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Surprisingly, there does not appear to be a comprehensive source of information relating to methamphetamine. While no list is ever complete, this one attempts to answer technical questions related to the chemical methamphetamine. Unfortunately, there tends to be a great deal of street lore that is blatantly wrong about methamphetamine and similar compounds. This document also attempts to point out some of the more common myths, and provide rational explanations. Do not use this information. I am not a chemist. This is for informational purposes only. Use of this information for illegal purposes is not condoned. The author makes no warranty, expressed or implied, of the suitability of this information for any particular purpose. The author does not endorse the abuse of any drugs, legal or otherwise. Methamphetamine also known as speed, meth, crystal, crank, and sometimes confusingly called ice is a chemical widely known for its stimulant properties on the human body. It is frequently confused with other drugs that share similar symptoms, including amphetamine, 4-methyl-aminorex, ephedrine, caffeine, and other chemicals, both legal and illegal. When precision is needed, we shall explicitly state one form or the other. The literature gives conflicting reports, due to the fact that many criterion are subjective, and probably also due to confusion over terminology. The pharmacological effects of methamphetamine are very similar to those of similarly structured molecules. Methamphetamine can be taken orally, snorted, smoked or injected, in approximately increasing order of immediacy of onset. Onset can be immediate in the case of injection , or can take as long as minutes if ingested orally. Duration is subjective, but is probably on the order of 4 — 8 hours. Delayed absorption for example, due to oral ingestion can prolong the effects relative to time of administration. Of course, larger doses last longer due to the fact that it is removed from the blood at a finite rate. The length of time that methamphetamine will stay in the plasma blood is between 4 to 6 hours. It can be detected in the urine one hour after use and up to 48 hours after use. A toxic reaction or overdose can occur at relatively low levels, 50 milligrams of pure drug for a non-tolerant user. These include euphoria, hyperexcitability, extreme nervousness, accelerated heartbeat, sweating, dizziness, restlessness, insomnia, tooth grinding, incessant talking, and other effects. Methamphetamine and other CNS stimulants have strong bronchodilation effects. Vasoconstriction tightening of blood vessels and pupil dilation are also common. Elevated blood pressure, heart rate, and other general symptoms of increased sympathetic nervous activity. The physical effects are almost assuredly due to interactions between the amphetamine structure and human physiology, probably due to the similarity to adrenaline epinephrine. Mental capacity is not diminished directly by the drug. In fact, some studies have shown slight increases in mental capacity on simple tasks. It has been prescribed for attention deficit disorder, among other things. Emotional responses may range from euphoria to anger and paranoia. Preliminary doses tend to produce the former, while continued use e. This is the easiest section to write, and the most fun, since I can be relatively sure of the facts. The basic structure is unchanged, but an HCl molecule has become attracted to the free base. In this case, the hydrogen from the HCl has become attracted to the nitrogen in the free base. You will notice that the salt form is much more common. This is for physiological reasons. The same reaction which attracts the free base to HCl could also attract it to other molecules, causing irritation and other symptoms. The human terms: The d- is cool, the l- is shit, remember. There are other recipes, but none to practical to attempt. Apartment manufacture of meth is not possible. The benefit of this method is that different amines can be used to produce novel N-alkyl amphetamines ethamphetamine, tert-butylamphetamine, etc. The only difference between methamphetamine and pseudo ephedrine is that damn alpha-hydroxy group. Reacting your ephedrine with thionyl chloride replaces the OH with Cl to produce N-methyl-alpha-chloroamphetamine as an intermediate. Hydrogenating this product is easy: use lithium aluminum hydride, sodium borohydride, or even hydrogen gas with nickel or platinum metal as a catalyst. The product of this step is N-methylamphetamine and HCl. Evaporate off the water and you have methamphetamine hydrochloride. If you start with dl-ephedrine, you get dl-meth. In this procedure, the alcohol grouping of ephedrine, pseudoephedrine, or PPA is reduced by boiling one of these compounds in a mixture of hydroiodic acid and red phosphorus. Hydroiodic acid works as a reducing agent because its dissociates at higher temperatures to iodine and hydrogen, which does the reducing. The dissociation is reversible. The equilibrium is shifted in favor of dissociation by adding red phosphorus to the mixture. The red phosphorus reacts with the iodine to produce PI 3 , which then further reacts with water to form phosphorus acid and more hydroiodic acid. Since the hydrogen atom of the HI is being absorbed by the ephedrine, the red phosphorus acts as a recycler. In some reductions, the need for HI is dispensed with just by mixing red phosphorus and iodine crystals in a water solution. The red phosphorus then goes on to make HI by the above mentioned process. With a small amount of due care, this is an excellent alternative to either purchasing, stealing, or making your own pure hydroiodic acid. This method has the advantage of being easy to do. It was formerly the most popular method of making meth from ephedrine. Now red phosphorus is on the California list of less restricted chemicals, so an increased level of subterfuge is called for to obtain significant amounts. One might think that this is easily gotten around by making your own red phosphorus, but this is a process I would not want to undertake. Ever hear of phosphorus shells? I would much rather face the danger of exploding champagne bottles. Those who insist on finding out for themselves, will see Journal of the American Chemical Society, volume 68, page Those with a knack for scrounging from industrial sources will profit from knowing that red phosphorus is used in large quantities in the fireworks and matchmaking industries. The determined experimenter could obtain a pile of red phosphorus by scraping off the striking pads of matchbooks with a sharp knife. Naturally, it is a tedious process to get large amounts of red phosphorus by scraping the striking pads off matchbooks. Another problem with this method is that it can produce a pretty crude product if some simple precautions are not followed. From checking out typical samples of street meth, it seems basic precautions are routinely ignored. I believe that the by-products in the garbage meth are iodoephedrine, and the previously mentioned azirine. If a careful fractional distillation is done, these products can be removed. They can be avoided in the first place if, when making hydroiodic acid from iodine and red phosphorus, the acid is prepared first, and allowed to come to complete reaction for 20 minutes before adding the ephedrine to it. This will be a hassle for some, because the obvious procedure to follow is to use the water extract of the ephedrine pills to make the HI in. The way around the roadblock here is to just boil off some more of the water from the ephedrine pill extract, and make the acid mixture in fresh pure water. Since the production of HI from iodine and red phosphorus gives off a good deal of heat, it is wise to chill the mixture in ice, and slowly add the iodine crystals to the red phosphorus-water mixture. To do the reaction, a ml round bottom flask is filled with grams of ephedrine hydrochloride or PPA-HCl. The use of the sulfate salt is unacceptable because HI reduces the sulfate ion, so this interferes with the reaction. This same acid and red phosphorus mixture can be prepared from adding grams of iodine crystals to grams of red phosphorus in ml of water. This should produce the strong hydroiodic acid solution needed. I can tell you that experiments have shown that one molar HI is ineffective at reducing ephedrine to meth. I would think that so long as one is over 3 molar acid, the reaction will work. With the ingredients mixed together in the flask, a condenser is attached to the flask, and the mixture is boiled for one day. This length of time is needed for best yields and highest octane numbers on the product. While it is cooking, the mixture is quite red and messy looking from the red phosphorus floating around in it. When one day of boiling under reflux is up, the flask is allowed to cool, then it is diluted with an equal volume of water. Next, the red phosphorus is filtered out. A series of doubled up coffee filters will work to get out all the red phosphorus, but real filter paper is better. The filtered solution should look a golden color. A red color may indicate that all the phosphorus is not yet out. If so, it is filtered again. The filtered-out phosphorus can be saved for use in the next batch. If filtering does not remove the red color, there may be iodine floating around the solution. It can be removed by adding a few dashes of sodium bisulfate or sodium thiosulfate. The next step in processing the batch is to neutralize the acid. A strong lye solution is mixed up and added to the batch with shaking until the batch is strongly basic. This brings the meth out as liquid free base floating on top of the water. The strongly basic solution is shaken vigorously to ensure that all the meth has been converted to the free base. With free base meth now obtained, the next step, as usual, is to form the crystalline hydrochloride salt of meth. To do this, a few hundred mls of toluene is added to the batch, and the meth free base extracted out as usual. If this is the case, the product is sufficiently pure to make nice white crystals just by bubbling dry HCl gas through the toluene extract as described in Chapter 5. If the toluene extract is darker colored, a distillation is called for to get pure meth free base. The procedure for that is also described in Chapter 5. The yield of pure methamphetamine hydrochloride should be from to grams. Reference: Ely, R. All the chemicals were reagent grade, with no special treatment of the tetrahydrofuran THF , and the atmosphere above the condensed ammonia was not flushed with nitrogen gas. A condenser was fitted in the center neck, an additional funnel containing l-ephedrine base in THF was fitted into one side neck, and a rubber stopper fitted with a glass tube extending to the bottom of the flask was fitted in the third neck. Anhydrous ammonia gas was condensed and collected in the flask. Small pieces of lithium metal were rinsed in petroleum ether, patted dry, and added to the condensed ammonia. A deep royal blue color was noted as the lithium metal dissolved in the condensed ammonia. The l-ephedrine was added drop wise to the lithium ammonia solution over a period of approximately 10 minutes with stirring. When all of the l-ephedrine had been added, ammonium chloride was added slowly to the solution. The flask was removed from the cooling bath, and the condensed ammonia was allowed to warm to room temperature and evaporate from the flask through the side necks. When most of the ammonia had evaporated, water was added to the remaining solution until it cleared and any remaining lithium metal was decomposed. The remaining solution was removed from the flask to a separatory funnel, where the aqueous layer was discarded. The THF layer was dried with magnesium sulfate, and the hydrochloride salt of the methamphetamine was made by bubbling hydrogen chloride through the THF. The same procedure was used, substituting phenylproponolamine and methylephedrine as the starting materials. A second synthesis was conducted with l-ephedrine, using the same procedure except that the reaction was not quenched with ammonium chloride. The reaction was found to reduce l-ephedrine to d-methamphetamine quickly and easily. Furthermore, it was found that the reaction converted phenylpropanolamine to amphetamine and methylephedrine to dimethylamphetamine. The time required for the reaction to proceed from the condensing of the ammonia gas in the reaction flask until the excess lithium was decomposed was approximately one hour. The majority of this time was spent waiting for the condensed ammonia to evaporate from the reaction flask. It was also found that the ephedrine would reduce to methamphetamine without the addition of ammonium chloride as a quenching agent. According to the infamous J. All in all, quite an entertaining and educational article ;-. This may be so in fact I read the same article , but typically a water quench leads to the alcohol, which is what we were trying to get rid of to start with. Apparently they were following the guys handwritten notes. Yep — apparently that would be the case. As well, any extra Li or Na if doing the straight Birch method would convert to the Hydroxide, which might fuck the product up a bit. Phenylalanine is 2-aminophenylpropanoic acid, which is more or less amphetamine with a COOH where the CH3 should be at the end of the chain. When that carbonyl is reduced, you now have amphetamine. Go back up to that first one I mentioned for upgrading amphetamine into methamphetamine. These are methods that are subjectively evaluated to be less useful, but still may serve as interesting lessons in applied chemistry. One of the easiest ways to make methamphetamine is from amphetamine. The difference between amphetamine and methamphetamine is the addition of a single methyl group CH 3 to the amino group sticking off the middle carbon atom in the chain. Fortunately, substituting amines is really simple. Vaporize your amine your amphetamine with a bunch of vaporized chloromethane CH 3 Cl, a solvent and some gaseous pyridine… voila, the amino group takes the methyl from the chloromethane and lets a hydrogen go. The hydrogen joins the liberated chlorine, and the resulting HCl is soaked up by the pyridine. The pyridine is optional. This last question is solved be reference to a principle called the law of mass action. An excess of methylamine will inhibit the secondary reactions. Typically, a reductive amination done in a parr bomb or using sodium cyanoborohydride is done with a five times molar excess of methylamine or methylamine hydrochloride. As with any distillation there will be some left over. Question is, how much ammonia and reducing agent are you willing to waste on making 2aminopropane? This tends to occlude a slight amount of solvent so keep your crystal size small and grind and dry the result. Both these solvents are easily available if you know where to look. Methamphetamine in its pure hydrochloride salt form is colorless. However, products on the market today are often not colorless. The following is a table of some common impurities and the colors associated with them. Note: There is no doubt a segment of the dealers who will add food coloring or some other such color to their drug to make it more appealing, with the philosophy that a brightly-colored product may sell better than an off color product. This is relatively uncommon however. I am not sure what the cause of this is, but its most likely some form of oil, either formed in the reaction or left over from a very poor solvent. It may or may not be harmless depending upon what it is. This oil is often removed with acetone, but ethyl-ether would be better suited for this as it dries faster. Pure methamphetamine HCl melts at around c f. The crystals can be carefully chopped and mixed with sodium carbonate, and when the resulting powder is heated and the methamphetamine HCl melts CO 2 and methamphetamine base vapor is given off. This is probably one of the more effective ways of smoking meth if you are careful, however the hydrochloride salt is often the form smoked as the base form is often an oil and is difficult to store, transport, and work with. You can test methamphetamine HCl for optical activity with the greyish-clear plastic pieces from a pocket video game. Dissolve the methamphetamine in distilled water, then place one of the optical filters the grayish clear things from the games LCD display in front, and one in behind of the solution. Rotate one filter, and note the angle that is brightest and the angle that is darkest. After you have done this, repeat the procedure with distilled water. Or a dealer uses Ephedrine as cut. It is advisable to become familiar with the many ways of synthesizing methcathinone from pseudo ephedrine, as just such a procedure can be used on freshly produced methamphetamine to verify that the pseudo ephedrine was in fact reduced. Suffice to say that it is sweet, pleasant, and to a cat-head, nirvana. You should become familiar with this as well, in order to be able to know if suspected methamphetamine is in fact actually methcathinone. It should first melt at over c then begin to fume. Often the fumes will ignite. Methcathinone HCl has a higher melting point than methamphetamine HCl like over c at least and a characteristic smell, giving it away in an instant. Amphetamine has a bitter taste, followed by some degree of numbness. Methamphetamine is also more active on serotonin that amphetamine according to net resources. It appears to some extent in almost all syntheses relying on reduction and typically appears at the very end of the process of forming the HCl salt by bubbling HCl through the mixture. The scans just sucked when I tried to scan as text 5 pages magically became of scrambled text. I am currently trying gif type scans. However, it will never dry out as completely one might suspect. Even drying under heavy vacuum leads to only a temporary solution. Once it is exposed to air it quickly becomes an oil again. Often this is a brown color as you stated for other by-products. As far as the rest of the post, I find it very useful and agree with it completely. Take a ball about the size of a lead pellet, and wrap it in tissue, and swallow, or you can put it in capsules and use it. You can smoke it, mix it with vitamin B, and snort it like cocaine. Remember, this is pure stuff!! Take one of the small bottles and spray starter fluid in it till it looks half-full. Then fill the rest of the way with water, cap the bottle and shake for 5 minutes. Then, draw off the top layer with the eyedropper, and throw away the water layer. Repeat this until you have about 3 oz. Put the cap on it, and put it in the refrigerator if you can. It is very easy to become delirious off the ether fumes, so be sure you are well ventilated, I mean it!!! Small, aspirin, or experiment bottles seem to work the best for smaller batches. Remember, this is the water you have to use to evaporate. This recipe is bogus! You have simple extracted pseudoephedrine! All this stuff will give you is engziety sp? The d- isomer is the one that every one wants and that Uncle Sam has declared is just too cool for any one except doctors. The only way to change between the two isomers is to oxidize the l-meth into phenylacetone, condense it with methylamine, then reduce it. Do not use ethyl ether near flame or non-sparkless motors. It is also an anaesthetic and can cause respiratory collapse if you inhale too much. Take the unmarked small bottle and spray starter fluid in it until it looks half-full. Let it sit for a minute or two, and tap the side to try and separate the clear upper layer. Then, draw off the top ether layer with the eyedropper, and throw away the lower water and cloudy layer. Place the ether in the marked container. Repeat this until you have about 1. Put the cap on it, and put it in the freezer if you can. Rinse the other bottle and let it stand. This is because the hydroxyl group the OH in ephedrine is on a very acidic carbon the first carbon away from the ring and a hydroxyl group is very basic. Your post was interesting, but this is not quite true. Direct hydrogenation over Pd or Pd on a carrier is well known and facile. Calls to numbers on a specific treatment center listing will be routed to that treatment center. Additional calls will also be forwarded and returned by one of our treatment partners below. Calls to any general helpline non-facility specific XX numbers for your visit will be answered by one of our treatment partners, a paid advertiser on Amphetamines. Learn More.
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Метамфетамин
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Methamphetamine \\\\\\\\\\[note 1\\\\\\\\\\] contracted from N - methylamphetamine is a potent central nervous system CNS stimulant that is mainly used as a recreational drug and less commonly as a second-line treatment for attention deficit hyperactivity disorder and obesity. It is rarely prescribed over concerns involving human neurotoxicity and potential for recreational use as an aphrodisiac and euphoriant , among other concerns, as well as the availability of safer substitute drugs with comparable treatment efficacy. Dextromethamphetamine is a much stronger CNS stimulant than levomethamphetamine. Both methamphetamine and dextromethamphetamine are illicitly trafficked and sold owing to their potential for recreational use. The highest prevalence of illegal methamphetamine use occurs in parts of Asia, Oceania, and in the United States, where racemic methamphetamine, levomethamphetamine, and dextromethamphetamine are classified as schedule II controlled substances. Levomethamphetamine is available as an over-the-counter OTC drug for use as an inhaled nasal decongestant in the United States. While dextromethamphetamine is a more potent drug, racemic methamphetamine is sometimes illicitly produced due to the relative ease of synthesis and limited availability of chemical precursors. In low to moderate doses, methamphetamine can elevate mood , increase alertness, concentration and energy in fatigued individuals, reduce appetite, and promote weight loss. At very high doses, it can induce psychosis , breakdown of skeletal muscle , seizures and bleeding in the brain. Chronic high-dose use can precipitate unpredictable and rapid mood swings , stimulant psychosis e. Heavy recreational use of methamphetamine may lead to a post-acute-withdrawal syndrome , which can persist for months beyond the typical withdrawal period. Unlike amphetamine , methamphetamine is neurotoxic to human midbrain dopaminergic neurons. Methamphetamine belongs to the substituted phenethylamine and substituted amphetamine chemical classes. It is related to the other dimethylphenethylamines as a positional isomer of these compounds, which share the common chemical formula : C 10 H 15 N 1. In the United States, dextromethamphetamine hydrochloride, under the trade name Desoxyn , has been approved by the FDA for treating ADHD and obesity in both adults and children; \\\\\\\\\\[23\\\\\\\\\\] \\\\\\\\\\[24\\\\\\\\\\] however, the FDA also indicates that the limited therapeutic usefulness of methamphetamine should be weighed against the inherent risks associated with its use. As methamphetamine is associated with a high potential for misuse, the drug is regulated under the Controlled Substances Act and is listed under Schedule II in the United States. Methamphetamine is often used recreationally for its effects as a potent euphoriant and stimulant as well as aphrodisiac qualities. According to a National Geographic TV documentary on methamphetamine, an entire subculture known as party and play is based around sexual activity and methamphetamine use. Methamphetamine is contraindicated in individuals with a history of substance use disorder , heart disease , or severe agitation or anxiety, or in individuals currently experiencing arteriosclerosis , glaucoma , hyperthyroidism , or severe hypertension. The physical effects of methamphetamine can include loss of appetite , hyperactivity, dilated pupils , flushed skin , excessive sweating , increased movement , dry mouth and teeth grinding leading to ' meth mouth ' , headache, irregular heartbeat usually as accelerated heartbeat or slowed heartbeat , rapid breathing , high blood pressure , low blood pressure , high body temperature , diarrhea, constipation, blurred vision , dizziness , twitching , numbness , tremors , dry skin, acne , and pale appearance. Methamphetamine users and addicts may lose their teeth abnormally quickly, regardless of the route of administration, from a condition informally known as meth mouth. They suggest the side effect has been exaggerated and stylized to create a stereotype of current users as a deterrence for new ones. Methamphetamine use was found to be related to higher frequencies of unprotected sexual intercourse in both HIV-positive and unknown casual partners, an association more pronounced in HIV-positive participants. Besides the sexual transmission of HIV, it may also be transmitted between users who share a common needle. The psychological effects of methamphetamine can include euphoria , dysphoria , changes in libido , alertness , apprehension and concentration , decreased sense of fatigue, insomnia or wakefulness , self-confidence , sociability, irritability, restlessness, grandiosity and repetitive and obsessive behaviors. Unlike amphetamine , methamphetamine is directly neurotoxic to dopamine neurons in both lab animals and humans. Magnetic resonance imaging studies on human methamphetamine users have also found evidence of neurodegeneration, or adverse neuroplastic changes in brain structure and function. Current models of addiction from chronic drug use involve alterations in gene expression in certain parts of the brain, particularly the nucleus accumbens. The frequent persistence of addiction suggests that long-lasting changes in gene expression may occur in particular regions of the brain, and may contribute importantly to the addiction phenotype. Recently a crucial role has been found for epigenetic mechanisms in driving lasting changes in gene expression in the brain. A review in \\\\\\\\\\[77\\\\\\\\\\] summarized a number of studies involving chronic methamphetamine use in rodents. Epigenetic alterations were observed in the brain 'reward' regions, including the ventral tegmental area , the nucleus accumbens , the dorsal striatum , the hippocampus , and the prefrontal cortex. Chronic methamphetamine use caused gene-specific histone acetylations, deacetylations and methylations. Gene-specific DNA methylations in particular regions of the brain were also observed. The various epigenetic alterations caused downregulations or upregulations of specific genes important in addiction. For instance, chronic methamphetamine use caused methylation of the lysine in position 4 of histone 3 located at the promoters of the c-fos and the C-C chemokine receptor 2 ccr2 genes, activating those genes in the nucleus accumbens NAc. In methamphetamine addicted rats, epigenetic regulation through reduced acetylation of histones, in brain striatal neurons, caused reduced transcription of glutamate receptors. A systematic review and network meta-analysis of 50 trials involving 12 different psychosocial interventions for amphetamine, methamphetamine, or cocaine addiction found that combination therapy with both contingency management and community reinforcement approach had the highest efficacy i. As of December \\\\\\\\\\[update\\\\\\\\\\] , there is no effective pharmacotherapy for methamphetamine addiction. Tolerance is expected to develop with regular methamphetamine use and, when used recreationally, this tolerance develops rapidly. While newborn babies addicted to opioids show the jittery signs of immediate withdrawal, methamphetamine-affected babies show little more than a tendency to sleep. Neonatologist Dr Ju Lee Oei of the University of New South Wales said not only were these babies often overlooked at birth, it was not until they approached school age that concerning behavioural and learning issues really started to emerge, by which time years of treatment opportunities had been missed. These children do not present with overt cerebral palsy or disability, but they have attention, behavioural and subtle cognitive losses that cannot be explained by anything else after accounting for lifestyle, environmental differences and genetic influences. Researcher and nurse, Dr Stacey Blythe , said 'Generally what would happen is the child presents as relatively healthy and they continue to grow and develop. A methamphetamine overdose may result in a wide range of symptoms. Abuse of methamphetamine can result in a stimulant psychosis which may present with a variety of symptoms e. Acute methamphetamine intoxication is largely managed by treating the symptoms and treatments may initially include administration of activated charcoal and sedation. Antipsychotics such as haloperidol are useful in treating agitation and psychosis from methamphetamine overdose. Methamphetamine has been identified as a potent full agonist of trace amine-associated receptor 1 TAAR1 , a G protein-coupled receptor GPCR that regulates brain catecholamine systems. In addition to the plasma membrane monoamine transporters, methamphetamine inhibits uptake and induces efflux of neurotransmitters and other substrates at the vesicular monoamine transporters, VMAT1 and VMAT2. Following oral administration, methamphetamine is well-absorbed into the bloodstream, with peak plasma methamphetamine concentrations achieved in approximately 3. The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination. Methamphetamine and amphetamine are often measured in urine or blood as part of a drug test for sports, employment, poisoning diagnostics, and forensics. Methamphetamine is a chiral compound with two enantiomers, dextromethamphetamine and levomethamphetamine. At room temperature, the free base of methamphetamine is a clear and colorless liquid with an odor characteristic of geranium leaves. Bleach exposure time and concentration are correlated with destruction of methamphetamine. Racemic methamphetamine may be prepared starting from phenylacetone by either the Leuckart \\\\\\\\\\[\\\\\\\\\\] or reductive amination methods. During World War II, methamphetamine was sold in tablet form under the brand name Pervitin not to be confused with Perviton , which is a synonym for Phenatine , produced by the Berlin-based Temmler pharmaceutical company. It was used extensively by all branches of the combined Wehrmacht armed forces of the Third Reich , and was popular with Luftwaffe pilots in particular, for its performance-enhancing stimulant effects and to induce extended wakefulness. Side effects were so serious that the army sharply cut back its usage in Suffering from a drug hangover and looking more like a zombie than a great warrior, he had to recover from the side effects. Obetrol , patented by Obetrol Pharmaceuticals in the s and indicated for treatment of obesity , was one of the first brands of pharmaceutical methamphetamine products. The production, distribution, sale, and possession of methamphetamine is restricted or illegal in many jurisdictions. It has been suggested, based on animal research, that calcitriol, the active metabolite of vitamin D , can provide significant protection against the DA- and 5-HT-depleting effects of neurotoxic doses of methamphetamine. From Wikipedia, the free encyclopedia. This article is about the free base and salts of methamphetamine, a stimulant drug. For other uses, see Meth disambiguation. US : C Risk not ruled out. IUPAC name. Interactive image. N C Cc1ccccc1 C C. See also: Party and play and the Recreational routes of methamphetamine administration. Main article: Meth mouth. Signaling cascade in the nucleus accumbens that results in psychostimulant addiction v t e. Note: colored text contains article links. Nuclear pore. Nuclear membrane. Plasma membrane. Metabolic pathways of methamphetamine in humans \\\\\\\\\\[sources 2\\\\\\\\\\]. Benzoic acid. Hippuric acid. Methamphetamine synthesis. Method of methamphetamine synthesis of methamphetamine via reductive amination. Methods of methamphetamine synthesis via the Leuckart reaction. Main article: History and culture of substituted amphetamines. Main article: Legal status of methamphetamine. Levomethamphetamine and dextromethamphetamine are also known as L-methamphetamine , R -methamphetamine , or levmetamfetamine International Nonproprietary Name \\\\\\\\\\[INN\\\\\\\\\\] and D-methamphetamine , S -methamphetamine , or metamfetamine INN , respectively. Text color Transcription factors. Methamphetamine, a central nervous system stimulant drug, is p-hydroxylated by CYP2D6 to less active p-OH-methamphetamine. United States Food and Drug Administration. Shire US Inc. December Archived PDF from the original on 30 December Retrieved 30 December PubChem Compound. National Center for Biotechnology Information. Sudbury, Mass. Archived from the original on 18 March Retrieved 4 September Clinical Toxicology. Drug profiles. Archived from the original on 15 April Retrieved 27 November University of Alberta. Archived from the original on 4 March Retrieved 16 January Archived from the original on 7 December Retrieved 1 January Archived from the original on 28 January Pubchem Compound. Archived from the original on 6 October April Topical nasal decongestants -- i For products containing levmetamfetamine identified in The product delivers in each milliliters of air 0. NBC News. Associated Press. Archived from the original on 12 August Retrieved 12 September Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons. Behav Neurol. Brain Res. Neuroimaging studies have revealed that METH can indeed cause neurodegenerative changes in the brains of human addicts Aron and Paulus, ; Chang et al. These abnormalities include persistent decreases in the levels of dopamine transporters DAT in the orbitofrontal cortex, dorsolateral prefrontal cortex, and the caudate-putamen McCann et al. The density of serotonin transporters 5-HTT is also decreased in the midbrain, caudate, putamen, hypothalamus, thalamus, the orbitofrontal, temporal, and cingulate cortices of METH-dependent individuals Sekine et al. Neuropsychological studies have detected deficits in attention, working memory, and decision-making in chronic METH addicts There is compelling evidence that the negative neuropsychiatric consequences of METH abuse are due, at least in part, to drug-induced neuropathological changes in the brains of these METH-exposed individuals These include loss of gray matter in the cingulate, limbic and paralimbic cortices, significant shrinkage of hippocampi, and hypertrophy of white matter Thompson et al. Elevated choline levels, which are indicative of increased cellular membrane synthesis and turnover are also evident in the frontal gray matter of METH abusers Ernst et al. Archived PDF from the original on 2 January Retrieved 6 January A critical review'. National Geographic Channel. August Archived from the original on 8 July Retrieved 7 July The Lancet. New York: McGraw-Hill. National Institute on Drug Abuse. National Institutes of Health , U. October Retrieved 15 March Medical News Today. Advanced Recovery Systems. American Dental Association. Archived from the original on June Retrieved 15 December AIDS and Behavior. Archived from the original on 4 June Retrieved 15 January Archived from the original PDF on 16 August Merck Manual for Health Care Professionals. Archived from the original on 6 May Retrieved 8 May Neurologic Clinics. Drug Alcohol Rev. Glial modulators as potential treatments of psychostimulant abuse. Advances in Pharmacology. Glia including astrocytes, microglia, and oligodendrocytes , which constitute the majority of cells in the brain, have many of the same receptors as neurons, secrete neurotransmitters and neurotrophic and neuroinflammatory factors, control clearance of neurotransmitters from synaptic clefts, and are intimately involved in synaptic plasticity. Despite their prevalence and spectrum of functions, appreciation of their potential general importance has been elusive since their identification in the mids, and only relatively recently have they been gaining their due respect. Neuroimmune basis of methamphetamine toxicity. International Review of Neurobiology. Collectively, these pathological processes contribute to neurotoxicity e. Curr Neuropharmacol. They are present in the organs that mediate the actions of METH e. In the brain, METH acts primarily on the dopaminergic system to cause acute locomotor stimulant, subchronic sensitized, and neurotoxic effects. Behavioural Neurology. The Journal of Pharmacology and Experimental Therapeutics. Pharmacol Rep. Archived PDF from the original on 16 July Retrieved 8 November Curr Drug Abuse Rev. Dialogues in Clinical Neuroscience. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict. Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February New England Journal of Medicine. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders DSM-5 referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe. Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder. This is known to occur on many genes including fosB and c-fos in response to psychostimulant exposure. Chronic exposure to psychostimulants increases glutamatergic \\\\\\\\\\[signaling\\\\\\\\\\] from the prefrontal cortex to the NAc. The Journal of General Physiology. Coincident and convergent input often induces plasticity on a postsynaptic neuron. The NAc integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex PFC , as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses Goto and Grace, KEGG Pathway. Retrieved 31 October Most addictive drugs increase extracellular concentrations of dopamine DA in nucleus accumbens NAc and medial prefrontal cortex mPFC , projection areas of mesocorticolimbic DA neurons and key components of the 'brain reward circuit'. Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain. Molecular Neurobiology. Nature Reviews Neuroscience. The net result is gene activation and increased CDK5 expression. The net result is c-fos gene repression. Clinical Psychopharmacology and Neuroscience. Drug Alcohol Abuse. Similar to environmental enrichment, studies have found that exercise reduces self-administration and relapse to drugs of abuse Cosgrove et al. There is also some evidence that these preclinical findings translate to human populations, as exercise reduces withdrawal symptoms and relapse in abstinent smokers Daniel et al. In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in or compulsive engagement in non-drug rewards such as gambling, shopping, or sex Evans et al. Archived from the original on 13 October Bibcode : PNAS.. Journal of Psychoactive Drugs. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Drugs of abuse induce neuroplasticity in the natural reward pathway, specifically the nucleus accumbens NAc , thereby causing development and expression of addictive behavior. Sexual behavior is highly rewarding Tenk et al. Moreover, sexual experience induces neural plasticity in the NAc similar to that induced by psychostimulant exposure, including increased dendritic spine density Meisel and Mullins, ; Pitchers et al. Finally, periods of abstinence from sexual experience were found to be critical for enhanced Amph reward, NAc spinogenesis Pitchers et al. Drug Alcohol Depend. J Subst Abuse Treat. Trends Pharmacol. PLOS Medicine. Expert Rev Clin Pharmacol. Despite concerted efforts to identify a pharmacotherapy for managing stimulant use disorders, no widely effective medications have been approved. Addiction Abingdon, England. Merck Manual Home Health Handbook. Archived from the original on 17 February Retrieved 26 September Cochrane Database Syst. Shoptaw SJ ed. The prevalence of this withdrawal syndrome is extremely common Cantwell ; Gossop with American Family Physician. Emergency Central. Unbound Medicine. Archived from the original on 26 September Retrieved 11 June Archived PDF from the original on 4 July Retrieved 2 January Shoptaw SJ, Ali R eds. A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis. New York: Oxford University Press. Methamphetamine Toxicity. Archived from the original on 9 April Retrieved 20 April Bibcode : PNAS International Union of Basic and Clinical Pharmacology. Archived from the original on 29 June Retrieved 8 December AMPH also increases intracellular calcium Gnegy et al. AMPH and METH also stimulate DA efflux, which is thought to be a crucial element in their addictive properties \\\\\\\\\\[80\\\\\\\\\\], although the mechanisms do not appear to be identical for each drug \\\\\\\\\\[81\\\\\\\\\\]. University of Paris. Archived from the original on 29 May Retrieved 29 May Retrieved 5 October Methamphetamine is rapidly absorbed from the gastrointestinal tract with peak methamphetamine concentrations occurring in 3. Methamphetamine is also well absorbed following inhalation and following intranasal administration. It is distributed to most parts of the body. Because methamphetamine has a high lipophilicity it is distributed across the blood brain barrier and crosses the placenta. The primary site of metabolism is in the liver by aromatic hydroxylation, N-dealkylation and deamination. At least seven metabolites have been identified in the urine, with the main metabolites being amphetamine active and 4-hydroxymethamphetamine. Other minor metabolites include 4-hydroxyamphetamine, norephedrine, and 4-hydroxynorephedrine. The simplest unsubstituted phenylisopropylamine, 1-phenylaminopropane, or amphetamine, serves as a common structural template for hallucinogens and psychostimulants. Amphetamine produces central stimulant, anorectic, and sympathomimetic actions, and it is the prototype member of this class The phase 1 metabolism of amphetamine analogs is catalyzed by two systems: cytochrome P and flavin monooxygenase. Amphetamine can also undergo aromatic hydroxylation to p -hydroxyamphetamine. Stereochemical course of the reaction' PDF. Archived PDF from the original on 7 October Retrieved 6 November Hydroxyamphetamine was administered orally to five human subjects The lack of effect of administration of neomycin to one patient indicates that the hydroxylation occurs in body tissues. Unfortunately, at the present time one cannot be completely certain that the hydroxylation of hydroxyamphetamine in vivo is accomplished by the same enzyme which converts dopamine to noradrenaline. Retrieved 12 October Clin Pharmacokinet. Disposition of toxic drugs and chemicals in man. Seal Beach, Ca. Archived from the original on 19 October Retrieved 17 October Bibcode : Chmsp.. Water Res. The Journal of Organic Chemistry. The Guardian. Archived from the original on 17 August Retrieved 17 August London: Routledge. Vermont Department of Health. Government of Vermont. Archived from the original on 26 June Retrieved 29 January ISRN Dentistry. Spiegel Online. Der Spiegel, 6 May Archived from the original on 19 December Retrieved 12 August Oxford University Press. Archived from the original on 23 March Retrieved 23 October New York University Press. Archived from the original on 5 April Retrieved 4 November Lundbeck: Desoxyn. Archived from the original on 30 November Recordati SP. Archived from the original on 7 July Retrieved 15 May New York: United Nations. Archived PDF from the original on 16 October Retrieved 11 November International Narcotics Control Board. United Nations. Archived from the original PDF on 5 December Retrieved 19 November Annals of the New York Academy of Sciences. Dexedrine ProCentra Zenzedi. Dextromethamphetamine Levomethamphetamine. Amphetamine dependence Meth mouth Prenatal methamphetamine exposure. United States Native Americans Australia. Recreational drug use. Calea zacatechichi Silene capensis. Coffee break Coffeehouse Latte art Tea house. Abuse Date rape drug Impaired driving Drug harmfulness Effects of cannabis Addiction Dependence Prevention Opioid replacement therapy Rehabilitation Responsible use Drug-related crime Fetal alcohol spectrum disorder Long-term effects of cannabis Neurotoxicity Overdose Passive smoking of tobacco or other substances. Alcohol legality Alcohol consumption Anabolic steroid legality Cannabis legality Annual use Lifetime use Cigarette consumption Cocaine legality Cocaine use Methamphetamine legality Opiates use Psilocybin mushrooms legality Salvia legality. Adapromine Amantadine Bromantane Memantine Rimantadine. Oxiracetam Phenylpiracetam Phenylpiracetam hydrazide. ATC code : N06B. ADHD pharmacotherapies. Amphetamine Mixed amphetamine salts , Levoamphetamine , Dextroamphetamine , Lisdexamfetamine Methamphetamine Methylphenidate Dexmethylphenidate. Atomoxetine Modafinil. Clonidine Guanfacine. Amantadine Carbamazepine. Monoamine releasing agents. Oxazolines: 4-Methylaminorex Aminorex Clominorex Fluminorex. Others: Indeloxazine Viqualine. Human trace amine-associated receptor ligands. N , N -Dimethylethylamine Trimethylamine. Sigma receptor modulators. Monoamine neurotoxins. Categories : Methamphetamine Anorectics Aphrodisiacs Carbonic anhydrase activators Cardiac stimulants Euphoriants Excitatory amino acid reuptake inhibitors Japanese inventions Management of obesity Norepinephrine-dopamine releasing agents Phenethylamines Sigma agonists Stimulants Substituted amphetamines Sympathomimetics TAAR1 agonists Treatment and management of attention deficit hyperactivity disorder VMAT inhibitors introductions. Namespaces Article Talk. Views Read View source View history. In other projects Wikimedia Commons Wikinews. By using this site, you agree to the Terms of Use and Privacy Policy. Medical: oral ingestion Recreational: oral , intravenous , intramuscular , subcutaneous , smoke inhalation , insufflation , rectal , vaginal. Varies widely \\\\\\\\\\[6\\\\\\\\\\]. Rapid \\\\\\\\\\[7\\\\\\\\\\]. Signaling cascade in the nucleus accumbens that results in psychostimulant addiction v t e Note: colored text contains article links. Nuclear pore Nuclear membrane Plasma membrane Ca v 1. Following presynaptic dopamine and glutamate co-release by such psychostimulants, \\\\\\\\\\[57\\\\\\\\\\] \\\\\\\\\\[58\\\\\\\\\\] postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation. Psychostimulant cross-sensitization. Psychostimulant self-administration. Psychostimulant conditioned place preference. Reinstatement of drug-seeking behavior. CREB phosphorylation in the nucleus accumbens. Sensitized dopamine response in the nucleus accumbens. Altered striatal dopamine signaling. Altered striatal opioid signaling. Changes in striatal opioid peptides. Number of dendrites in the nucleus accumbens. Dendritic spine density in the nucleus accumbens. Metabolic pathways of methamphetamine in humans \\\\\\\\\\[sources 2\\\\\\\\\\] Methamphetamine 4-Hydroxymethamphetamine 4-Hydroxyphenylacetone Phenylacetone Benzoic acid Hippuric acid Amphetamine Norephedrine 4-Hydroxyamphetamine 4-Hydroxynorephedrine The primary metabolites of methamphetamine are amphetamine and 4-hydroxymethamphetamine. Wikimedia Commons has media related to Dextromethamphetamine.
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