Enflurane (2-chloro-1,1,2,-trifluoroethyl-difluoromethyl ether) is a halogenated ether structural isomer of isoflurane. Developed by Ross Terrell in 1963, it was first used clinically in 1966. It was increasingly used for inhalational anesthesia during the 1970s and 1980s but is no longer in common use. Clinically, enflurane produces a dose-related depression of myocardial contractility with an associated decrease in myocardial oxygen consumption. Between 2% and 5% of the inhaled dose is oxidized in the liver, producing fluoride ions and difluoromethoxy-difluoroacetic acid. This is significantly higher than the metabolism of its structural isomer isoflurane. The exact mechanism of the action of general anesthetics has not been delineated. Enflurane acts as a positive allosteric modulator of the GABAA, glycine, and 5-HT3 receptors, and as a negative allosteric modulator of the AMPA, kainate, and NMDA receptors, as well as of nicotinic acetylcholine receptors.

Dexmedetomide (biologically active dextroisomer of medetomidine) is an alpha2-adrenergic agonist which was approved by FDA for the sedation purposes. Upon administration the drug activates the alpha2 receptors thus inhibiting the release of norepinephrine and terminating the propagation of pain signals. Also it inhibits sympathetic activity and thus can decrease blood pressure and heart rate.

Desflurane is a non-flammable liquid administered via vaporizer as a general anesthetic. It is halogenated exclusively with fluorine and is very resistant to defluorination. For this reason, it is not associated with nephrotoxicity, as is the case with other inhalational anesthetics. Desflurane is indicated for the induction and/or maintenance of anesthesia and adults, and for maintenance of anesthesia in pediatric patients following the induction with other agents.

Ketamine (brand name Ketalar) is a cyclohexanone derivative used for induction of anesthesia. Ketalar is indicated as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation; also, it is indicated for the induction of anesthesia prior to the administration of other general anesthetic agents. Ketamine blocks NMDA receptors through an interaction with sites thought to be located within the ion channel pore region. However, the complete pharmacology of ketamine is more complex, and it is known to directly interact with a variety of other sites to varying degrees. Recently, it was shown that inclusion of the NR3B subunit does not alter the ketamine sensitivity of recombinant NR1/NR2 receptors expressed in oocytes. Likewise, 100 μM ketamine produced only weak inhibition of the glycine-induced current of NR1/NR3A/NR3B receptors. The side effects of ketamine noted in clinical studies include psychedelic symptoms (hallucinations, memory defects, panic attacks), nausea/vomiting, somnolence, cardiovascular stimulation and, in a minority of patients, hepatoxicity. The recreational use of ketamine is increasing and comes with a variety of additional risks ranging from bladder and renal complications to persistent psychotypical behaviour and memory defects. Ketamine was first synthesized in 1962 by Calvin Stevens at Parke-Davis Co (now Pfizer) as an alternative anesthetic to phencyclidine. It was first used in humans in 1965 by Corssen and Domino and was introduced into clinical practice by 1970.