The myth and mending of ketamine
Thursday, January 12, 2012
The origins of ketamineKetamine, a chemical derivative of phencyclidine (PCP), was first synthesized by Calvin Lee Stevens, Professor of organic chemistry at Wayne State University. Initially evaluated under the clinical number CI-581, the pharmacological actions were tested on volunteers from the population of Jackson Prison, Michigan in 1964. It was shown to be an effective analgesic and anaesthetic agent that gave patients a feeling of being ‘disconnected’ from the environment. The term ‘dissociative anaesthetic’ was coined by Toni Domino, the wife of one of the lead researchers, to describe the clinical effects of the drug (Domino, 2010).For many years, the mechanism of action of ketamine has been thought to be mainly due to the non-competitive antagonism of N-methyl-d-aspartate glutamate (NMDA) receptors. Glutamate is a major excitatory transmitter in the central nervous system—antagonizing the receptor leads to a decrease in neuronal activity and therefore anaesthesia.However, this is not the whole story. Ketamine appears to have several different sites of action and has been reported to interact with many systems such as opioid, monoamine, cholinergic, purinergic and adenosine receptors, as well as having local anaesthetic effects(White et al, 1982; Persson, 2010).‘Although ketamine is currently successfully used for analgesia in emergency medicine and the developing world, it is still unfairly demonized in some circles’The racemic mixture of ketamine, containing equal amounts of two ketamine enantiomers, S (+) and R (−), was approved for general clinical use in 1970 (White et al, 1982). During the past 41 years, the appropriate use of ketamine has divided opinion, and some controversial beliefs still muddy the waters of debate.
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