 (1): 98–107. doi:10.1038/sj.bjp.0705942. PMID 15644873. 







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