Lysergic Acid Diethylamide (LSD) is an indolealkylamine discovered by Albert Hoffman of Sandoz Laboratories in 1943.1 It may be synthesized from lysergic acid and diethylamine. Lysergic acid, a naturally occurring ergot alkaloid, is present in grain parasitized by the fungus Claviceps purpurea. A closely related alkaloid, lysergic acid amide, is present in morning glory seeds and the Hawaiian baby wood rose.1 In the 1950s, LSD was used as an aid in the treatment of alcoholism, opioid addiction, pyschoneurosis, and sexual disorders, but currently it is classified under Schedule I of the federal Controlled Substances Act with no accepted medical use in the U.S. It is available illicitly as a powder, tablet, or gelatin capsule, or impregnated in sugar cubes, gelatin squares, blotter paper, or postage stamps.
LSD is a potent centrally acting drug. The d-isomer is pharmacologically active while the l-isomer is apparently inactive.1 Neuropharmacological studies have shown that LSD exerts a selective inhibitory effect on the brain's raphe system by causing a cessation of the spontaneous firing of serotonin containing neurons of the dorsal and median raphe nuclei. In this way, LSD acts as an indirect serotonin antagonist. However, inhibition of raphe firing is not sufficient to explain the psychotomimetic effects of LSD because the compound lisuride is a more potent inhibitor of the raphe system yet does not demonstrate hallucinogenic potential in humans. Therefore, other post-synaptic mechanisms such as action on glutamate or serotonin receptors, may be involved.2 Also, there is evidence that LSD indirectly exerts effects on the cytoskeleton by reducing the amount of serotonin released by the raphe system.3 LSD produces sympathomimetic, parasympathomimetic and neuromuscular effects which include mydriasis, lacrima-tion, tachycardia, and tremor.
LSD may be self administered orally, nasally, or by parenteral ingestion; however, the oral route is the most common. Doses of 50 to 300 ug are ingested, with a minimum effective dose of 20 to 25 ug. Absorption is rapid and complete regardless of the route of administration. However, food in the stomach slows absorption when ingested. Effects are observed within 5 to 10 min, with psychosis evident after 15 to 20 min. Peak effects have been reported 30 to 90 min after dosing; effects decline after 4 to 6 h.4 The duration of effects may be 8 to 12 h.
Pharmacokinetic studies in humans are limited with much of the data dating from the 1960s. Following intravenous administration of 2 ug/kg, a peak plasma LSD concentration of 5 ng/mL was observed after 1 h.1 At 8 h, the plasma concentration had declined to 1 ng/mL.1
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