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Most ketamine is racemic, i.e. it is composed of equal parts S/(+) and R/(-) ketamine. The (+) isomer of ketamine is more potent than the (-) isomer. It also seems that (+) ketamine would be superior as a psychedelic tool, for a number of reasons.
Some facts/differences worth noting:
In a study which used male adults, the amount of ketamine needed for total anaesthesia was ~271 mg (+) ketamine vs ~409 mg racemic ketamine.
(+) ketamine is generally considered to be approx. 2-3 times more potent than (-) ketamine.
(+) ketamine is cleared from the body in HALF the time it takes for racemic ketamine. The clearance of (-) ketamine takes only slightly longer than racemic ketamine.
(-) ketamine significantly inhibits the clearance of (+) ketamine. This means that if you have pure (+) ketamine, after you come out of a k-hole, the aftereffects of the k will wear off more quickly than they would if you had done racemic ketamine.
(+) ketamine inhibits the dopamine transporter 8 times more potently than (-) ketamine.[2]

However, application of S(+)-ketamine was associated with a remarkably smoother emergence period, a profound postoperative analgesia, a more rapid recovery of cerebral functions, and a greater preference by the study persons. The incidence of psychotomimetic phenomena appeared to be negligibly less after S(+)-ketamine in comparison to racemic ketamine, but their quality was described as far less unpleasant. Clinical use of S(+)-ketamine administered at one-half of the usual dose is thus not only associated with a reduction of undesirable adverse effects without altering ketamine’s anaesthetic and analgesic potency, but also offers distinctive improvements due to the reduced drug load. Moreover, increasing experimental evidence supports a remarkable neuroprotective effect of S(+)-ketamine, which may become a promising drug for new therapeutic approaches to neuroprotection.

It was found that (S)-ketamine binds with a 3-4 time higher affinity to the PCP binding site of the NMDA receptor than (R)-ketamine, and that at these concentrations (R)-ketamine interacts also weakly with the sigma receptor sites, where (S)-ketamine binds only negligibly….R)-ketamine did not produce psychotic symptoms, but a state of relaxation. The (S)-ketamine-induced metabolic hyperfrontality appears to parallel similar metabolic findings in acute psychotic schizophrenic patients and encourages further investigations of glutamatergic disturbances in schizophrenia.
This leads me to believe that the psychedelic effects of racemic ketamine are being produced by the (+) isomer. This would further lead me to conclude that pure (+) ketamine would be more psychedelic in its subjective effects — as well as less sedating (as noted in the study).
With sub-anaesthetic doses of ketamine in humans, 50% of the test subjects who took racemic ketamine experienced anterograde amnesia (could not remember portions of the k-experience) , while only 8% of those who took (+) ketamine experienced amnesia. This means that your ability to recall a ketamine trip would be greatly improved if you were taking pure (+) ketamine.

Subjective mood was judged by the volunteers to be significantly better after S-(+)-ketamine, and volunteers found S-(+)-ketamine to be more acceptable than racemic ketamine. The frequency of dreams was the same after both drugs. No unpleasant dreams were reported after S-(+)-ketamine, but one of the volunteers who received racemic ketamine had uncomfortable dreams. It seems that (+) ketamine has a distinct positive vibe to it, unlike racemic ketamine which is more neutral (or even negative) in its psychological effects.

Buy Ketamine HCL Online is an unusual drug and people have found themselves freaked out, hurt, robbed or groped – all because they weren’t aware of Ketamines ‘disassociative’ aspects. Although K only lasts between 15-40 mins, it disassociates the mind from the body, so you won’t be able to feel or control your body with any certainty. It may be impossible to walk, run, or even move at all – all of which can be dangerous if you suddenly find yourself in a dodgy situation. There’s some particular info it’s good to know about with K, even if you think you know it all anyway coz you take K all the time – here are some tips to stay safe and get the best out of your K experience. Read these tips for safer K trips. (Another article on how K works as a drug, its history, its drug culture etc, is following shortly, stay tuned to our site).
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The only known source of Ketamine  is via diversion of prescription products. There have been reports of veterinarian offices being robbed of their ketamine stock. Also, according to the DEA, a major U.S. source of illicit ketamine arrives across the border from Mexico.
Widespread ketamine abuse began in the late 1970s as subcultures (e.g., mind explorers, new agers, spiritualists) experimented with the drug. Ketamine may be injected intravenously or intramuscularly, used intranasally (“snorted”), consumed orally, or added to marijuana and smoked. In social situations, illicit ketamine is most frequently used orally or intranasally.
Doses of 1 to 2 milligram per kilogram of body weight produce intense hallucinogenic and dissociative effects for roughly one hour. Sensations may include floating, stimulation and visual effects. Larger doses may result in the “k-hole”, where users are near full sedation and are said to mimic an “out-of-body” or “near-death” experience. High doses may dangerously reduce breathing, lead to muscles spasms or weakness, dizziness, balance difficulty, impaired vision, slurred speech, nausea and vomiting, and severe confusion.Buy Ketamine HCL Liquid Online | buy ketamine online usa.
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Buy Ketamine HCL Liquid Online has been demonstrated to be sufficient in treating discouragement in patients with bipolar issue who have not responded to antidepressants. In persons with significant depressive turmoil, it forms a snappy stimulant effect, acting inside two hours instead of the a few weeks taken by ordinary antidepressants to work. Its hydrochloride salt is sold as Ketanest, Ketaset, and Ketalar. Pharmacologically, ketamine is viewed as a Nmda receptor adversary. At high, totally soothing level estimations, ketamine has similarly been found to attach to μ-opioid receptors sort 2 in taught human neuroblastoma cells – regardless, without agonist development – and to sigma receptors in rats.also,` ketamine chips in with muscarinic receptors, plunging monoaminergic torment pathways and voltage-gated calcium.
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