Ketamine HCL POWDER is a rapid-acting general anesthetic and NMDA receptor antagonist used for induction of anesthesia in diagnostic and surgical procedures, typically in combination with a muscle relaxant.
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. Furthermore, 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.
TypeSmall MoleculeGroupsApproved, Vet approvedStructure
weight average 237.725
Ketamine is indicated as an anesthetic agent for recommended diagnostic and surgical procedures. If skeletal muscle relaxation is needed, it should be combined with a muscle relaxant. If the surgical procedure involves visceral pain, it should be supplemented with an agent that obtunds visceral pain. Ketamine can be used for induction of anesthesia prior to other general anesthetic agents and as a supplement to low-potency agents.
Reports have indicated the potential use of ketamine as a therapeutic tool for the management of depression when administered in lower doses. These reports have increased the interest in ketamine in this area and several clinical trials are launched for this indication.
Induction and Maintenance of General Anesthesia
Contraindications & Black box Warnings
Ketamine HCL POWDER
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 transient and minimal respiratory depression. The anesthetic state produced by Ketamine has been termed “dissociative anesthesia” in that it appears to selectively interrupt association pathways of the brain before producing sympathetic sensory blockade. It may selectively depress the thalamocortical system before significantly bounding the more ancient cerebral centers and pathways (reticular-activating and limbic systems).
Ketamine enhances descending inhibiting serotoninergic pathways and can exert anti-depressive 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 an analgesic by the prevention of central sensitization in dorsal horn neurons, as well as by the inhibition of the synthesis of nitric oxide. Ketamine can present cardiovascular changes and bronchi dilatation.
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 anesthetic agents, ketamine does not interact with GABA receptors.