Fenciclidina

Salvar

La fenciclidina ( PCP ), también conocida como polvo de ángel, entre otros

nombres, es una droga que se usa para sus efectos que alteran la
mente. [5]PCP puede causar alucinaciones , percepciones distorsionadas de
sonidos y comportamiento violento . [7] [8] Como droga recreativa ,
generalmente se fuma , pero se puede tomar por
boca, inhalar o inyectar . [7] [4] También se puede mezclar
con cannabis o tabaco . [5]
Los efectos adversos pueden incluir convulsiones , coma , adicción y un mayor
riesgo de suicidio . [7] Flashbacks puede ocurrir a pesar de parar
uso. [8] Químicamente, PCP es un miembro de la clase arylcyclohexylamine ,
y farmacológicamente , es un anestésico disociativo . [9] [10] PCP funciona
principalmente como un antagonista del receptor NMDA . [9]
PCP es el más comúnmente utilizado en los Estados Unidos. [11] Mientras que
el uso alcanzó su punto máximo en la década de 1970, [12] entre 2005 y 2011
se produjo un aumento en las visitas a los departamentos de emergencia como
resultado de la droga. [7] A partir de 2017 en los Estados Unidos,
aproximadamente el 1% de las personas en el grado doce informaron haber
usado PCP en el año anterior, mientras que el 2.9% de las mayores de 25
informó haberlo usado en algún momento de su vida. [13]
PCP se creó inicialmente en 1926 y se comercializó
como medicamento anestésico en la década de 1950. [10] [14] Su uso en
humanos no se permitió en los Estados Unidos en 1965 debido a las altas
tasas de efectos secundarios, mientras que su uso en otros animales no se
permitió en 1978. [5] [15] [10] Además, la ketamina era descubierto y fue mejor
tolerado como un anestésico. [15] PCP actualmente es ilegal en los Estados
Unidos, donde está clasificado como un medicamento de la Lista II . [5] Se han
vendido varios derivados de PCP para uso recreativo y no médico. [dieciséis]
Usos recreativos
Efectos
Los efectos del comportamiento pueden variar según la dosis. Las dosis bajas
producen un entumecimiento en las extremidades y la intoxicación,
caracterizadas por una marcha tambaleante e inestable, dificultad para hablar,
ojos inyectados en sangre y pérdida del equilibrio. Las dosis moderadas (5-10
mg intranasal, o 0.01-0.02 mg / kg por vía intramuscular o intravenosa)
producirán analgesia y anestesia. Las dosis altas pueden
provocar convulsiones . [17] La droga a menudo se produce ilegalmente en
condiciones mal controladas; esto significa que los usuarios pueden
desconocer la dosis real que están tomando. [18]
Los efectos psicológicos incluyen cambios severos en la imagen
corporal, pérdida de los límites del
ego , paranoia y despersonalización . También se
informan alucinaciones, euforia e impulsos suicidas , así como el
comportamiento agresivo ocasional. [19] : 48-49 [17] Como muchas otras
drogas, se sabe que la PCP altera los estados de ánimo de una manera
impredecible, provocando que algunas personas se despeguen y otras que se
animan. PCP puede inducir sentimientos de fuerza, poder e invulnerabilidad,
así como un efecto entumecedor en la mente. [4]
Los estudios realizados por la Red de advertencia de abuso de drogas en la
década de 1970 muestran que los informes de los medios de violencia inducida
por PCP son muy exagerados y que los incidentes de violencia son inusuales y
a menudo se limitan a individuos con reputación de agresión
independientemente del consumo de drogas. [19] : 48 Aunque poco común, se
han dado a conocer los eventos de individuos intoxicados con PCP que actúan
de manera impredecible, posiblemente impulsados por sus delirios o
alucinaciones. Un ejemplo es el caso de Big Lurch , un ex rapero con
antecedentes de crímenes violentos, que fue condenado por el asesinato y el
canibalismo de su compañero de habitación bajo la influencia de
PCP. [20]Otros tipos de incidentes comúnmente citados incluyen infligir daño a
la propiedad y automutilación de varios tipos, como sacarse los propios
dientes. [19] : 48 [20] Sin embargo, estos efectos no se observaron en su uso
medicinal en las décadas de 1950 y 1960, y los informes de violencia física
sobre PCP a menudo han demostrado ser infundados. [21] [22]
Las dosis recreativas de la droga también ocasionalmente parecen inducir un
estado psicótico que se asemeja a un episodio esquizofrénico , que a veces
dura meses. [23] Los usuarios generalmente informan que se sienten ajenos a
la realidad. [24]
Los síntomas se resumen en el dispositivo mnemónico RED DANES:
furia, eritema (enrojecimiento de la piel), pupilas dilatadas,
delirios, amnesia , nistagmo (oscilación del globo ocular cuando se mueve
lateralmente), excitación y sequedad de la piel. [25]
Adiccion
La PCP se autoadministra e induce la expresión de ΔFosB en las neuronas
espinosas medianas de tipo D1 del núcleo accumbens , [1] [26]y, en
consecuencia, se sabe que el uso excesivo de PCP
causa adicción . [1] Los efectos de recompensa y refuerzo de PCP están
mediados, al menos en parte, bloqueando los receptores de NMDA en las
entradas glutamatérgicas a las neuronas espinosas de tipo D1 en el núcleo
accumbens. [1] Se ha demostrado que PCP produce aversión
placentaria condicionada y preferencia de lugar condicionada en estudios con
animales. [27]
Métodos de administración
La PCP se presenta en forma líquida y en polvo (la base de PCP se disuelve
con mayor frecuencia en éter ), pero generalmente se pulveriza sobre un
material frondoso como el cannabis , la menta , el orégano , el tabaco ,
el perejil o las hojas de jengibre y luego se fuma.

 PCP puede ser ingerido por fumar. "Fry" es un término callejero para los
cigarrillos de marihuana o tabaco que se sumergen en PCP y luego se
secan. [28]
 El clorhidrato de PCP se puede insuflar (inhalar), dependiendo de la pureza.
 La base libre es bastante hidrófoba y puede absorberse a través de la piel y
las membranas mucosas (a menudo inadvertidamente).

Manejo de la intoxicación
El tratamiento de la intoxicación por PCP consiste principalmente en cuidados
de apoyo, que controlan la respiración, la circulación y la temperatura corporal,
y, en las primeras etapas, en el tratamiento de los síntomas
psiquiátricos. [29] [30] [31] Las benzodiazepinas , como lorazepam , son
las drogas de elección para controlar la agitación y las convulsiones (cuando
están presentes). Los antipsicóticos típicos , como las fenotiazinas y
el haloperidol, se han usado para controlar los síntomas psicóticos, pero
pueden producir muchos efectos secundarios indeseables, como la distonía ,
por lo que ya no se prefiere su uso; Las fenotiazinas son particularmente
riesgosas, ya que pueden reducir el umbral convulsivo, empeora
la hipertermia y aumenta los efectos anticolinérgicos de la PCP. [29] [30] Si se
administra un antipsicótico, se ha recomendado
haloperidol intramuscular . [31] [32] [33]
La diuresis ácida forzada (con cloruro de amonio o, con más seguridad, ácido
ascórbico ) puede aumentar el aclaramiento de la PCP del cuerpo, y en el
pasado se recomendaba algo polémicamente como medida
de descontaminación . [29] [30] [31] Sin embargo, ahora se sabe que solo
alrededor del 10% de una dosis de PCP es eliminada por los riñones, lo que
aumentaría el aclaramiento urinario de poca importancia; además,
la acidificación urinaria es peligrosa, ya que puede inducir acidosis y empeorar
la rabdomiolisis (degradación muscular), que no es una manifestación inusual
de toxicidad por PCP. [29] [30]
Farmacología
Farmacodinamia
Fenciclidina [34] [35]
Sitio K (nM) Acción Especies Árbitro
NMDA 44-59 Antagonista Humano [36] [37]
DAKOTA DEL
MOR > 10,000 Humano [36]
NORTE
DAKOTA DEL
INSECTO > 10,000 Humano [36]
NORTE
DAKOTA DEL
KOR > 10,000 Humano [36]
NORTE
DAKOTA DEL
NOP > 10,000 Humano [36]
NORTE
σ > 10,000 Agonista conejillo de indias [36] [38]
σ 136 Agonista Rata [36]
DAKOTA DEL
re > 10,000 Humano [36]
NORTE
2.7-4.3 144 Rata /
D alto Agonista [39] [40] [41]
( EC ) humano humano
DAKOTA DEL
5-HT > 10,000 Humano [36]
NORTE
5-HT alto ≥5,000 Agonista? Rata [40] [42]
SERT 2,234 Inhibidor Humano [36]
RED > 10,000 Inhibidor Humano [36]
DAT > 10,000 Inhibidor Humano [36]
DAKOTA DEL
PCP 154 Humano [37]
NORTE
[ 3 H] 5-HTcaptación 1,424 (IC ) Inhibidor Rata [43]
[ 3 H] NISunión 16,628 (IC) Inhibidor Rata [43]
[ 3 H] DAabsorción 347 (IC) Inhibidor Rata [43]
[ 3 H] CFTvinculante 1,547 (IC) Inhibidor Rata [43]
Values are K (nM). The smaller the value, the more strongly the drug binds to the site.
PCP is well known for its primary action on the NMDA receptor, an ionotropic
glutamate receptor, in rats and in rat brain homogenate.[44][41]As such, PCP is
an NMDA receptor antagonist. The role of NMDAR antagonism in the effect of
PCP, ketamine, and related dissociative agents was first published in the early
1980s by David Lodge[45] and colleagues.[16] Other NMDA receptor
antagonists include ketamine,[46] tiletamine,[47] dextromethorphan,[48] nitrous
oxide, and dizocilpine (MK-801).
Research also indicates that PCP inhibits nicotinic acetylcholine
receptors(nAChRs) among other mechanisms. Analogues of PCP exhibit
varying potency at nACh receptors[49] and NMDA receptors.[50] Findings
demonstrate that presynaptic nAChRs and NMDA receptor interactions
influence postsynaptic maturation of glutamatergic synapses and consequently
impact synaptic development and plasticity in the brain.[51]These effects can
lead to inhibition of excitatory glutamate activity in certain brain regions such as
the hippocampus[52] and cerebellum[53]thus potentially leading to memory loss
as one of the effects of prolonged use. Acute effects on the cerebellum manifest
as changes in blood pressure, breathing rate, pulse rate, and loss of muscular
coordination during intoxication.[8]
PCP, like ketamine, also acts as a potent dopamine DHigh receptor partial
agonist in rat brain homogenate[41] and has affinity for the human cloned
DHigh receptor.[54] This activity may be associated with some of the other
more psychotic features of PCP intoxication, which is evidenced by the
successful use of D receptor antagonists (such as haloperidol) in the treatment
of PCP psychosis.[55]
In addition to its well explored interactions with NMDA receptors, PCP has also
been shown to inhibit dopamine reuptake, and thereby leads to increased
extracellular levels of dopamine and hence
increased dopaminergic neurotransmission.[56] However, PCP has
little affinity for the human monoamine transporters, including the dopamine
transporter(DAT).[36] Instead, its inhibition of monoamine reuptake may be
mediated by interactions with allosteric sites on the monoamine
transporters.[36]PCP is notably a high-affinity ligand of the PCP site 2 (K =
154 nM), a not-well-characterized site associated with monoamine reuptake
inhibition.[37]
Studies on rats indicate that PCP interacts indirectly with opioid
receptors(endorphin and enkephalin) to produce analgesia.[57]
A binding study assessed PCP at 56 sites including neurotransmitter
receptors and transporters and found that PCP had K values of >10,000 nM at
all sites except the dizocilpine (MK-801) site of the NMDA receptor (K = 59 nM),
the σ receptor (PC12) (K = 136 nM), and the serotonin transporter (K =
2,234 nM).[36] The study notably found K values of >10,000 nM for the D
receptor, the opioid receptors, the σ receptor, and
the dopamine and norepinephrine transporters.[36] These results suggest that
PCP is a highly selective ligand of the NMDAR and σ receptor.[36]However,
PCP may also interact with allosteric sites on the monoamine transporters to
produce inhibition of monoamine reuptake.[36]
Neurotoxicity
Some studies found that, like other NMDA receptor antagonists, PCP can cause
a kind of brain damage called Olney's lesions in rats.[58][59]Studies conducted
on rats showed that high doses of the NMDA receptor
antagonist dizocilpine caused reversible vacuoles to form in certain regions of
the rats' brains. All studies of Olney's lesions have only been performed on non-
human animals and may not apply to humans. One unpublished study by Frank
Sharp reportedly showed no damage by the NDMA antagonist, ketamine, a
similar drug, far beyond recreational doses,[60] but due to the study never
having been published, its validity is controversial.
PCP has also been shown to cause schizophrenia-like changes in N-
acetylaspartate and N-acetylaspartylglutamate levels in the rat brain, which are
detectable both in living rats and upon necropsy examination of brain
tissue.[61] It also induces symptoms in humans that mimic
schizophrenia.[62] PCP not only produced symptoms similar to schizophrenia, it
also yielded electroencephalogram changes in the thalamocortical pathway
(increased delta decreased alpha) and in the hippocampus (increase theta
bursts) that were similar to those in schizophrenia.[63] PCP induced
augmentation of dopamine release may link the NMDA and DA hypothesis of
schizophrenia.[64]
Pharmacokinetics
PCP is metabolized into PCHP, PPC and PCAA.
When smoked, some of the compound is broken down by heat into 1-
phenylcyclohexene (PC) and piperidine.
Conversion of PCP into PC and piperidine by heat.

Chemistry
PCP is an arylcyclohexylamine.
Analogues

Possible analogues of PCP

Fewer than 30 different analogues of PCP were reported as being used on the
street during the 1970s and 1980s, mainly in the United States.[16] The best
known of these are rolicyclidine (PCPy or 1-(1-
phenylcyclohexyl)pyrrolidine); eticyclidine(PCE or N-ethyl-1-
phenylcyclohexylamine); and tenocyclidine (TCP or 1-(1-(2-
thienyl)cyclohexyl)piperidine).[65] Only of a few of these compounds were
widely used.[16]
The generalized structural motif required for PCP-like activity is derived from
structure-activity relationship studies of PCP derivatives, and summarized in the
illustration (right). All of these derivatives are likely to share some of their
psychoactive effects with PCP itself, although a range of potencies and varying
mixtures of anesthetic, dissociative and stimulant effects are known, depending
on the particular drug and its substituents. In some countries such as the United
States, Australia, and New Zealand, all of these compounds would be
considered controlled substance analogues of PCP, and are hence illegal drugs
if sold for human consumption, even though many of them have never been
made or tested.[66][67]
Other analogues of PCP include 3-HO-PCP, 3-MeO-PCMo, and 3-MeO-PCP.
Usage
PCP began to emerge as a recreational drug in major cities in the United States
in 1960s.[7] 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 number of high schoolstudents admitting to trying PCP at
least once fell from 13% in 1979 to less than 3% in 1990.[19]:46–49
History
It is commonly mistakenly reported that PCP was first synthesized in
1926.[68] This early synthesis, in fact, refers to the
PCP intermediate PCC.[16]PCP was actually discovered by Victor Maddox, a
chemist at Parke-Davisin Michigan, while investigating synthetic analgesic
agents. Although unexpected, PCP was identified as potentially interesting, and
as such, was submitted for pharmacological testing. The promising results of
these pharmacological investigations led to the rapid development of PCP. It
was approved for use as an investigational drug under the brand names Sernyl
and Sernylan in the 1950s as an anesthetic, but because of its long terminal
half-life and adverse side effects, such as hallucinations, mania, delirium,
and disorientation, it was removed from the market in 1965 and limited to
veterinary use.[16][69][70]
Regulation
PCP is a Schedule II substance in the United States and its ACSCN is
7471.[71] Its manufacturing quota for 2014 was 19 grams.[72]
It is a Schedule I drug by the Controlled Drugs and Substances act in Canada,
a List I drug of the Opium Law in the Netherlands, and a Class Asubstance in
the United Kingdom.[73]
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