Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.16.2 (PCP)
3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most street hallucinogens contain either LSD or phenycyclidine HCl (PCP). Because the acute phase of LSD and PCP mimic several other drugs and conditions, it is important to exclude these other possibilities. When faced with LSD or PCP, "talking down" usually suffices for the mild case; management becomes more complex should hyperpyrexia, coma, seizures or a hypertensive crisis ensue. Diazepam, not a phenothiazine, is preferred for sedation.
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PMID:Management of hallucinogen abuse. 106 15

Repeated acquisition behavioral performances of normotensive and renovascular hypertensive baboons were tested before, during, and following chronic oral dosing with the beta-adrenergic antagonists atenolol HCl (2.6 mg/kg/day PO), and d,l propranolol HCl (6.8 mg/kg twice daily PO) in separate studies. Each study administered active drug for 21 consecutive days preceded and followed by 14-day baseline and recovery periods, respectively. Animals pressed five keys in sequence for food reinforcement during daily experimental sessions which consisted of alternating acquisition (new sequence learning) and performance (previously learned) task components. Atenolol increased response latencies during acquisition in comparison to performance components, and during early portions of sessions. Propranolol also increased response latencies during acquisition components in early periods of sessions, but fewer dependent measures were affected, and the magnitude of increases in response latencies was smaller (12% +/- 5 SEM) as compared with atenolol (47% +/- 13). Test doses of phencyclidine HCl (PCP) increased latencies to the same degree as atenolol. PCP markedly reduced accuracy, while atenolol or propranolol did not. Blood pressures remained stable under atenolol, and decreased by approximately 10-15 mmHg under propranolol. No differences between renovascular hypertensive and normotensive baboons were found as a function of drug conditions. Drug effects were not dependent on plasma propranolol concentration.
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PMID:Performance of baboons under a repeated acquisition procedure during chronic oral exposure to atenolol and propranolol. 136 67

Tris-HCl is the most commonly used buffer in studies of radioligand binding to sigma receptors, with concentrations as high as 50 or 100 mM often used. We report here that these concentrations of Tris substantially inhibit (+)-[3H]SKF-10,047 binding to sigma receptors. The well-established inhibitory effect of Tris-HCl on ligand binding to PCP receptors did not contribute to the presently reported inhibition of (+)-[3H]SKF-10,047 binding. The IC50 of Tris, determined in the presence of 10 mM potassium phosphate buffer, was 15.4 +/- 1.2 mM (n = 3, pH 8.0, 25 degrees C, 1 nM radioligand). Equilibrium saturation studies revealed an apparent competitive inhibition of binding.
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PMID:Tris inhibits (+)-[3H]SKF-10,047 binding to sigma receptors. 143 40

1. Anesthetized dogs were given phencyclidine HCl (PCP) by intracerebroventricular (i.c.v.) injection. 2. Physiological parameters were monitored after consecutive doses of 0.5, 1.0 and 2.0 mg of PCP. 3. Dose-related changes seen, including bradycardia, hypotension and bradypnea, were opposite to those produced by i.v. doses. 4. Single doses of 1.0 or 2.0 mg of PCP confirmed the prior observations, and the latter provided the baseline for further observations on dogs receiving PCP before various i.c.v. pretreatments--atropine, haloperidol, phentolamine or propranolol--in efforts to characterize the central neurotransmitter system(s) involved in the PCP effects.
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PMID:Respiratory and circulatory effects of centrally administered phencyclidine in anesthetized dogs. 176 Dec

Neurochemical interactions of tiletamine, a potent phencyclidine (PCP) receptor ligand, with the N-methyl-D-aspartate (NMDA)-coupled and -uncoupled PCP recognition sites were examined. Tiletamine potently displaced the binding of [3H]1-(2-thienyl)cyclohexylpiperidine with an IC50 of 79 nM without affecting sigma-, glycine, glutamate, kainate, quisqualate, or dopamine (DA) receptors. Like other PCP ligands acting via the NMDA-coupled PCP recognition sites, tiletamine decreased basal, harmaline-, and D-serine-mediated increases in cyclic cGMP levels and induced stereotypy and ataxia. Tiletamine was nearly five times more potent than PCP at inhibiting the binding of 3-hydroxy[3H]PCP to its high-affinity NMDA-uncoupled PCP recognition sites. However, following parenteral administration, dizocilpine maleate (MK-801), ketamine, PCP, dexoxadrol, and 1-(2-thienyl)cyclohexylpiperidine HCl, but not tiletamine, increased rat pyriform cortical DA metabolism and/or release, a response modulated by the NMDA-uncoupled PCP recognition sites. Pretreatment with tiletamine did not attenuate the MK-801-induced increases in rat pyriform cortical DA metabolism, a result suggesting that tiletamine is not a partial agonist of the NMDA-uncoupled PCP recognition sites in this region. However, following intracerebroventricular administration (100-500 micrograms/rat), tiletamine increased pyriform cortical DA metabolism with a bell-shaped dose-response curve. These data indicate a differential interaction of tiletamine with the NMDA-coupled and -uncoupled PCP recognition sites. The paradoxical effects of tiletamine suggest that tiletamine might activate receptor(s) or neuronal pathways of unknown pharmacology.
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PMID:Contrasting neurochemical interactions of tiletamine, a potent phencyclidine (PCP) receptor ligand, with the N-methyl-D-aspartate-coupled and -uncoupled PCP recognition sites. 184 86

The dependence-producing properties of 10 days of chronic i.v. infusions of phencyclidine (PCP) and the relationship between PCP serum concentrations and behavioral effects were studied in Sprague-Dawley rats. For dependence studies, rats were trained to respond for food under a fixed-ratio 30 schedule during half-hour response periods every 6 hr. After training, implantation of jugular catheters, and restabilization of behavior, the rats were infused with PCP.HCl at 3.2, 5.6, 10.0 or 17.8 mg/kg/day (n = 5 or 6 per dose). The two higher doses initially decreased response rates, but tolerance developed within 4 to 5 days. When PCP infusions were terminated, dose-dependent decreases in session response rate occurred in the three highest dose groups (P less than .05). Mild, overt signs of abstinence were observed only in the highest dose group. Response rates returned to base line within 2 to 3 days after stopping PCP infusions. PCP serum concentrations in rats infused with 10 mg of PCP.HCl/kg/day for 10 days were stable from hour 24 to day 10 (mean steady-state concentration (+/- S.D.) = 97 (+/- 20) ng of PCP/ml; n = 4). The average terminal elimination half-life after stopping infusions on day 10 was 4.6 hr. Comparison of the average response rates with the average serum concentrations showed that during the first 24 hr of infusions, the rate of responding for food decreased as PCP concentrations increased; however, once the animals became tolerant to PCP there was no relationship. In contrast, during the first 24 hr after stopping infusions, response rates decreased as serum concentrations decreased.
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PMID:Phencyclidine dependence: the relationship of dose and serum concentrations to operant behavioral effects. 207 96

Recently, it was found in studies in vitro and in vivo that phencyclidine hydrochloride (PCP, 'angel dust') can induce cerebral arterial and arteriolar spasms, in psychotomimetic concentrations, by acting on specific PCP receptors, which is followed by rupture of cerebral and postcapillary venules. We wondered whether a chemical substance which has the ability to block Ca2+ channels, neurotransmitter release, intracellular Ca2+ release and the NMDA-glutamate receptor channel, viz., Mg2+, might block the PCP receptor which subserves cerebral contractile events and thereby prevent rupture of microvessels. In vivo experiments carried out on cerebral microvessels in a rat pial brain preparation revealed that different dose regimens of Mg aspartate HCl administered intravenously attenuated cerebrovasospasms induced by PCP and shifted PCP concentration-effect curves (ED50) rightward to higher concentrations. These data suggest that Mg2+ may alter the binding of PCP for its vascular receptors. Since Mg2+ prevented rupture of the cerebral microvessels, it may prove useful, clinically, in prevention and treatment of PCP-intoxicated victims.
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PMID:Mg2+ protects against PCP-induced cerebrovasospasms and vascular damage in rat brain. 215 88

Rats were chronically infused with phencyclidine (PCP, 13.3 mg PCP.HCl/kg/day) or saline, s.c., for 10 days using osmotic minipumps (n = 5 for each group). Twenty-four hours after the cessation of dosing, the rats were sacrificed, and brains were removed for analysis of PCP receptor binding. Saturation studies of the binding of [3H]-TCP to brain homogenates revealed statistically significant increases in the maximum binding capacity (Bmax) and decreases in the affinity for [3H]-TCP in the PCP-treated group.
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PMID:Alterations in rat brain [3H]-TCP binding following chronic phencyclidine administration. 217 62

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

Tritium-labelled phencyclidine (PCP) hydrochloride (12 mg/kg) was injected SC for six consecutive days into two groups of eight male rats maintained at 85% of their initial free-feeding weights. Eight days after the last injection, electric footshock raised fat levels of PCP 28% over nonshocked controls, and lowered blood levels 18%, but did not alter brain levels of the drug significantly. Thus, application of an acute stressor does result in redistribution of tissue stores of phencyclidine as predicted in the literature; however, the direction of the redistributions was to fat, rather than to brain. To explore the relation of a long-term stressor (one that eliminates adipose tissue as a sink for mobilized PCP), exploratory behavior was evaluated in male rats during six days of food deprivation commencing after six daily injections of PCP HCl (2 or 4 mg/kg, SC). Exploratory behavior of the 4 mg/kg dose group was abruptly altered, compared to saline controls, at six days of food deprivation, when the rats' body weights were about 70% of initial weights and when body fat would be severely reduced or depleted. To assess replicability and generalizability of this phenomenon, PCP HCl (4 or 8 mg/kg, SC) or dextroamphetamine sulfate (3.2 or 6.4 mg/kg, SC) was injected into male rats for six days and food deprivation followed afterward for nine consecutive days, or until similar body weight reductions as in the first experiment were achieved. Again, exploratory behavior was altered in comparison to saline controls in phencyclidine-treated rats (at the 4 mg/kg dose level) when rats reached about 70% of initial weights.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delayed effects of amphetamine or phencyclidine: interaction of food deprivation, stress and dose. 237 46


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