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Results for “LYSERGIC ACID DIETHYLAMIDE”

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PubMed1983

Morphologic alterations in the Purkinje neuron of the rat induced by lysergic acid diethylamide and fixation.

The effect of lysergic acid diethylamide (LSD) on the morphology of the cerebellar cortex of the rat was studied with electron microscopy. Hippocampal electrical activity was used as an objective measure of drug efficacy. At a dose of 1700 micrograms/kg, the amplitude from the hippocampus was diminished (in 2 to 5 min) and this effect lasted for about 65 to 165 min. A morphologic alteration consisting of cisternal stacks occurred in the dendrites of Purkinje neurons of rats treated with this dose of LSD, with the perfusion carried out correctly. These stacks of smooth endoplasmic reticulum were seen 2 h after injection and persisted for at least 8 h. A reduction in the volume of perfused fluid to less than 500 ml caused similar changes in the dendrites of the Purkinje neuron of untreated rats; this was one way to experimentally induce a faulty perfusion. With LSD and faulty perfusion (reduced volume) more severe changes occurred in the dendrites and small stacks of smooth endoplasmic reticulum were seen in the Purkinje soma; similar changes were also seen when the perfusion of a control animal was mismanaged during the initial 3 min. The Purkinje neuron seems to manifest morphologic alterations, generally of two types, with exposure to a variety of noxious agents. The LSD caused some perturbation of this neuron, and this was found under properly controlled conditions of fixation. The results are interpreted as indicating that LSD is causing a metabolic alteration which could disrupt the synaptic activity over several hours.

Animals↗
PubMed1967

Congenital malformations induced by mescaline, lysergic acid diethylamide, and bromolysergic acid in the hamster.

Malformations of the brain, spinal cord, liver, and other viscera; body edema; and localized hemorrhages were found in fetal hamsters from mothers injected subcutaneously with a single dose of mescaline, lysergic acid diethylamide, or 2-bromo-D lysergic acid diethylamide on the 8th day of pregnancy. In addition, all three drugs produced an increase in the percentages of small fetuses per litter, of resorptions, and of fetal mortality.

Abnormalities, Drug-Induced↗
PubMed1980

Enzymic formation of dehydrogenated and hydroxylated metabolites from lysergic acid diethylamide by rat liver microsomes.

1. The metabolism of lysergic acid diethylamide (LSD) was studied using rat liver microsomes, and two minor metabolites were obtained in addition to lysergic acid ethylamide and N6-desmethyl-lysergic acid diethylamide (nor-LSD) which were reported previously. 2. One of the metabolites was identified as lysergic acid ethylvinylamide, apparently formed by dehydrogenation of a diethylamide group in the side chain at the 8-position, and the other as the phenol 13-hydroxy-LSD. 3. The formation of both lysergic acid ethylamide and lysergic acid ethylvinylamide was similarly induced by pretreatment of rats with either phenobarbitone sodium or 3-methylcholanthrene, while nor-LSD formation was induced only by phenobarbitone and that of 13-hydroxy-LSD only by methylcholanthrene.

Anaerobiosis↗
PubMed1977

Hyperthermic effects of D-lysergic acid diethylamide (LSD) and its derivatives in rabbits and rats.

Several D-lysergic acid diethylamide (LSD) derivatives including metabolites of LSD in animals liver and Streptomyces such as D-lysergic acid ethyl, 2-hydroxyethylamide (LEO), D-lysergic acid ethylamide (LAE), D-norlysergic acid diethylamide (norLSD) and synthetic N6-allyl-D-norlysergic acid diethylamide (allyl-nor LSD) were studied with rabbits and rats. In rabbits, the order of the hyperthermic activities was allyl-norLSD greater than LSD greater than LEO, LAE, nor-LSD, and this order was parallel to that of 5-hydroxytryptamine-like activities of these compounds which was previously studied. However, the order was LAE greater than LSD greater than norLSD IN RATS. The hyperthermic effect of LSD in rabbits was attenuated by methysergide, but not by atropine when these drugs were intraventricularly administered. These results suggest the possibility that the metabolites of LSD contribute to the hyperthermic effect of LSD in rats but not in rabbits, and support the idea that 5-HT receptors are involved in the hyperthermia induced by LSD in rabbits.

5-Hydroxytryptophan↗
PubMed1973

Lysergic acid diethylamide: radioimmunoassay.

A radioimmnunoassay for d-lysergic acid diethylamide (LSD) is described. Antibodies to LSD were obtained by immunizing rabbits with a conjugate of LSD and human serum albumin. The specificity of the antibody was shown by competitive binding studies. The method has been used to detect the presence of LSD in human urines. Picogram amounts can be measured by this assay.

Animals↗
PubMed1998

Indirect enzyme-linked immunosorbent assay for the quantitative estimation of lysergic acid diethylamide in urine.

A new antibody to lysergic acid diethylamide (LSD) was used to develop a novel indirect ELISA for the quantification of drug in urine. Evaluation of the new assay with the commercially available LSD ELISA (STC Diagnostics) shows improved performance. The test requires 50 microL of urine, which is used to measure concentrations of drug in the microg/L to ng/L range. The limit of detection was 8 ng/L compared with 85 ng/L in the commercial assay, and analytical recoveries were 98-106%. Our test detected 0.1 microg/L of LSD in urine with an intraassay CV of 2.4% (n = 8) compared with 6.0% for a 0.5 microg/L sample in the commercial assay (n = 20). The upper and lower limits of quantification were estimated to be 7 microg/L and 50 ng/L, respectively. Specificity was evaluated by measuring the extent of cross-reactivity with 24 related substances. Drug determination using the new assay offers both improved sensitivity and precision compared with existing methods, thus facilitating the preliminary quantitative estimation of LSD in urine at lower concentrations with a greater degree of certainty.

Benzidines↗
PubMed1973

An inhibition of post-ganglionic motor transmission in the mammalian vas deferens by D-lysergic acid diethylamide.

1. Under certain conditions D-lysergic acid diethylamide (LSD), 10(-9)-10(-6) g/ml., exerted an immediate, prolonged and slowly reversible inhibitory effect upon the post-ganglionic motor transmission in desheathed guinea-pig vas deferens preparations.2. The most critical factor influencing this action of LSD appeared to be the train length. With short trains of less than 4 or 5 pulses the twitch inhibition produced by LSD was often total. With longer trains (5-20 pulses), the degree of inhibition declined with increase in train length. These results suggest the existence of two components in the motor response to post-ganglionic stimulation, distinguished by their susceptibility to LSD.3. The inhibition of the LSD-susceptible component was related to the dose of LSD in the range 10(-9)-10(-6) g/ml., reaching a maximum at 0.5-1 x 10(-6) g/ml. The response remnants elicited by trains of more than 5 pulses under these conditions could not be reduced further by a ten- to twenty-fold increase in LSD concentration to 10(-5) g/ml. and were in fact slightly potentiated.4. The inhibition of post-ganglionic motor transmission by LSD was not explicable on the basis of an alpha-adrenoceptor blockade because it was not associated with any reduction in motor responses to noradrenaline.5. The use of propranolol excluded mediation of the LSD-inhibition by beta-adrenoceptors.6. The LSD effect was not due to a non-specific smooth muscle depression because it was not associated with any reduction in motor responses to acetylcholine, ATP or bradykinin.7. The inhibitory effect of LSD on post-ganglionic transmission resembled that of noradrenaline in that it was antagonized by phentolamine; another alpha-adrenoceptor blocking agent, phenoxybenzamine, was less effective than phentolamine in this respect.8. The LSD-inhibition was obtained in preparations taken from reserpinized guinea-pigs.9. The inhibition of motor transmission in the vas deferens by LSD was confirmed in rats, Meriones shawii and rabbits.10. The inhibition of post-ganglionic transmission by LSD was unrelated to its ability to antagonize 5-hydroxytryptamine (5-HT), to which the longitudinal muscle of the guinea-pig vas deferens is insensitive. The more potent 5-HT antagonists, methysergide and BOL 148 were either virtually inactive or considerably weaker than LSD.

Acetylcholine↗
PubMed2002

Optimization of the separation of lysergic acid diethylamide in urine by a sweeping technique using micellar electrokinetic chromatography.

The separation and on-line concentrations of lysergic acid diethylamide (LSD), iso-lysergic acid diethylamide (iso-LSD) and lysergic acid N,N-methylpropylamide (LAMPA) in human urine were investigated by capillary electrophoresis-fluorescence spectroscopy using sodium dodecyl sulfate (SDS) as an anionic surfactant. A number of parameters such as buffer pH, SDS concentration, Brij-30 concentration and the content of organic solvent used in separation, were optimized. The techniques of sweeping-micellar electrokinetic chromatography (sweeping-MEKC) and cation-selective exhaustive injection-sweep-micellar electrokinetic chromatography (CSEI-sweep-MEKC) were used for determining on-line concentrations. The advantages and disadvantages of this procedure with respect to sensitivity, precision and simplicity are discussed and compared.

Chromatography, Micellar Electrokinetic Capillary↗
PubMed1969

Lysergic acid diethylamide: role in conversion of plasma tryptophan to brain serotonin (5-hydroxytryptamine).

Injections of D-lysergic acid diethylamide decrease the turnover rate of 5-hydroxytryptamine of rat brain, as measured from the conversion of (14)C-tryptophan into (14)C-5-hydroxytryptamine. The 2-bromolysergic acid diethylamide given in doses fivefold greater than those of lysergic acid diethylamide fails to change the rate of (14)C-tryptophan conversion into (14)C-5-hydroxytryptamine. The effect of D-lysergic acid diethylamide is discussed with regard to its action on brain serotonergic neurons and its psychotomimetic effects.

Animals↗
PubMed1975

Lysergic acid diethylamide: effect on histone acetylation in rabbit brain.

Lysergic acid diethylamide increased acetylation of histones in rabbit cerebral hemispheres and midbrain 30 minutes after intravenous administration of the drug at doses of 10 and 100 micrograms per kilogram of body weight. Evidence for the stimulation of acetylation in individual histone bands was obtained after separation by electrophoresis on polyacrylamied gels.

Acetylation↗