An NFL tight end is worried about what some douche bags at the club think of him? He plays for the fucking Patriots, one of the most popular and successful teams in the most popular sport in America.
Phencyclidine (a complex clip of the chemical name 1-(1-phenylcyclohexyl)piperidine), commonly initialized as PCP and known colloquially as angel dust, KJ (kristal joint), Ashy Larry, illy, or wet, is a recreational dissociative drug. It was brought to market in the 1950s as an anesthetic pharmaceutical drug but was taken off the market in 1965 due to its dissociative hallucinogenic side effects.
In chemical structure, PCP is an arylcyclohexylamine derivative, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA receptor and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.[1][2] Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan and nitrous oxide.
As a recreational drug, PCP may be ingested, smoked, inhaled or injected.[3]
Contents [hide] 1 Biochemistry and pharmacology 1.1 Pharmacodynamics 1.2 Pharmacokinetics 1.3 Structural analogues 1.4 Brain effects 1.5 History and medicinal use 2 Recreational uses 2.1 Methods of administration 2.2 Effects 3 Management of intoxication 4 See also 5 References 6 External links Biochemistry and pharmacology[edit] Pharmacodynamics[edit] PCP is well known for its primary action on ionotropic glutamate receptors, such as the NMDA receptor in rats and in rat brain homogenate.[4][5] As such, PCP is an NMDA receptor antagonist. NMDA receptors mediate excitation,[6] however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans[7] and rodents.[8]
Research also indicates that PCP inhibits nicotinic acetylcholine (nACh) receptors. Analogues of PCP exhibit varying potency at nACh receptors[citation needed] and NMDA receptors.[9] In some brain regions, these effects are believed to act synergistically by inhibiting excitatory activity.[citation needed]
PCP, like ketamine, also acts as a D2 receptor partial agonist in rat brain homogenate.[5] This activity may be associated with some of the other more psychotic features of PCP intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP psychosis.[10]
Studies on rats indicate that PCP indirectly interacts with endorphin and enkephalin receptors to produce analgesia.[11]
PCP may also work as a dopamine reuptake inhibitor.[12]
Pharmacokinetics[edit] PCP is metabolized into PCHP, PPC and PCAA.
When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.
Conversion of PCP into PC and piperidine by heat. Structural analogues[edit]
Possible Analogues of PCP More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. 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). These compounds were never widely used and did not seem to be as well accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.[13][citation needed]
The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarized below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.[14][15][clarification needed]
Brain effects[edit] Some studies found that, like other NMDA receptor antagonists, phencyclidine can cause a kind of brain damage called Olney's lesions in rats.[16][17] 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, [18] but due to the study never having been published, its validity is highly controversial.
Phencyclidine has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[19] It also induces symptoms in humans that mimic schizophrenia.[20]
History and medicinal use[edit] PCP was first synthesized in 1926,[21] and was developed by Parke-Davis under the tradename named Sernyl in the 1950s as an anesthetic but because of its long 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.[22][23]
Recreational uses[edit]
Illicit PCP seized by the DEA in several forms. PCP began to emerge as a recreational drug in major cities in the United States in 1967.[24]:46 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 school students admitting to trying PCP at least once fell from 13% in 1979 to less than 3% in 1990.[24]:46–49
PCP comes in both powder and liquid forms (PCP base is dissolved most often in ether), but typically it is sprayed onto leafy material such as cannabis, mint, oregano, tobacco, parsley, or ginger leaves, then smoked.[citation needed]
PCP is a Schedule II substance in the United States, 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 A substance in the United Kingdom.
Methods of administration[edit] In its pure (free base) form, PCP is a yellow oil (usually dissolved in petroleum ether, diethyl ether, or tetrahydrofuran). Upon treatment with hydrogen chloride gas, or isopropyl alcohol saturated with hydrochloric acid, this oil precipitates into white-tan crystals or powder (PCP hydrochloride). In this, the salt form, PCP can be insufflated, depending upon the purity. However, most PCP on the illicit market often contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass.[citation needed] These contaminants can range from unreacted piperidine and other precursors, to carcinogens like benzene and cyanide-like compounds such as PCC (piperidinocyclohexyl carbonitrile).[citation needed]
The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette is dipped, to be ingested through smoking, commonly known as "boat" or "water." The name most likely originated from the somatic "numbing" effect and feelings of dissociation induced by PCP, and has led to the widespread and mistaken belief that the liquid is made up of or contains real embalming fluid. Occasionally, however, some users and dealers could have, believing this myth, used real embalming fluid mixed with, or in place of, PCP.[25][26] Smoking PCP is known as "getting wet", and a cigarette or joint which has been dipped in PCP may be referred to on the street as a "fry stick," "sherm," "leak," "amp," "lovely," "KJ (an abbreviation for 'Killer Joint')," "toe tag", "dipper", "happy stick," or "wet stick." "Getting wet" may have once been a popular method of using PCP, especially in the western United States where it may have been sold for about $10 to $25 per cigarette.[citation needed]
Effects[edit] Behavioral effects can vary by dosage. Low doses produce a numbness in the extremities and intoxication, characterized by staggering, unsteady gait, slurred speech, bloodshot eyes, and loss of balance. Moderate doses (5–10 mg intranasal, or 0.01–0.02 mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.[27] Users frequently do not know how much of the drug they are taking due to the tendency of the drug to be made illegally in uncontrolled conditions.[28]
Psychological effects include severe changes in body image, loss of ego boundaries, paranoia and depersonalization. Hallucinations, euphoria, and suicidal impulses are also reported, as well as occasional aggressive behavior.[27][24]:48–49 Like many other drugs, phencyclidine has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. PCP may induce feelings of strength, power, and invulnerability as well as a numbing effect on the mind.[3]
Studies by the Drug Abuse Warning Network in the 1970s show that media reports of PCP-induced violence are greatly exaggerated and that incidents of violence are unusual and often (but not always) limited to individuals with reputations for aggression regardless of drug use.[24]:48 This said, there have been a few, very-televised events of PCP-intoxicated individuals acting in an unpredictable fashion, possibly driven by their delusions or hallucinations. One famous example is the case of Big Lurch, a former rapper with a history of violent crime, who was convicted of murdering and cannibalizing his roommate while under the influence of PCP.[29] Other commonly cited types of incidents include inflicting property damage and self-mutilation of various types, such as pulling one's own teeth.[29][24]:48 These effects were not noted in its medicinal use in the 1950s and 1960s, however, and reports of physical violence on phencyclidine have often been shown to be unfounded.[30] [31]
Recreational doses of the drug also occasionally appear to induce a psychotic state that resembles a schizophrenic episode, sometimes lasting for months at a time.[32] Users generally report feeling detached from reality.[33]
Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.[34]
Management of intoxication[edit] Management of phencyclidine intoxication mostly consists of supportive care – controlling breathing, circulation, and body temperature – and, in the early stages, treating psychiatric symptoms.[35][36][37] Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such as phenothiazines and haloperidol have been used to control psychotic symptoms, but may produce many undesirable side effects – such as dystonia – and their use is therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia, and boost the anticholinergic effects of PCP.[35][36] If an antipsychotic is given, intramuscular haloperidol has been recommended.[37][38][39]
Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was somewhat controversially recommended in the past as a decontamination measure.[35][36][37] However, it is now known that only around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence; furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is not an unusual manifestation of PCP toxicity.[35][36]
----
You're thinking of ketamine. Similar, but pcp is a hallucinogenic and ketamine is a dissociative.
Phencyclidine (a complex clip of the chemical name 1-(1-phenylcyclohexyl)piperidine), commonly initialized as PCP and known colloquially as angel dust, KJ (kristal joint), Ashy Larry, illy, or wet, is a recreational dissociative drug. It was brought to market in the 1950s as an anesthetic pharmaceutical drug but was taken off the market in 1965 due to its dissociative hallucinogenic side effects.
In chemical structure, PCP is an arylcyclohexylamine derivative, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA receptor and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.[1][2] Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan and nitrous oxide.
As a recreational drug, PCP may be ingested, smoked, inhaled or injected.[3]
Contents [hide] 1 Biochemistry and pharmacology 1.1 Pharmacodynamics 1.2 Pharmacokinetics 1.3 Structural analogues 1.4 Brain effects 1.5 History and medicinal use 2 Recreational uses 2.1 Methods of administration 2.2 Effects 3 Management of intoxication 4 See also 5 References 6 External links Biochemistry and pharmacology[edit] Pharmacodynamics[edit] PCP is well known for its primary action on ionotropic glutamate receptors, such as the NMDA receptor in rats and in rat brain homogenate.[4][5] As such, PCP is an NMDA receptor antagonist. NMDA receptors mediate excitation,[6] however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans[7] and rodents.[8]
Research also indicates that PCP inhibits nicotinic acetylcholine (nACh) receptors. Analogues of PCP exhibit varying potency at nACh receptors[citation needed] and NMDA receptors.[9] In some brain regions, these effects are believed to act synergistically by inhibiting excitatory activity.[citation needed]
PCP, like ketamine, also acts as a D2 receptor partial agonist in rat brain homogenate.[5] This activity may be associated with some of the other more psychotic features of PCP intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP psychosis.[10]
Studies on rats indicate that PCP indirectly interacts with endorphin and enkephalin receptors to produce analgesia.[11]
PCP may also work as a dopamine reuptake inhibitor.[12]
Pharmacokinetics[edit] PCP is metabolized into PCHP, PPC and PCAA.
When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.
Conversion of PCP into PC and piperidine by heat. Structural analogues[edit]
Possible Analogues of PCP More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. 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). These compounds were never widely used and did not seem to be as well accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.[13][citation needed]
The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarized below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.[14][15][clarification needed]
Brain effects[edit] Some studies found that, like other NMDA receptor antagonists, phencyclidine can cause a kind of brain damage called Olney's lesions in rats.[16][17] 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, [18] but due to the study never having been published, its validity is highly controversial.
Phencyclidine has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[19] It also induces symptoms in humans that mimic schizophrenia.[20]
History and medicinal use[edit] PCP was first synthesized in 1926,[21] and was developed by Parke-Davis under the tradename named Sernyl in the 1950s as an anesthetic but because of its long 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.[22][23]
Recreational uses[edit]
Illicit PCP seized by the DEA in several forms. PCP began to emerge as a recreational drug in major cities in the United States in 1967.[24]:46 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 school students admitting to trying PCP at least once fell from 13% in 1979 to less than 3% in 1990.[24]:46–49
PCP comes in both powder and liquid forms (PCP base is dissolved most often in ether), but typically it is sprayed onto leafy material such as cannabis, mint, oregano, tobacco, parsley, or ginger leaves, then smoked.[citation needed]
PCP is a Schedule II substance in the United States, 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 A substance in the United Kingdom.
Methods of administration[edit] In its pure (free base) form, PCP is a yellow oil (usually dissolved in petroleum ether, diethyl ether, or tetrahydrofuran). Upon treatment with hydrogen chloride gas, or isopropyl alcohol saturated with hydrochloric acid, this oil precipitates into white-tan crystals or powder (PCP hydrochloride). In this, the salt form, PCP can be insufflated, depending upon the purity. However, most PCP on the illicit market often contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass.[citation needed] These contaminants can range from unreacted piperidine and other precursors, to carcinogens like benzene and cyanide-like compounds such as PCC (piperidinocyclohexyl carbonitrile).[citation needed]
The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette is dipped, to be ingested through smoking, commonly known as "boat" or "water." The name most likely originated from the somatic "numbing" effect and feelings of dissociation induced by PCP, and has led to the widespread and mistaken belief that the liquid is made up of or contains real embalming fluid. Occasionally, however, some users and dealers could have, believing this myth, used real embalming fluid mixed with, or in place of, PCP.[25][26] Smoking PCP is known as "getting wet", and a cigarette or joint which has been dipped in PCP may be referred to on the street as a "fry stick," "sherm," "leak," "amp," "lovely," "KJ (an abbreviation for 'Killer Joint')," "toe tag", "dipper", "happy stick," or "wet stick." "Getting wet" may have once been a popular method of using PCP, especially in the western United States where it may have been sold for about $10 to $25 per cigarette.[citation needed]
Effects[edit] Behavioral effects can vary by dosage. Low doses produce a numbness in the extremities and intoxication, characterized by staggering, unsteady gait, slurred speech, bloodshot eyes, and loss of balance. Moderate doses (5–10 mg intranasal, or 0.01–0.02 mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.[27] Users frequently do not know how much of the drug they are taking due to the tendency of the drug to be made illegally in uncontrolled conditions.[28]
Psychological effects include severe changes in body image, loss of ego boundaries, paranoia and depersonalization. Hallucinations, euphoria, and suicidal impulses are also reported, as well as occasional aggressive behavior.[27][24]:48–49 Like many other drugs, phencyclidine has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. PCP may induce feelings of strength, power, and invulnerability as well as a numbing effect on the mind.[3]
Studies by the Drug Abuse Warning Network in the 1970s show that media reports of PCP-induced violence are greatly exaggerated and that incidents of violence are unusual and often (but not always) limited to individuals with reputations for aggression regardless of drug use.[24]:48 This said, there have been a few, very-televised events of PCP-intoxicated individuals acting in an unpredictable fashion, possibly driven by their delusions or hallucinations. One famous example is the case of Big Lurch, a former rapper with a history of violent crime, who was convicted of murdering and cannibalizing his roommate while under the influence of PCP.[29] Other commonly cited types of incidents include inflicting property damage and self-mutilation of various types, such as pulling one's own teeth.[29][24]:48 These effects were not noted in its medicinal use in the 1950s and 1960s, however, and reports of physical violence on phencyclidine have often been shown to be unfounded.[30] [31]
Recreational doses of the drug also occasionally appear to induce a psychotic state that resembles a schizophrenic episode, sometimes lasting for months at a time.[32] Users generally report feeling detached from reality.[33]
Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.[34]
Management of intoxication[edit] Management of phencyclidine intoxication mostly consists of supportive care – controlling breathing, circulation, and body temperature – and, in the early stages, treating psychiatric symptoms.[35][36][37] Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such as phenothiazines and haloperidol have been used to control psychotic symptoms, but may produce many undesirable side effects – such as dystonia – and their use is therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia, and boost the anticholinergic effects of PCP.[35][36] If an antipsychotic is given, intramuscular haloperidol has been recommended.[37][38][39]
Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was somewhat controversially recommended in the past as a decontamination measure.[35][36][37] However, it is now known that only around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence; furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is not an unusual manifestation of PCP toxicity.[35][36]
----
You're thinking of ketamine. Similar, but pcp is a hallucinogenic and ketamine is a dissociative.
Comments
linePCP is a hell of a drug
PCP is for horses, not humans, dumbass.
In chemical structure, PCP is an arylcyclohexylamine derivative, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA receptor and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.[1][2] Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan and nitrous oxide.
As a recreational drug, PCP may be ingested, smoked, inhaled or injected.[3]
Contents [hide]
1 Biochemistry and pharmacology
1.1 Pharmacodynamics
1.2 Pharmacokinetics
1.3 Structural analogues
1.4 Brain effects
1.5 History and medicinal use
2 Recreational uses
2.1 Methods of administration
2.2 Effects
3 Management of intoxication
4 See also
5 References
6 External links
Biochemistry and pharmacology[edit]
Pharmacodynamics[edit]
PCP is well known for its primary action on ionotropic glutamate receptors, such as the NMDA receptor in rats and in rat brain homogenate.[4][5] As such, PCP is an NMDA receptor antagonist. NMDA receptors mediate excitation,[6] however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans[7] and rodents.[8]
Research also indicates that PCP inhibits nicotinic acetylcholine (nACh) receptors. Analogues of PCP exhibit varying potency at nACh receptors[citation needed] and NMDA receptors.[9] In some brain regions, these effects are believed to act synergistically by inhibiting excitatory activity.[citation needed]
PCP, like ketamine, also acts as a D2 receptor partial agonist in rat brain homogenate.[5] This activity may be associated with some of the other more psychotic features of PCP intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP psychosis.[10]
Studies on rats indicate that PCP indirectly interacts with endorphin and enkephalin receptors to produce analgesia.[11]
PCP may also work as a dopamine reuptake inhibitor.[12]
Pharmacokinetics[edit]
PCP is metabolized into PCHP, PPC and PCAA.
When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.
Conversion of PCP into PC and piperidine by heat.
Structural analogues[edit]
Possible Analogues of PCP
More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. 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). These compounds were never widely used and did not seem to be as well accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.[13][citation needed]
The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarized below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.[14][15][clarification needed]
Brain effects[edit]
Some studies found that, like other NMDA receptor antagonists, phencyclidine can cause a kind of brain damage called Olney's lesions in rats.[16][17] 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, [18] but due to the study never having been published, its validity is highly controversial.
Phencyclidine has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[19] It also induces symptoms in humans that mimic schizophrenia.[20]
History and medicinal use[edit]
PCP was first synthesized in 1926,[21] and was developed by Parke-Davis under the tradename named Sernyl in the 1950s as an anesthetic but because of its long 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.[22][23]
Recreational uses[edit]
Illicit PCP seized by the DEA in several forms.
PCP began to emerge as a recreational drug in major cities in the United States in 1967.[24]:46 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 school students admitting to trying PCP at least once fell from 13% in 1979 to less than 3% in 1990.[24]:46–49
PCP comes in both powder and liquid forms (PCP base is dissolved most often in ether), but typically it is sprayed onto leafy material such as cannabis, mint, oregano, tobacco, parsley, or ginger leaves, then smoked.[citation needed]
PCP is a Schedule II substance in the United States, 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 A substance in the United Kingdom.
Methods of administration[edit]
In its pure (free base) form, PCP is a yellow oil (usually dissolved in petroleum ether, diethyl ether, or tetrahydrofuran). Upon treatment with hydrogen chloride gas, or isopropyl alcohol saturated with hydrochloric acid, this oil precipitates into white-tan crystals or powder (PCP hydrochloride). In this, the salt form, PCP can be insufflated, depending upon the purity. However, most PCP on the illicit market often contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass.[citation needed] These contaminants can range from unreacted piperidine and other precursors, to carcinogens like benzene and cyanide-like compounds such as PCC (piperidinocyclohexyl carbonitrile).[citation needed]
The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette is dipped, to be ingested through smoking, commonly known as "boat" or "water." The name most likely originated from the somatic "numbing" effect and feelings of dissociation induced by PCP, and has led to the widespread and mistaken belief that the liquid is made up of or contains real embalming fluid. Occasionally, however, some users and dealers could have, believing this myth, used real embalming fluid mixed with, or in place of, PCP.[25][26] Smoking PCP is known as "getting wet", and a cigarette or joint which has been dipped in PCP may be referred to on the street as a "fry stick," "sherm," "leak," "amp," "lovely," "KJ (an abbreviation for 'Killer Joint')," "toe tag", "dipper", "happy stick," or "wet stick." "Getting wet" may have once been a popular method of using PCP, especially in the western United States where it may have been sold for about $10 to $25 per cigarette.[citation needed]
Effects[edit]
Behavioral effects can vary by dosage. Low doses produce a numbness in the extremities and intoxication, characterized by staggering, unsteady gait, slurred speech, bloodshot eyes, and loss of balance. Moderate doses (5–10 mg intranasal, or 0.01–0.02 mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.[27] Users frequently do not know how much of the drug they are taking due to the tendency of the drug to be made illegally in uncontrolled conditions.[28]
Psychological effects include severe changes in body image, loss of ego boundaries, paranoia and depersonalization. Hallucinations, euphoria, and suicidal impulses are also reported, as well as occasional aggressive behavior.[27][24]:48–49 Like many other drugs, phencyclidine has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. PCP may induce feelings of strength, power, and invulnerability as well as a numbing effect on the mind.[3]
Studies by the Drug Abuse Warning Network in the 1970s show that media reports of PCP-induced violence are greatly exaggerated and that incidents of violence are unusual and often (but not always) limited to individuals with reputations for aggression regardless of drug use.[24]:48 This said, there have been a few, very-televised events of PCP-intoxicated individuals acting in an unpredictable fashion, possibly driven by their delusions or hallucinations. One famous example is the case of Big Lurch, a former rapper with a history of violent crime, who was convicted of murdering and cannibalizing his roommate while under the influence of PCP.[29] Other commonly cited types of incidents include inflicting property damage and self-mutilation of various types, such as pulling one's own teeth.[29][24]:48 These effects were not noted in its medicinal use in the 1950s and 1960s, however, and reports of physical violence on phencyclidine have often been shown to be unfounded.[30] [31]
Recreational doses of the drug also occasionally appear to induce a psychotic state that resembles a schizophrenic episode, sometimes lasting for months at a time.[32] Users generally report feeling detached from reality.[33]
Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.[34]
Management of intoxication[edit]
Management of phencyclidine intoxication mostly consists of supportive care – controlling breathing, circulation, and body temperature – and, in the early stages, treating psychiatric symptoms.[35][36][37] Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such as phenothiazines and haloperidol have been used to control psychotic symptoms, but may produce many undesirable side effects – such as dystonia – and their use is therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia, and boost the anticholinergic effects of PCP.[35][36] If an antipsychotic is given, intramuscular haloperidol has been recommended.[37][38][39]
Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was somewhat controversially recommended in the past as a decontamination measure.[35][36][37] However, it is now known that only around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence; furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is not an unusual manifestation of PCP toxicity.[35][36]
----
You're thinking of ketamine. Similar, but pcp is a hallucinogenic and ketamine is a dissociative.
This was hilarious and I'm drunk. Abundance!
agree
Rāsāẏanika gaṭhana sālē, pisipira ēkaṭi arylcyclohexylamine byuṯpanna, ēbaṁ, phārmākōlaji, ēṭā dissociative anesthetics paribārēra ēkajana sadasya. Pisipira sabacēẏē antiglutamatergic hyālusinōjēnas mata, hyālusinōjēnas an'yān'ya bibhāga tulanāẏa ullēkhayōgyabhābē ārō bipajjanaka yā blaka NMDA risēpaṭara kāryakalāpa ēbaṁ ēkaṭi NMDA risēpaṭara pratidbandbī hisēbē prāthamikabhābē kāja karē. [1] [2 ] An'ya NMDA risēpaṭara antagonists ketamine, tiletamine, dextromethorphan antarbhukta Ō nā'iṭrāsa aksā'iḍa.
Ēkaṭi binōdanamūlaka ḍrāga hisābē, pisipira, pākasthalitē grahaṇa smōkaḍa, niḥśbāsēra bā inajēkaśanēra hatē pārē. [3]
Sūcipatra [cāmaṛā]
1 Bāẏōkēmisṭri ō phārmākōlaji
1.1 Pharmacodynamics
1.2 Haya
1.3 Kāṭhāmōgata analogues
1.4 Mastiṣka prabhāba
1.5 Itihāsa ō bhēṣaja byabahāra
2 Binōdanamūlaka byabahāra
Praśāsanēra 2.1 Pad'dhati
2.2 Ēphēkṭasa
Nēśā haẏa 3 myānējamēnṭa
4 Āra'ō dēkhuna
5 Tathyasūtra
6 Bahiḥsanyōga
Bāẏōkēmisṭri ō phārmākōlaji [sampādanā]
Pharmacodynamics [sampādanā]
Pisipira bhāla yēmana im̐dura ō im̐dura mastiṣkēra homogenate madhyē NMDA risēpaṭara hisābē ionotropic gluṭāmēṭa risēpṭara, tāra pradhāna karma jan'ya paricita. [4] [5] Ē'i kāraṇē, pisipira ēkaṭi NMDA risēpaṭara pratidbandbī haẏa. NMDA risēpṭara [6] tabē, gabēṣaṇā pisipira apratyāśitabhābē mānuṣēra [7] ēbaṁ tīkṣṇadanta prāṇī madhyē sāragarbha karaṭikāla ayākṭibhēśana utpādana karē dēkhānō haẏēchē, uttējanā madhyasthatā. [8]
Gabēṣaṇā thēkē pisipira nicotinic acetylcholine (Nach) risēpṭara inhibits yē iṅgita dēẏa. Nach risēpṭara ē pisipira pradarśanī nānārakama śakti ēra analogues [talaba praẏōjana] ēbaṁ NMDA risēpṭara. [9] Kichu mastiṣka añcalē, ē'i prabhāba uddīpaka kāryakalāpa inhibiting dbārā synergistically kāja balē biśbāsa karā haẏa. [Talaba praẏōjana]
Pisipira, ketamine mata, ēchāṛā'ō im̐dura mastiṣkēra homogenate ēkaṭi D2 risēpaṭara ānśika agonist hisābē kāja karē. [5] Ē'i kāryakalāpa D2 risēpaṭara antagonists saphala byabahārēra pramāṇa yā pisipira nēśā, an'yān'ya ārō manōrōgēra baiśiṣṭya kichu (saṅgē yukta hatē pārē Yēmana pisipira manōrōgēra cikitsāra jan'ya) haloperidol hisēbē. [10]
Im̐durēra upara gabēṣaṇā pramāṇa karē pisipira parōkṣabhābē bēdanāra upaśama utpādana endorphin ēbaṁ enkephalin risēpṭara sāthē mithaskriẏā iṅgita. [11]
Pisipira ēkaṭi ḍōpāmina reuptake niṣēdhātmaka hisābē kāja karatē pārē. [12]
Haya [sampādanā]
Pisipira PCHP, PPC ēbaṁ PCAA madhyē metabolized haẏa.
Dhūmapāna, ēṭi kichu 1- phenyl -1- cyclohexene (pisi) ēbaṁ piriḍina madhyē tāpa nicē naṣṭa haẏē gēchē.
Tāpa dbārā pisi ēbaṁ piriḍina madhyē pisipira rūpāntara.
Kāṭhāmōgata analogues [sampādanā]
Pisipira sambhābya Analogues
Pisipira bēśī 30 bibhinna analogues pradhānata mārkina yuktarāṣṭrēra, 1970 ēbaṁ 1980 samaẏa rāstāẏa byabahr̥ta hacchē hisābē ripōrṭa karā haẏēchila. Sērā ēra madhyē paricita rolicyclidine haẏa (PCPy bā 1 - (1- phenylcyclohexyl) pyrrolidine); Eticyclidine (PCE bā n- ETHYL -1- phenylcyclohexylamine); Ēbaṁ tenocyclidine (TCP athabā 1 - (1 - (2- thienyl) cyclohexyl) piriḍina). Ē'i yaugēra byāpaka bhābē byabahr̥ta nā haẏa ēbaṁ pāśāpāśi pisipira nijē'i hisēbē byabahārakārīdēra dbārā gr̥hīta habē balē manē hacchē nā, tabē tārā saba kāraṇa tādēra abaidha anurūpa prabhāba niẏantrita upādānēra ēkṭa ēra sūci āmi sam'mukhēra yōga karā haẏa ni. [13] [Talaba praẏōjana]
Pisipira mata karmakānḍēra jan'ya praẏōjana sādhāraṇa sṭrākacārāla mōṭipha pisipira analogues gaṭhana - karmakānḍēra samparka gabēṣaṇā thēkē prāpta, ēbaṁ nīcēra saṅkṣipta karā haẏa. Ē'i analogues saba, pisipira nijēkē kichuṭā anurūpa prabhāba āchē ēkaṭi potencies paridhi ō byabahr̥ta biśēṣa substituents upara nirbhara abēdanika ēra nānārakama miśraṇa, dissociative ēbaṁ uddīpaka prabhāba saṅgē, yadi'ō. Yēmana mārkina yuktarāṣṭra, asṭrēliẏā ō ni'ujilyānḍa hisābē kichu dēśē, ē'isaba yaugēra saba pisipira niẏantrita padārtha analogues bibēcita, ēbaṁ haẏa habē tā'i tādēra anēka praṇīta bā parīkṣita haẏēchē nā yadi'ō abaidha ōṣudha, . [14] [15 ] [Byākhyā praẏōjana]
Mastiṣka prabhāba [sampādanā]
Kaẏēkaṭi samīkṣāẏa an'yān'ya NMDA risēpaṭara antagonists mata, Phencyclidine im̐durēra madhyē Olney ēra kṣata nāmaka mastiṣkēra kṣati ēka dharanēra sr̥ṣṭi karatē pārē, yē khum̐jē pā'ōẏā yāẏa ni. Im̐durēra ōpara paricālita [16] [17] sṭāḍija NMDA risēpaṭara pratidbandbī dizocilpine ēra ucca mātrā ulaṭākara Vacuoles gaṭhana sr̥ṣṭikārī dēkhiẏēchēna Im̐dura' ghilu nirdiṣṭa añcalē. Olney ēra kṣata saba gabēṣanāra ēkamātra a - mānaba prāṇīra upara sañcālita haẏēchē ēbaṁ mānuṣēra kṣētrē prayōjya nā'ō hatē pārē. Phrāṅka śārpa karē ēka aprakāśita gabēṣaṇāẏa janaśruti NDMA pratidbandbī dbārā kōna kṣati, ketamine, dūrē binōdanamūlaka mātrāẏa parē'ō ēkaṭi anurūpa mādaka, , [18] dēkhiẏēchēna kintu kāraṇē gabēṣaṇā prakāśita haẏēchē kakhana'ō karatē, tāra baidhatā atyanta bitarkita haẏa.
Phencyclidine ēchāṛā'ō jībanta im̐durēra madhyē ēbaṁ mastiṣkēra ṭisyura maẏanā tadanta parīkṣāra upara ubhaẏa nirdhāraṇayōgya yā im̐dura mastiṣkē n- acetylaspartate ō n- acetylaspartylglutamate sālē sijōphrēniẏāra mata paribartana, kāraṇa dēkhānō haẏēchē. [19] Ēṭi anukaraṇamūlaka yē mānuṣēra madhyē upasarga dēẏa Sijōphrēniẏāra. [20]
Itihāsa ō bhēṣaja byabahāra [sampādanā]
Pisipira prathama 1926 sālē sanślēṣita haẏa, [21] ēbaṁ ēkaṭi abēdanika hisēbē 1950 sālē Sernyl nāmē tradename adhīna kintu kāraṇa yēmana hyālusinēśana, bā'i, pralāpa hisābē tāra dīrgha ardha jībana ēbaṁ pratikūla pārśba pratikriẏā, ēra Parke - ḍēbhisa dbārā unnata chila, ēbaṁ Disorientation, ēṭi 1965 sālē bājāra thēkē sarānō haẏēchē ēbaṁ paśucikiṯsā byabahārēra madhyē'i sīmābad'dha chila. [22] [23]
Binōdanamūlaka byabahāra [sampādanā]
Abaidha pisipira bibhinna pharma DEA dbārā bājēẏāpta.
Pisipira 1967 sālē mārkina yuktarāṣṭra pradhāna śaharē ēkaṭi binōdanamūlaka ḍrāga hisābē ut'thāna śuru [24]: . 1978 Sālē 46, pipala myāgājina ō pisipira dēśēra" ēka nambara" mādaka samasyā nāmaka 60 miniṭa ēra mā'ika ōẏālēsa. Mādakēra binōdanamūlaka byabahārēra sabasamaẏa'i apēkṣākr̥ta kama haẏēchē, ēṭi 1980 sālē ullēkhayōgyabhābē kamē śuru karēna. Sārbhē ina, antata ēkabāra pisipira cēṣṭā karatē admitting hā'i skula chātra saṅkhyā 1990 sālē kama 3% thēkē 1979 sālē 13% thēkē paṛē giẏēchilēna. [24]:46 -49
Pisipira pā'uḍāra ō tarala pharama (pisipira bēsa thāra madhyē prāẏaśa'i drabībhūta karā haẏa) ubhaẏēra madhyē āsē, kintu sādhāraṇata ēṭi yēmana gām̐jā, pudinā, ōrēgānō, tāmāka, pārsalē, bā ādā pātā, tārapara dhūmapāna hisābē śāka upādāna sam'mukhēra sprē karā haẏa. [Talaba praẏōjana]
Pisipira kānāḍā, nēdāralyānḍa āphiṁ ā'ina ēbaṁ ēkaṭi klāsa yuktarājya ēkaṭi padārtha ēkaṭi tālikā āmi mādaka kāja mārkina yuktarāṣṭra, niẏantrita ḍrāgasa ēbaṁ bastugulira dbārā ēkaṭi sūci āmi mādaka ēkaṭi sūci dbitīẏa padārtha haẏa.
Praśāsanēra pad'dhati [sampādanā]
Tāra biśud'dha (bināmūlyē bēsa) pharma, pisipira (sādhāraṇata pēṭrōliẏāma thāra, DIETHYL thāra, athabā ṭēṭrāhā'iḍrōphi'urāna drabībhūta) ēkaṭi haluda tēla haẏa. Labaṇāmna saṅgē sampr̥kta hā'iḍrōjēna klōrā'iḍa gyāsa, bā isopropyl ēlakōhala saṅgē cikitsā karāra parē, ē'i tēla sādā Tan sphaṭika bā pā'uḍāra (pisipira hā'iḍrōklōrā'iḍa) madhyē precipitates. Ē'i ina, labaṇa pharma, pisipira biśud'dhatā upara nirbhara karē, insufflated karā yābē. Tabē, abaidha bājārē sabacēẏē pisipira prāẏa'i raṅa kaṣā thēkē bādāmī abadhi bistr̥ta habē yāra phalē asthāẏī uṯpādana phalē hisābē dūṣaṇakārī ēkaṭi nambara, , ēbaṁ pā'uḍāra thēkē ēkaṭi āṭhāyukta bhara abadhi bistr̥ta karatē aikya raẏēchē. [Tathyasūtra praẏōjana] ē'i dūṣaṇakārī pārēna Unreacted piriḍina ēbaṁ an'yān'ya prikārsara thēkē, yēmana PCC (piperidinocyclohexyl carbonitrile) hisēbē bēnajina ēbaṁ sāẏānā'iḍa mata yaugēra mata kyānsāra utpādaka thēkē parisīmā. [Talaba praẏōjana]
Śabdaṭi" embalming tarala" prāẏa'i ēkaṭi sigārēṭa sādhāraṇabhābē" naukā" athabā nāmē'ō paricita dhūmapāna, mādhyamē pākasthalitē grahaṇa karā, cubāna haẏa yā tarala pisipira paṛuna byabahāra karā haẏa" jala. " Nāma sambhabata prabhāba ō pisipira dbārā prabartita pr̥thakīkaraṇa anubhūti" numbing" dēhagata thēkē sambhūta, ēbaṁ tarala gaṭhita bā bāstaba embalming tarala dhāraṇa karē yē byāpaka ō bhrānta biśbāsa nētr̥tbādhīna haẏēchē. Mājhēmadhyē, kintu, kichu byabahārakārīdēra ēbaṁ bikrētā hatē pārē, ē'i śruti biśbāsī, saṅgē, bā pisipira, sthānē miśiẏē bāstaba embalming tarala byabahr̥ta. [25] [26] Dhūmapāna pisipira"bhējā pēẏē" hisābē paricita haẏa, ēbaṁ ēkaṭi sigārēṭa bā yugma Pisipira madhyē cubāna karā haẏēchē, yā ēkaṭi" bhājā lāṭhi," " sherm," " lika," " rahamāna," " atība sundara," " KJ (' hatyākārī sanyukta' jan'ya ēkaṭi samāhāra)," " hisābē rāstāẏa ullēkha karā yētē pārē Aṅgulī ṭyāga"," nuliẏā"," śubha lāṭhi, "bā" bhējā lāṭhi. " "Bhējā patha" ēkabāra biśēṣa karē ēṭi sigārēṭēra prati prāẏa $ 10 thēkē $ 25 jan'ya bikri karā haẏē thākatē pārē yēkhānē paścima mārkina yuktarāṣṭra, pisipira byabahāra karē ēkaṭi janapriẏa pad'dhati tairi hatē pārē. [Talaba praẏōjana]
Prabhāba [sampādanā]
Byabahārika prabhāba ḍōja dbārā paribartana ha'ōẏāra sambhābanā raẏēchē. Nimna mātrāẏa ēkaṭi ṭalaṭalāẏamāna, naṛabaṛa gē'iṭa dbārā cihnita pā ō nēśā madhyē asāṛatā, , slurred baktr̥tā, raktarāṅā cōkha, ēbaṁ bhārasāmya kṣati utpādana. Sanyamī mātrāẏa (5-10 miligrāma Intranasal, athabā 0.01-0.02 Miligrāma/ intramuscular bā śirāẏa pradānēra jan'ya kēji) bēdanāra upaśama ēbaṁ abēdana utpādana habē. Ucca mātrāẏa khim̐cuni hatē pārē. [27] Byabahārakārīrā prāẏa'i tārā kāraṇē abaśa abasthāẏa abaidhabhābē tairi karā mādakēra prabaṇatā thēkē grahaṇa karā haẏa kata mādakēra jāni nā. [28]
Manastāttbika prabhāba tībra śarīra imēja paribartana, ahaṁ gaṇḍi kṣati, mastiṣkabikr̥tibiśēṣa ēbaṁ byaktitbahāni antarbhukta. Hyālusinēśana, ramaramā, ēbaṁ ātmaghātī impulses ēchāṛā'ō mājhē madhyē ākramanātmaka ācaraṇa, yēmana ripōrṭa karā haẏa. Phencyclidine ēkaṭi anirdēśya phyāśana mējāja yuktarāṣṭra paribartana karā haẏēchē paricita anēka an'yān'ya ōṣudha, bhālō lēgēchē [27] [24]:48 -49, Karāra kichu byakti ghaṭācchē Bicuyata haẏē, ēbaṁ an'yadēra prāṇabanta haẏē. Pisipira śakti, kṣamatā, ēbaṁ invulnerability sē'isāthē manēra upara ēkaṭi numbing prabhāba anubhūti rāji karānō hatē pārē. [3]
1970 Sālē ḍrāga apabyabahāra satarkabāṇī nēṭa'ōẏārka dbārā sṭāḍija pisipira inaḍi'usaḍa sahinsatāra miḍiẏā ripōrṭa atiśaẏa atirañjita yē ō sahinsatāra ghaṭanā asbābhābika haẏa ēbaṁ prāẏa'i (kintu sabasamaẏa naẏa) nirbiśēṣē mādaka byabahārēra āgrāsana jan'ya reputations mānuṣadēra sīmābad'dha karēna. [24 ]: 48 Ē'i sambhabata tādēra bibhrama bā hyālusinēśana dbārā cālita ēkaṭi anirdēśya phyāśana, abhinaẏa PCP - matta byaktira kaẏēka khuba'i - pracārita ghaṭanā āchē, tini balēna. Ēka bikhyāta yēmana biga andhakāra, yakhana pisipira prabhāba adhīna tāra ēka'i gharē bāsindā hanana ēbaṁ cannibalizing dōṣī sābyasta karā haẏa yārā sahinsa aparādha, ēkaṭi itihāsa saṅgē sābēka rāpāra ēra kēsa. Ghaṭanā [29] an'yān'ya sādhāraṇabhābē udāhr̥ta dharanēra inflicting sampattira kṣati hala ēbaṁ Yēmana nijēra dām̐ta kāchē bibhinna dharanēra, ēra sba - aṅgahāni [29] [24].: 48 Ē'i prabhāba 1950 ēbaṁ 1960 sālē ēra auṣadhi byabahāra lakṣanīẏa chila nā, kintu, ēbaṁ Phencyclidine nēbhigēśana śārīrika sahinsatāra ripōrṭa prāẏa'i dēkhānō haẏēchē Amūlaka habē. [30] [31]
Mādakēra binōdanamūlaka mātrāẏa ēchāṛā'ō mājhē mājhē kakhanō kakhanō ēkaṭi samaẏē māsa dīrghasthāẏī, ēkaṭi sijōphrēniẏā ākrānta parbēra yē barṇanāra anurūpa ēkaṭi mānasika rāṣṭra prabr̥tta haẏa. [32] Byabahārakārīrā sādhāraṇata bāstabatā thēkē bicchinna bōdha ripōrṭa. [33]
Lakṣaṇa smr̥tisaṅkrānta ḍibhā'isa lāla ḍēnisa dbārā saṅkṣipta karā haẏa.: Rage, erythema (tbakēra lālatā), dilated chātradēra, bibhrama, smr̥tilōpa, nystagmus (pārśbata sarānōra samaẏa sāmanā ēra dōlana), uttējanā, ēbaṁ tbaka śōṣa [34]
Nēśā haẏa byabasthāpanā [sampādanā]
Phencyclidine nēśā haẏa myānējamēnṭa bēśirabhāga sahāẏaka yatna niẏē gaṭhita - niẏantraṇa śbāsa, sañcālana, ēbaṁ śarīrēra tāpamātrā. - Ō, prāthamika paryāẏē, mānasika upasargēra cikitsā [35] [36] [37] ē'i dharanēra lorazepam hisābē Benzodiazepines, , pachandēra ōṣudhēra haẏa Cāgāṛa ēbaṁ hr̥darōgēra (yakhana bartamāna) niẏantraṇa. Yēmana phenothiazines ēbaṁ haloperidol hisābē baiśiṣṭasūcaka ēnṭisā'ikōṭikēra manōrōgēra upasarga niẏantraṇa karatē byabahr̥ta haẏēchē, kintu anēka abāñchita pārśba pratikriẏā tairī karatē pārē - yēmana dystonia hisābē - ēbaṁ tādēra byabahāra tā'i ēkhana āra pachanda haẏa; Tārā pākaṛa thrēśahōlḍa kama hā'ipārathārmiẏā khārāpa, ēbaṁ pisipira. [35] [36] Ēkaṭi ēnṭisā'ikōṭika dē'ōẏā haẏa, intramuscular haloperidol supāriśa karā haẏēchē. [37] [38] [39 Anticholinergic prabhāba anumōdana pārē phenothiazines, biśēṣa karē jhum̐kipūrṇa ]
(Niśādala bā, ārō nirāpadē, ayāsakarabika ayāsiḍa diẏē) jōrapūrbaka ayāsiḍa mūtrabardhaka auṣadha śarīra thēkē pisipira kliẏārēnsa br̥d'dhi hatē pārē, ēbaṁ kichuṭā bitarkitabhābē ēkaṭi biśud'dhatā parimāpa hisēbē atītē supāriśa karā haẏa. [35] [36] [37] Yā'ihōka, ēṭā haẏa Ēkhana pisipira ēkaṭi ḍōja mātra prāẏa 10% sāmān'ya phala ēra bardhita prasrābē kliẏārēnsa yābē nā, yā kiḍani, dbārā muchē phēlā habē yē paricita; Ēṭi raktē amlādhikyajanita bikāra prabartita ō pisipira biṣāktatāra ēkaṭi asbābhābika udbhāsa nā yā rhabdomyolysis (pēśī bhāṅganēra), khārāpa hatē pārē hisābē uparantu, prasrābē amlīkaraṇa, bipajjanaka. [35] [36]