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Inhalational Durg Abuse
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard Rowley, Herbert D. Kleber, Peter Jatlow
Evidence that chronic use of phencyclidine may produce long-term neurologic, cognitive, and behavioral dysfunction is suggested. Studies of chronic PCP users have shown some tolerance to the drug, as well as anxiety, fatigue, irritability, depression, paranoid psychosis, and memory loss (Stillman and Petersen, 1979) and a chronic dementia (Millman, 1985).
The Molecular Basis of Action of Abused Substances
Published in Frank Lynn Iber, Alcohol and Drug Abuse as Encountered in Office Practice, 2020
Phencyclidine has effects similar to those of amphetamines and barbiturates. This agent enhances the sedative effects of both ethanol and barbiturates. Binding occurs at two disparate central nervous system sites. The omega opiate binding is highly specific, but the functional alteration is unknown. It also binds to the GABA-benzodiazepine ionophore chloride channel. This component is required to complete that regulatory system.
Stimulants and psychedelics
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
Mescaline, derived from the Mexican peyote and other cacti, is the least potent of all the classical hallucinogens (Nichols, 2004). Psilocybin derived from mushrooms (magic mushroom) and LSD both have their main mechanism of action at the serotonin 2A receptor (5-HT2A). All of these hallucinogenic substances produce similar effects and show cross-tolerance when multiple hallucinogens are used (Nichols, 2004). Phencyclidine (PCP) is a dissociative anaesthetic similar in action to ketamine. PCP is known by a variety of names but is commonly referred to as ‘Angel dust’. PCP is an N-methyl-D-aspartate (NMDA) receptor agonist and also a partial D2 receptor agonist and the sites of action produce a variety of effects including physical and psychological changes. PCP is one of many dissociate anaesthetic compounds that are available for non-medical use. A review of these substances, published in 2014, suggested that, currently, at least 12 dissociatives are available and almost half of them were unknown in the scientific literature prior to their introduction (Morris and Wallach, 2014).
Pre-bout hypertension in the combat sports athlete: clearance recommendations
Published in The Physician and Sportsmedicine, 2023
Kevin deWeber, Ken S Ota, Cicely Dye
Pre-bout hypertension may also be a sign of drug, exogenous hormone, and/or supplement use. Many prescription medications and illicit drugs can cause elevated BP; common culprits are listed in Table 2. Illicit drug users have a 6.5-times increased risk of hemorrhagic and ischemic stroke; cocaine, amphetamines, Ecstasy, ephedrine, phencyclidine, and LSD are known culprits [24]. Hemorrhagic strokes have also been reported after the use of pre-workout supplements [25–27]. Cocaine use can cause sudden cardiac death, life-threatening arrhythmias, myocardial ischemia and infarction, dilated cardiomyopathy, and acute myocarditis [28]. Amphetamines can cause myocardial infarction [29], and energy drinks have been linked to myocardial ischemia [30]. Androgenic anabolic steroid abuse has been linked to arterial hypertension, accelerated progression of coronary artery disease, and increased risk of myocardial infarction [31]. Participating in combat sports, with its vigorous high-static/high-dynamic exercise and repeated head trauma, while these substances are in the body may compound the risk of significant adverse events.
Novel Sunifiram-carbamate hybrids as potential dual acetylcholinesterase inhibitor and NMDAR co-agonist: simulation-guided analogue design and pharmacological screening
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Khalid A. Agha, Nader E. Abo-Dya, Abdul Rashid Issahaku, Clement Agoni, Mahmoud E. S. Soliman, Eatedal H. Abdel-Aal, Zakaria K. Abdel-Samii, Tarek S. Ibrahim
N-methyl-D-aspartate receptor (NMDAR) is another approach in enhancing cognition,8 it is a glutamate receptor and ion channel protein found in nerve cells as tetrameric complex and is a promising target for cognitive enhancement since it is centrally involved in cognitive processes.9 It was shown that transient activation of NMDAR is the trigger for the induction of long-term potentiation (LTP) at synapses of neurons in the hippocampus which are likely to explain their importance for learning and memory.10 Also, it has the ability to increase acetylcholine release and its inhibition result in decrease in acetylcholine secretion.11,12 Biochemical and molecular studies of NMDA receptor showed that both mRNA and protein levels of NMDARs are reduced in AD brain and AD model, suggesting hypofunction of NMDAR with increasing AD pathologic severity.13 These observations supported by findings that blocking NMDAR by ketamine and phencyclidine can induce schizophrenic like symptoms including cognitive decline in healthy individuals and exacerbate cognitive deficit in schizophrenic individuals.14,15
Characterizing Trends in Synthetic Cannabinoid Receptor Agonist Use from Patient Clinical Evaluations during Medical Toxicology Consultation
Published in Journal of Psychoactive Drugs, 2021
Collin Tebo, Maryann Mazer-Amirshahi, Paul Wax, Sharan Campleman, Edward Boyer, Jeffrey Brent, Amit Sheth, Raminta Daniuaityte, Robert Carlson
Three SCRA users indicated an attempt at self-harm. One patient was a 27-year-old white male with bipolar disorder who was single and had some high school education. He presented to the ED with delirium/toxic psychosis. On the day he came into the ED, he had smoked a synthetic cannabinoid joint that had been dipped in phencyclidine. A second patient who expressed an attempt at self-harm was an 18-year-old white male in high school who was found confused and falling. His clinical effects included coma/central nervous system depression. His friends gave him an SCRA called, “Toochi,” that “people take to trip out.” The third patient who attempted self-harm was a single white male, age 21, who had smoked an SCRA called “Sexy Monkey,” and had injected the drug 2 C (a phenethylamine similar in structure to MDMA, Ecstasy). On the day he presented to the ED, he had also reported using heroin, cocaine, and hydroxyzine, reporting that he was attempting suicide. The effects of the drugs “felt great and [I] realized I did not want to die,” he said.