Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phencyclidine (PCP) is a potent sympathomimetic and hallucinogenic dissociative anesthetic agent. As an abused street drug, it is most often smoked, thus allowing the user to titrate the dose. The clinical signs of PCP intoxication can be viewed in three dose-related stages, but waxing and waning of signs through the three stages is not uncommon. Treatment protocols for each stage address drug therapy and both clinical and psychological supportive measures.
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PMID:Emergency management of acute phencyclidine intoxication. 43 46

Phencyclidine (PCP) is a dissociative veterinary anesthetic and tranquilizer that at present is being abused as a psychedelic and hallucinogenic agent with increasing frequency. The cases of two young patients suffering from phencyclidine toxicity are reported. In each, central nervous system depression was accompanied by an acute dystonic motor reaction resulting in acute rhabdomyolysis and myoglobinuria. Skeletal muscle injury was felt to be the result of excessive involuntary isometrimc motor activity rather than a direct effect of phencyclidine on skeletal muscle. Patients suffering from phencyclidine intoxication should be screened for acute rhabdomyolysis. Phencyclidine intoxication should be included in the differential of nontraumatic rhabdomyolysis and should be considered among the potential causes of acute myoglobinuric renal failure.
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PMID:Phencyclidine-associated acute rhabdomyolysis. 62 51

A 23-year old white man presented an acute PCP intoxication. His EEG showed a monomorphic nonreactive generalized theta rhythm which is the typical activity of PCP overdose. This background was interrupted by periodic bilaterally synchronous high voltage slow paroxysms similar to those described in subacute sclerosing panencephalitis. This unusual finding supports the hypothesis that PCP may act by reversible deafferentation of cortical neurons.
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PMID:Pseudoperiodic bilateral EEG paroxysms in a case of phencyclidine intoxication. 65 79

A survey of 104 deaths involving phencyclidine (PCP) occurring from 1981 through 1986 in metropolitan St. Louis, Missouri, is presented. Four black males (22-33 yr) died from fatal PCP intoxication. PCP was detected in an additional 100 deaths: 81 homicides, 13 suicides, and 6 accidental deaths. Seventy-five of these deaths were homicides of Black males (mean age 27 years) typically dying from gunshot wounds, 64 cases. In 50% of deaths where PCP was detected, other drugs were co-administered: ethanol (35%) and cocaine (20%) being the most common mixtures. A dramatic continuous increase in PCP abuse from 1984 through 1986 was demonstrated by drug abuse indicator data: treatment admissions, emergency room episodes, police exhibits, and driving under the influence of PCP arrests. Increased abuse of PCP in St. Louis has been associated with increased medical emergencies and violence against persons.
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PMID:Phencyclidine and violent deaths in St. Louis, Missouri: a survey of medical examiners' cases from 1977 through 1986. 228 25

Phencyclidine (PCP) abuse is reaching alarming proportions. PCP has recently been shown to induce hypertensive encephalopathies, microvascular cerebrovasospasm and acute intracerebral hemorrhage. Since we have shown in vitro that cerebral vasospasms induced by PCP could be completely reversed, or prevented, by use of organic calcium antagonists, we utilized a television microscope recording system to determine whether magnesium ions (Mg2+) could inhibit the ability of PCP to induce contraction of pial arterioles and its sequelae of microvascular damage. Administration of either MgCl2 or Mg aspartate HCl, i.a. or i.v. (1, 10, and 20 mumol/min), before or after administration of PCP produced dose-dependent inhibition (30-80%) of PCP-induced arteriolar spasms and the subsequent vascular damage. A variety of pharmacologic receptor antagonists and cyclooxygenase inhibitors failed to influence PCP-induced cerebrovasospasms. These data suggest that a naturally-occurring Ca2+ antagonist, viz. Mg2+, may be useful in the treatment of PCP intoxication and its cerebral vascular consequences.
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PMID:Magnesium ions prevent phencyclidine-induced cerebrovasospasms and rupture of cerebral microvessels: direct in-vivo microcirculatory studies on the rat brain. 236 50

Phencylidine (PCP) is a major drug of abuse in the United States. It produces a toxic confusional psychosis in man. We show here that nanomolar to micromolar concentrations of PCP and behaviorally active congeners selectively block voltage-regulated noninactivating (or very slowly inactivating) presynaptic K channels in the brain. The rank order of potency for blockage of these K channels parallels both the relative ability of these agents to produce characteristic behavioral deficits in rats and their ability to displace [3H]PCP from its high-affinity binding sites in brain. In view of the enhanced voltage-gated Ca influx that would be expected to accompany blockage of presynaptic K channels, this mechanism could explain the excessive neurotransmitter release that is characteristic of PCP intoxication.
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PMID:Phencyclidine in low doses selectively blocks a presynaptic voltage-regulated potassium channel in rat brain. 241 37

PCP or "angel dust" is a dissociative anesthetic agent with notoriety as an abuse substance. Numerous members of many subcultures are frequent users of this drug. It is well known in California's psychedelia, along the East Coast, and in the middle- and working-class suburbs of the Midwest. It is important that practitioners become acquainted with the drug and its effects. Persons intoxicated with PCP have murdered their own children and have even jumped out of high-rise apartment buildings. States of florid psychosis lasting for days can follow a brief encounter with PCP. Inadvertent administration of narcotics and barbiturates to patients with acute PCP intoxication can lead to a crisis that could prove to be fatal.
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PMID:Phencyclidine (PCP) abuse. A close-up look at a growing problem. 293 52

Studies were conducted to determine whether single or combination treatments of charcoal, paraffin, cholestyramine, and/or ammonium chloride (NH4Cl), would alter the rotarod-measured motor dysfunction induced by 10 to 90 mg/kg of phencyclidine (PCP). Additionally, the effect of NH4Cl/charcoal treatment of the biodisposition of 50 mg/kg PCP was evaluated in order to assess whether amelioration of behavioral effects could be correlated to alterations in brain levels, plasma levels, and/or the renal clearance of PCP and metabolites. NH4Cl/charcoal treatment proved more effective at reducing intoxication than either treatment singly, though effectiveness was reduced by larger doses of PCP. NH4Cl/charcoal treatment reduced intoxification by 40, 16, and 21% at PCP doses of 10, 25, and 50 mg/kg. However, the reduction in motor dysfunction observed at 25 and 50 mg/kg PCP was greater than the sum of the individual treatments. In contrast, the effect of combined NH4Cl and charcoal treatment on the biodisposition of 50 mg/kg PCP is not synergistic, but appears instead to be due simply to the additive effects of the individual treatments. Thus the amelioration of PCP intoxication cannot be fully explained by alterations in PCP biodisposition.
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PMID:Modification of phencyclidine intoxification and biodisposition by charcoal and other treatments. 317 69

1. Efflux of 86Rb from synaptosomes prepared from rat forebrain was used to assess voltage-gated changes in K+ permeability in mammalian central nerve terminals. 2. Although they are structurally unrelated to phencyclidine (PCP), the sigma-ligands, N-allyl-normetazocine (NANM; SKF 10,047) and cyclazocine, generalize to PCP in behavioral assays, displace [3H]PCP from a high-affinity binding site in brain, and potently block the same voltage-gated K+ channel as PCP itself. 3. The block of the voltage-gated K+ channel in nerve terminals by NANM and cyclazocine was stereoselective and was unaffected by the opioid antagonist naloxone. Moreover, in our experiments the relative activity of the stereoisomers of NANM and cyclazocine compared favourably with their relative activity in behavioural paradigms and binding assays. 4. Dexoxadrol, the D-isomer of dioxodrol, which produces PCP-like behavioural effects and displaces bound [3H]PCP, was a potent blocker of the PCP-sensitive, voltage-gated K+ channel. The corresponding L-isomer, levoxadrol, which produces morphine-like antinociception and sedation, but does not produce PCP-like behaviour nor displace bound [3H]PCP, was a very weak blocker of the voltage-gated K+ channel. 5. Levoxadrol, but not dexoxadrol, activated a separate K+ channel, as manifested by an increase in 86Rb efflux. This effect was blocked by naloxone. 6. We conclude that one of the PCP-sigma-ligand binding sites in the brain may be associated with the voltage-gated, non-inactivating K+ channel we observe in nerve terminals. Our findings are also consistent with the view that some of the behavioural manifestations of PCP intoxication are mediated by block of presynaptic K+ channels.
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PMID:Psychotomimetic sigma-ligands, dexoxadrol and phencyclidine block the same presynaptic potassium channel in rat brain. 325 23

Rats were trained to obtain food pellets in an 8-arm radial maze until a criterion of 89% efficiency, i.e., all arms entered within 9 arm entries, was reached in 5 consecutive sessions. Decreases in efficiency caused by phencyclidine (PCP; 4 to 9 mg/kg, IP, 15 min before testing) or ketamine (25 mg/kg, IP, 5 min) were attenuated when subjects were pretreated with clonidine (0.05 mg/kg, IP, 30 min). However, significant improvements in performance in the maze were not observed when clonidine (0.05 to 0.4 mg/kg, IP) was administered 15 min after PCP (9 mg/kg, IP, 45 min). Subsequent studies of righting reflex demonstrated an increased frequency and duration of anesthesia when clonidine (0.05 mg/kg, IP) was administered 15 minutes before PCP (12.5 to 50 mg/, IP) or ketamine (50 to 100 mg/kg, IP). When clonidine (0.05 mg/kg, IP) was administered 15 minutes before [3H]PCP (40 microCi/kg, IP), brain levels of tritium were reduced by 42 to 55%. The present findings do not support the suggestion that clonidine may be useful in the treatment of PCP intoxication. The data does indicate that pretreatment of surgical patients with clonidine may reduce the dose of ketamine required for anesthesia.
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PMID:Interactions of clonidine with phencyclidine and ketamine: studies of radial maze performance and righting reflex in rats. 356 94


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