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A team of researchers at Parke-Davis, led by V. Harold Maddox and Robert F. Parcell, [Maddox et al., ''J. Med Chem, 1965''] proceeded to synthesize phencyclidine and nearly fifty other derivatives as well. The parent compound, which would eventually gain FDA approval under the trade-name of ''Sernyl'', got its name, as legend would have it, to evoke a feeling of "serenity" or "tranquility" - thus leading to ''Sernyl'' as the marketed name of the hydrochloride salt of this compound, primarily administered via IV during initial clinical trials. The compound was withdrawn from human clinical research in 1962, a relatively "short" life as a medicinal agent used officially in humans. Parke-Davis voluntarily withdrew ''Sernyl'' from the human clinical market in 1965. Shortly thereafter, in 1967, Parke-Davis re-introduced phencyclidine as a veterinary anesthetic under the trade name of ''Sernylan''.
A team of researchers at Parke-Davis, led by V. Harold Maddox and Robert F. Parcell, [Maddox et al., ''J. Med Chem, 1965''] proceeded to synthesize phencyclidine and nearly fifty other derivatives as well. The parent compound, which would eventually gain FDA approval under the trade-name of ''Sernyl'', got its name, as legend would have it, to evoke a feeling of "serenity" or "tranquility" - thus leading to ''Sernyl'' as the marketed name of the hydrochloride salt of this compound, primarily administered via IV during initial clinical trials. The compound was withdrawn from human clinical research in 1962, a relatively "short" life as a medicinal agent used officially in humans. Parke-Davis voluntarily withdrew ''Sernyl'' from the human clinical market in 1965. Shortly thereafter, in 1967, Parke-Davis re-introduced phencyclidine as a veterinary anesthetic under the trade name of ''Sernylan''.


The full extent of the pharmacology of this compound in the human CNS is not fully understood to this day; primarily its interactions are as an non-competitive antagonist at the 3A-subunit [epsilon subunit] of the NMDAR in ''Homo sapiens''. Phencyclidine also binds to a bewildering array of other receptor sites; as has been stated previously, the full extent of its pharmacological interactions within the mammalian and human CNS still have yet to be discovered. Phencyclidine is known to bind, with relatively high affinity, to the D2 subunit of the human '''DAT''' (Dopamine Transporter), in additional to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR). It also binds to the mu-opioid receptor, which seems to be a central part of the mechanism of action of drugs in this class. (For example, Dizocilpine [MK-801] shows little appreciable analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits - this may well be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR certainly does play a role in transmission of pain signal transmission).
The full extent of the pharmacology of this compound in the human CNS is not fully understood to this day; primarily its interactions are as an non-competitive antagonist at the 3A-subunit [epsilon subunit] of the NMDAR in ''Homo sapiens''. Phencyclidine also binds to a bewildering array of other receptor sites; as has been stated previously, the full extent of its pharmacological interactions within the mammalian and human CNS still have yet to be discovered. Phencyclidine is known to bind, with relatively high affinity, to the D2 subunit of the human '''DAT''' (Dopamine Transporter), in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR). It also binds to the mu-opioid receptor, which seems to be a central part of the mechanism of action of drugs in this class. (For example, Dizocilpine [MK-801] shows little appreciable analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits - this may well be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR certainly does play a role in transmission of pain signal transmission).
'''Phencyclidine''' (a [[Clipping (morphology)|complex clip]] of the chemical name '''1-(1-phenylcyclohexyl)piperidine''', commonly [[Initialism|initialized]] as '''PCP'''), also known as '''angel dust''' and other [[Drug subculture|street names]], is a recreational, [[dissociative drug]] formerly used as an [[anesthesia|anesthetic]] agent, exhibiting [[hallucinogen]]ic and [[neurotoxic]] effects.<ref>{{cite book |title=Drug Use and Abuse |last=Maisto |first=Stephen A. |coauthors=Mark Galizio, Gerard Joseph Connors |year=2004 |publisher=Thompson Wadsworth |isbn=0155085174 }}</ref> Developed in 1926,<ref>[http://www.cesar.umd.edu/cesar/drugs/pcp.pdf Development of PCP]</ref> it was first patented in 1952 by the [[Parke-Davis]] pharmaceutical company and marketed under the brand name '''Sernyl'''. In [[Chemistry|chemical]] structure, PCP is an arylcyclohexylamine derivative, and, in [[pharmacology]], it is a member of the family of [[dissociative anesthetic]]s. PCP works primarily as an [[NMDA receptor antagonist]], which blocks the activity of the [[NMDA receptor]] and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.<ref>Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8</ref><ref>Kapur, S. and P. Seeman. "[http://www.nature.com/mp/journal/v7/n8/full/4001093a.html NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors¾implications for models of schizophrenia]" ''Molecular Psychiatry''. '''7'''(8): 837–844 (2002)</ref> Other NMDA receptor antagonists include [[ketamine]], [[tiletamine]], and [[dextromethorphan]]. Although the primary psychoactive effects of the drug lasts for a few hours, the total elimination rate from the body typically extends 8 days or longer.
'''Phencyclidine''' (a [[Clipping (morphology)|complex clip]] of the chemical name '''1-(1-phenylcyclohexyl)piperidine''', commonly [[Initialism|initialized]] as '''PCP'''), also known as '''angel dust''' and other [[Drug subculture|street names]], is a recreational, [[dissociative drug]] formerly used as an [[anesthesia|anesthetic]] agent, exhibiting [[hallucinogen]]ic and [[neurotoxic]] effects.<ref>{{cite book |title=Drug Use and Abuse |last=Maisto |first=Stephen A. |coauthors=Mark Galizio, Gerard Joseph Connors |year=2004 |publisher=Thompson Wadsworth |isbn=0155085174 }}</ref> Developed in 1926,<ref>[http://www.cesar.umd.edu/cesar/drugs/pcp.pdf Development of PCP]</ref> it was first patented in 1952 by the [[Parke-Davis]] pharmaceutical company and marketed under the brand name '''Sernyl'''. In [[Chemistry|chemical]] structure, PCP is an arylcyclohexylamine derivative, and, in [[pharmacology]], it is a member of the family of [[dissociative anesthetic]]s. PCP works primarily as an [[NMDA receptor antagonist]], which blocks the activity of the [[NMDA receptor]] and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.<ref>Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8</ref><ref>Kapur, S. and P. Seeman. "[http://www.nature.com/mp/journal/v7/n8/full/4001093a.html NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors¾implications for models of schizophrenia]" ''Molecular Psychiatry''. '''7'''(8): 837–844 (2002)</ref> Other NMDA receptor antagonists include [[ketamine]], [[tiletamine]], and [[dextromethorphan]]. Although the primary psychoactive effects of the drug lasts for a few hours, the total elimination rate from the body typically extends 8 days or longer.

Revision as of 05:59, 23 July 2010

Phencyclidine
Clinical data
Routes of
administration		Smoked, Insufflated, Oral
ATC code
  • none
Legal status
Legal status
Pharmacokinetic data
Elimination half-life7-46 hours
Identifiers
  • 1-(1-phenylcyclohexyl)piperidine
CAS Number
PubChem CID
DrugBank
ChemSpider
CompTox Dashboard (EPA)
ECHA InfoCard100.150.427 Edit this at Wikidata
Chemical and physical data
FormulaC17H25N
Molar mass243.387 g/mol g·mol−1
Data page
Phencyclidine (data page)
  (verify)

Phencyclidine, chemically 1-(1-phenylcyclohexyl)piperidine, was first written-up in the German Journal für Praktische Chemie in 1926 [Kotz ünd Merkel. Journal für Praktische Chemie, 1926, which may be found here, after which it faded into obscurity for a time before being picked up by a team of researchers at Parke-Davis & Company based in Detroit, MI, USA the early fifties as a potential novel human anesthetic agent.

A team of researchers at Parke-Davis, led by V. Harold Maddox and Robert F. Parcell, [Maddox et al., J. Med Chem, 1965] proceeded to synthesize phencyclidine and nearly fifty other derivatives as well. The parent compound, which would eventually gain FDA approval under the trade-name of Sernyl, got its name, as legend would have it, to evoke a feeling of "serenity" or "tranquility" - thus leading to Sernyl as the marketed name of the hydrochloride salt of this compound, primarily administered via IV during initial clinical trials. The compound was withdrawn from human clinical research in 1962, a relatively "short" life as a medicinal agent used officially in humans. Parke-Davis voluntarily withdrew Sernyl from the human clinical market in 1965. Shortly thereafter, in 1967, Parke-Davis re-introduced phencyclidine as a veterinary anesthetic under the trade name of Sernylan.

The full extent of the pharmacology of this compound in the human CNS is not fully understood to this day; primarily its interactions are as an non-competitive antagonist at the 3A-subunit [epsilon subunit] of the NMDAR in Homo sapiens. Phencyclidine also binds to a bewildering array of other receptor sites; as has been stated previously, the full extent of its pharmacological interactions within the mammalian and human CNS still have yet to be discovered. Phencyclidine is known to bind, with relatively high affinity, to the D2 subunit of the human DAT (Dopamine Transporter), in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR). It also binds to the mu-opioid receptor, which seems to be a central part of the mechanism of action of drugs in this class. (For example, Dizocilpine [MK-801] shows little appreciable analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits - this may well be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR certainly does play a role in transmission of pain signal transmission).

Phencyclidine (a complex clip of the chemical name 1-(1-phenylcyclohexyl)piperidine, commonly initialized as PCP), also known as angel dust and other street names, is a recreational, dissociative drug formerly used as an anesthetic agent, exhibiting hallucinogenic and neurotoxic effects.[1] Developed in 1926,[2] it was first patented in 1952 by the Parke-Davis pharmaceutical company and marketed under the brand name Sernyl. In chemical structure, PCP is an arylcyclohexylamine derivative, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA receptor and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.[3][4] Other NMDA receptor antagonists include ketamine, tiletamine, and dextromethorphan. Although the primary psychoactive effects of the drug lasts for a few hours, the total elimination rate from the body typically extends 8 days or longer.

Biochemistry and pharmacology

Biochemical action

The N-methyl-D-Aspartate (NMDA) receptor, a type of ionotropic receptor, is found on the dendrites of neurons and receives signals in the form of neurotransmitters. It is a major excitatory receptor in the brain. Normal physiological function requires that the activated receptor fluxes cations through the channel part of the receptor. PCP enters the ion channel from the outside of the neuron and binds, reversibly, to a site in the channel pore, blocking the flux of positive ions into the cell. PCP therefore inhibits depolarization of neurons and interferes with cognitive and other functions of the nervous system.

In a similar manner, PCP and analogues also inhibit nicotinic acetylcholine receptor channels (nAChR). Some analogues have greater potency at nAChR than at NMDAR. In some brain regions, these effects act synergistically to inhibit excitatory activity.[citation needed]

PCP (and ketamine) also act as potent D2 receptor partial agonists,[5] as well as dopamine reuptake inhibitors.[citation needed]

PCP is retained in fatty tissue and is broken down by the human metabolism into PCHP, PPC and PCAA.

The most troubling clinical effects are most likely produced by the action of phencyclidine on the D2 receptor. This has been suggested to account for most of the psychotic features.[6] The relative immunity to pain is likely produced by indirect interaction with the endogenous endorphin and enkephalin system in rats.[7][clarification needed]

When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.

Conversion of PCP into PC and piperidine by heat. (Image in the PD)

Structural analogs

Possible Analogues of PCP

More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. The best known of these are PCPy (rolicyclidine, 1-(1-phenylcyclohexyl)pyrrolidine); PCE (eticyclidine, N-ethyl-1-phenylcyclohexylamine); and TCP (tenocyclidine, 1-(1-(2-Thienyl)cyclohexyl)piperidine). These compounds were never widely-used and did not seem to be as well-accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.[8][citation needed]

The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarized below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.[9][10][clarification needed]

Brain effects

Like other NMDA receptor antagonists, it is postulated that phencyclidine can cause a certain kind of brain damage called Olney's lesions.[11][12] Studies conducted on rats showed that high doses of the NMDA receptor antagonist MK-801 caused irreversible vacuoles to form in certain regions of the rats' brains, and experts say that it is possible that similar brain damage can occur in humans.[citation needed] All studies of Olney's Lesions have only been performed on animals and may not apply to humans. The research into the relationship between rat brain metabolism and the creation of Olney's Lesions has been discredited and may not apply to humans, as has been shown with ketamine.[13][14]

Phencyclidine has also been shown to cause schizophrenia-like changes in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[15] It also induces symptoms in humans that are virtually indistinguishable from schizophrenia.[16]

History and medicinal use

PCP was first synthesized in 1926, and later tested after World War II as a surgical anesthetic. Because of its adverse side effects, such as hallucinations, mania, delirium, and disorientation, it was shelved until the 1950s. In 1953, it was patented by Parke-Davis and named Sernyl (referring to serenity), but was withdrawn from the market two years later because of side-effects. In 1967, it was given the trade name Sernylan and marketed as a veterinary anesthetic, but was again discontinued. Its side effects and long half-life in the human body made it unsuitable for medical applications.

PCP began to emerge as a recreational drug in major cities in the United States in 1967.[17] In 1978, People magazine and Mike Wallace of 60 Minutes called PCP the country's "number one" drug problem. Although recreational use of the drug had always been relatively low, it began declining significantly in the 1980s. In surveys, the amount of high school students admitting to trying PCP at least once fell from 13% in 1979 to less than 3% in 1990.[18]

Recreational use

Illicit PCP seized by the DEA in several forms.

PCP comes in both powder and liquid forms (PCP base is dissolved most often in ether), but typically it is sprayed onto leafy material such as cannabis, mint, oregano, parsley, or ginger leaves, then smoked.

PCP is a Schedule II substance in the United States, a List I drug of the Opium Law in the Netherlands and a Class A substance in the United Kingdom.

Method of absorption

The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette is dipped, to be ingested through smoking, commonly known as "boat" or "water." The name most likely originated from PCP's somatic "numbing" effect and the feeling of physical dissociation from the body, and has led to the widespread (mistaken) belief that the liquid is made up of or contains real embalming fluid. Occasionally, however, some users and dealers have, believing this myth, used real embalming fluid mixed with (or in place of) PCP.[19][20] Smoking PCP is known as "getting wet", and a tobacco or cannabis cigarette dipped in PCP may be referred to on the street as a "fry stick," "sherm," "amp," "toe tag", "dippa", "happy stick," or "wet stick." "Getting wet" is an increasingly popular method of using PCP, especially in the western United States where it is sold for about $10 to $25 per cigarette.

In its pure (base) form, PCP is a yellow oil (usually dissolved in petroleum or diethyl ether or tetrahydrofuran). Upon treatment with hydrogen chloride gas, or isopropyl alcohol saturated with HCl, this oil precipitates into white-tan crystals or powder (PCP hydrochloride) In this form, PCP can be insufflated, depending upon the purity. However, most PCP on the illicit market contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass. These contaminants can range from unreacted piperidine and other precursors, to carcinogens like benzene and cyanide-like compounds such as PCC (piperidinocyclohexyl carbonitrile).

Effects

Behavioral effects can vary by dosage. Small doses produce a numbness in the extremities and intoxication, characterized by staggering, unsteady gait, slurred speech, bloodshot eyes, and loss of balance. Moderate doses (5–10 mg intranasal, or 0.01-0.02 mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.[21]

Psychological effects include severe changes in body image, loss of ego boundaries, paranoia and depersonalization. Hallucinations, euphoria, suicidal impulses and aggressive behavior are reported infrequently.[21][22]

The drug has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. Intoxicated individuals may act in an unpredictable fashion, possibly driven by their delusions and hallucinations. However, studies by the Drug Abuse Warning Network in the 1970s show that media reports of PCP-induced violence are greatly exaggerated and that incidents of violence were unusual and often limited to individuals with reputations for aggression regardless of drug use.[23]

Included in the portfolio of behavioral disturbances are acts of self-injury including suicide, and attacks on others or destruction of property. The analgesic properties of the drug can cause users to feel less pain, and persist in violent or injurious acts as a result. Recreational doses of the drug can also induce a psychotic state that resembles schizophrenic episodes which can last for months at a time with toxic doses.[citation needed] Users generally report an "out-of-body" experience where they feel detached from reality, or one's consciousness seems somewhat disconnected from consensus reality.[citation needed]

Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.[24]

Management of intoxication

Management of phencyclidine intoxication mostly consists of supportive care — controlling breathing, circulation, and body temperature — and, in the early stages, treating psychiatric symptoms.[25][26][27] Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such as phenothiazines and haloperidol have been used to control psychotic symptoms, but may produce many undesirable side effects — such as dystonia — and their use is therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia, and boost the anticholinergic effects of PCP.[25][26] If an antipsychotic is given, intramuscular haloperidol has been recommended.[27][28][29]

Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was somewhat controversially recommended in the past as a decontamination measure.[25][26][27] However, it is now known that only around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence; furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is not an unusual manifestation of PCP toxicity.[25][26]

See also

References

  • Inciardi, James A. (1992). The War on Drugs II. Mayfield Publishing Company. ISBN 1-55934-016-9.
  1. ^ Maisto, Stephen A. (2004). Drug Use and Abuse. Thompson Wadsworth. ISBN 0155085174. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  2. ^ Development of PCP
  3. ^ Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8
  4. ^ Kapur, S. and P. Seeman. "NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors¾implications for models of schizophrenia" Molecular Psychiatry. 7(8): 837–844 (2002)
  5. ^ Seeman P, Guan HC, Hirbec H (2009). "Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil". Synapse (New York, N.Y.). 63 (8): 698–704. doi:10.1002/syn.20647. PMID 19391150. {{cite journal}}: Unknown parameter |DUPLICATE DATA: doi= ignored (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. ^ Giannini AJ, Nageotte C, Loiselle RH, Malone DA, Price WA (1984). "Comparison of chlorpromazine, haloperidol and pimozide in the treatment of phencyclidine psychosis: DA-2 receptor specificity". Journal of Toxicology. Clinical Toxicology. 22 (6): 573–9. doi:10.3109/15563658408992586. PMID 6535849.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Castellani S, Giannini AJ, Adams PM (1982). "Effects of naloxone, metenkephalin, and morphine on phencyclidine-induced behavior in the rat". Psychopharmacology. 78 (1): 76–80. doi:10.1007/BF00470593. PMID 6815700.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ PCP synthesis and effects: table of contents
  9. ^ Itzhak Y, Kalir A, Weissman BA, Cohen S. New analgesic drugs derived from phencyclidine. Journal of Medicinal Chemistry. 1981; 24(5):496–499
  10. ^ Chaudieu I, Vignon J, Chicheportiche M, Kamenka JM, Trouiller G, Chicheportiche R. Role of the aromatic group in the inhibition of phencyclidine binding and dopamine uptake by PCP analogs. Pharmacology Biochemistry and Behaviour. 1989 Mar;32(3):699–705.
  11. ^ Olney J, Labruyere J, Price M (1989). "Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs". Science. 244 (4910): 1360–2. doi:10.1126/science.2660263. PMID 2660263.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Hargreaves R, Hill R, Iversen L (1994). "Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology". Acta Neurochir Suppl (Wien). 60: 15–9. PMID 7976530.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0966001974
  14. ^ Erowid DXM Vault : Response to "The Bad News Isn't In": Please Pass The Crow, by William E. White
  15. ^ Reynolds, Lindsay M. (March 1, 2005). "Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain". Schizophrenia Research. 73 (2–3): 147–152. doi:10.1016/j.schres.2004.02.003. PMID 15653257. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  16. ^ Murray JB (2002). "Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research". J Psychol. 136 (3): 319–27. PMID 12206280. {{cite journal}}: Unknown parameter |month= ignored (help)
  17. ^ Inciardi 1992, p. 46.
  18. ^ Inciardi 1992, pp. 46-49.
  19. ^ http://abcnews.go.com/US/story?id=92771&page=1 Kids Use Embalming Fluid as Drug
  20. ^ http://www.syracuse.com/news/index.ssf/2009/08/_syracuse_ny_the.html Illegal drug users dip into embalming fluid By Douglass Dowty / The Post-Standard August 03, 2009
  21. ^ a b Diaz, Jaime. How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall, 1996.
  22. ^ Inciardi 1992, p. 48-49.
  23. ^ Inciardi 1992, p. 48.
  24. ^ AJ Giannini. Drugs of Abuse--Second Edition. Los Angeles, Practice Management Information Corp.,1997,pg. 126. ISBN 1-57066-053-0.
  25. ^ a b c d Helman RS, Habal R (October 6, 2008). "Phencyclidine Toxicity". eMedicine. Retrieved on November 3, 2008.
  26. ^ a b c d Olmedo R (2002). "Chapter 69: Phencyclidine and ketamine". In Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS (eds.) (ed.). Goldfrank's Toxicologic Emergencies. New York: McGraw-Hill. pp. 1034–41. ISBN 0-07-136001-8. {{cite book}}: |editor= has generic name (help)CS1 maint: multiple names: editors list (link) Retrieved on November 3, 2008 through Google Book Search.
  27. ^ a b c Milhorn HT (1991). "Diagnosis and management of phencyclidine intoxication". American Family Physician. 43 (4): 1293–302. PMID 2008817. {{cite journal}}: Unknown parameter |month= ignored (help)
  28. ^ Giannini AJ. Price WA. PCP: Management of acute intoxication. Medical Times. 1985;113(9):43-49
  29. ^ Giannini AJ, Eighan MS, Loiselle RH, Giannini MC (1984). "Comparison of haloperidol and chlorpromazine in the treatment of phencyclidine psychosis". Journal of Clinical Pharmacology. 24 (4): 202–4. PMID 6725621. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
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