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)

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

The central effects of phencyclidine (PCP) were investigated using electrophysiological, biochemical, and behavioral techniques. PCP produced depressions of neuronal firing of several brain regions when applied locally or parenterally. At the cerebellar locus coeruleus Purkinje neuron pathway PCP produced depressions of spontaneous firing. Use of lesion techniques and receptor antagonists revealed that at this synapse PCP acted as an agonist, i.e., an indirect sympathomimetic in that it caused release and or blocked reuptake of norepinephrine. PCP also produce alterations in behavioral measures such as stereotypy and rotarod performance. In addition PCP, like norepinephrine, produced increases in cyclic AMP levels in cerebellar slices. Inhibition of central neuron firing, and alterations in behavior were correlated with brain and blood levels of PCP. Many effects of PCP were antagonized by neuroleptics. It can be concluded that PCP has profound effects on several indices of central neuron function and such changes can be related to the psychosis and other effects of this drug.
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PMID:Candidate mechanisms underlying phencyclidine-induced psychosis: an electrophysiological behavioral, and biochemical study. 612 73

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17

A field study was performed at two police agencies to evaluate the utility and accuracy of five on-site urine analysis drug-testing devices when used to test driving under the influence (DUI) arrestees. The devices evaluated were AccuSign, Rapid Drug Screen, TesTcup-5, TesTstik, and Triage. Standard workplace screening cut-off concentrations were used and samples were tested for marijuana, cocaine and metabolites, amphetamine(s), opiates, and PCP (except opiates 300 ng/mL). Four-hundred arrestees were recruited at each site, informed consent was obtained, and urine specimens were collected from each subject for analysis. Police officers conducted the testing with one device, and trained technicians performed testing with the other four devices. The device used by the officers was rotated. All positive and 5% of the negative samples were confirmed in a laboratory using mass spectrometry. Laboratory cut-off concentrations were 4 ng/mL for carboxy-THC; 50 ng/mL for benzoylecgonine; 100 ng/mL for amphetamines; 50 ng/mL for opiates; and 5 ng/mL for PCP. Approximately one-third (36%) of the subjects tested positive for at least one drug. No randomly selected sample, that tested negative on the devices, tested positive at the laboratory. Based on 800 specimens, the false-negative rate for each device was < 1% for all drug classes. A false positive was defined as testing positive with the device, but the specimen did not contain detectable drug, given the study reporting criteria. For marijuana, benzoylecgonine, and opiates, all devices had < or = 0.25% false-positive rates. For PCP, the false-positive rates were all < or = 1.5%. For amphetamine(s), the false-positive rates were all < or = 1.75%. These rates were adjusted because study confirmation batteries included methylenedioxyamphetamine, methylenedioxymethamphetamine (MDMA), additional over-the-counter sympathomimetic amines, hydromorphone, and hydrocodone. Without the expanded confirmation battery, false-positive rates approached 4% (Triage) for amphetamines and were > or = 2.25% for opiates. Fifty to 90% of the positive amphetamine(s) samples contained MDMA. A similar percentage of the opiate-positive samples contained hydromorphone or hydrocodone. When additional drugs were included in the confirmation testing, it was concluded that the on-site urine analysis drug-testing results were useful in DUI investigations.
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PMID:A field evaluation of five on-site drug-testing devices. 1242 6

Ketamine is a dissociative anaesthetic that is being used in non-medical contexts. The effects of ketamine are very similar to those of phencyclidine, another dissociative anaesthetic that has enjoyed considerable popularity as a recreational drug. The effects of ketamine include analgesia, cardiovascular and respiratory stimulation, dissociation, hallucinations and anaesthesia. The potential dangers of uncontrolled ketamine use include psychosis and violence, accidents and marked psychomotor and cognitive impairment. Although studies have shown potential for tolerance to and physical dependence on ketamine, further investigation of these phenomena is needed. Ketamine is thought to produce most of its effects through antagonist activity at the PCP site of the NMDA receptor complex. Ketamine has sympathomimetic properties resulting from enhancement of catecholamine, and particularly dopamine, activity. While opioid receptor activity has been identified, this is relatively weak and the contribution to the effects of ketamine is not clear. Although much is known of the clinical uses and effects of ketamine, as yet little is understood of ketamine as a recreational drug and potential drug of dependence.
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PMID:Pharmacological properties of ketamine. 1620 65

NMDA receptor antagonists include the prescription medication ketamine, the illicit xenobiotics PCP, MXE, and other novel PCP analogs, and the OTC medication DXM. The NMDA receptor antagonist most commonly abused by adolescents in the United States is DXM. These xenobiotics cause dissociative effects by non-competitively inhibiting the action of glutamate at the NMDA receptor. Additionally, these agents modulate the actions of monoamine neurotransmitters, agonize opioid receptors, and inhibit nitric oxide synthase. Patients typically present with sympathomimetic and neuropsychiatric clinical manifestations after abuse of NMDA receptor antagonists. Treatment is generally symptomatic and supportive. Interventions include benzodiazepines, propofol, fluids, antiemetics, aggressive cooling, and respiratory support.
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PMID:Generation Z: Adolescent Xenobiotic Abuse in the 21st Century. 2728 13