Ketamine is an NMDA receptor antagonist with a potent anesthetic effect. It was developed in 1963 as a replacement for phencyclidine (PCP) by Calvin Stevens at Parke Davis Laboratories. It started being used for veterinary purposes in Belgium and in 1964 was proven that compared to PCP, it produced minor hallucinogenic effects and shorter psychotomimetic effects. It was FDA approved in 1970, and from there, it has been used as an anesthetic for children or patients undergoing minor surgeries but mainly for veterinary purposes.


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Ketamine is a rapid-acting general anesthetic producing an anesthetic state characterized by profound analgesia,

normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and

respiratory stimulation, and occasionally a transient and minimal respiratory depression. The anesthetic state

produced by Ketamine has been termed as “dissociative anesthesia” in that it appears to selectively interrupt

association pathways of the brain before producing somesthetic sensory blockade. It may selectively depress the

thalamoneocortical system before significantly obtunding the more ancient cerebral centers and pathways

(reticular-activating and limbic systems).

Ketamine enhances descending inhibiting serotoninergic pathways and can exert antidepressive effects. These effects are seen in concentrations ten times lower than the needed concentration for anesthetic proposes. The effect of ketamine can be described as analgesic by the prevention of central sensitization in dorsal horn neurons as well as by the inhibition on the synthesis of nitric oxide. Ketamine can present cardiovascular changes and bronchodilatation.

Mechanism of action

Ketamine interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels. Unlike other general anaesthetic agents, ketamine does not interact with GABA receptors.



100g, 10g, 25g, 50g


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