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PubMed2004

Quantitation of lysergic acid diethylamide in urine using atmospheric pressure matrix-assisted laser desorption/ionization ion trap mass spectrometry.

A quantitative method was developed for analysis of lysergic acid diethylamide (LSD) in urine using atmospheric pressure matrix-assisted laser desorption/ionization ion trap mass spectrometry (AP MALDI-ITMS). Following solid-phase extraction of LSD from urine samples, extracts were analyzed by AP MALDI-ITMS. The identity of LSD was confirmed by fragmentation of the [M + H](+) ion using tandem mass spectrometry. The quantification of LSD was achieved using stable-isotope-labeled LSD (LSD-d(3)) as the internal standard. The [M + H](+) ion fragmented to produce a dominant fragment ion, which was used for a selected reaction monitoring (SRM) method for quantitative analysis of LSD. SRM was compared with selected ion monitoring and produced a wider linear range and lower limit of quantification. For SRM analysis of samples of LSD spiked in urine, the calibration curve was linear in the range of 1-100 ng/mL with a coefficient of determination, r(2), of 0.9917. This assay was used to determine LSD in urine samples and the AP MALDI-MS results were comparable to the HPLC/ ESI-MS results.

Atmospheric Pressure↗
PubMed1975

The effects of lysergic acid diethylamide on the response to field stimulation of the rat vas deferens and the rat and cat anococcygeus muscles.

1. The effect of lysergic acid diethylamid (LSD) on the response to field stimulation in vitro of the rat vas deferens and anococcygeus muscle was examined. 2. LSD in concentrations from 10(-9) to 10(-6) M caused an increase in tone or rhythmic activity in both tissues, effects identical to those produced by guanethidine or tyramine. The motor effects of all three drugs were abolished by phentolamine 2 x 10(-6) M. Methysergide 2 x 10(-7) M given before LSD reduced the motor effect but was ineffective once the LSD contraction had developed. 3. LSD 10(-9) to 10(-6) M reduced and eventually abolished the response to motor adrenergic nerve stimulation in the anococcygeus muscle with no effect on the response to noradrenaline (NA) and no evidence of differential sensitivity according to the number of stimulating pulses. In the vas deferens LSD abolished the initial twitch component with no effect on the secondary slow contraction. LSD had no effect on the response to inhibitory nerve stimulation in the anococcygeus. 4. These results suggest that in the anococcygeus LSD closely resembles guanethidine in its effects as an adrenergic neurone blocking drug with indirect sympathomimetic actions. In the vas deferens these properties would explain the block of the initial twitch component in the motor response to field stimulation and the increase in rhythmic activity but do not explain the resistance of the secondary slow component of the motor response.

Animals↗
PubMed1983

Heat shock protein in mammalian brain and other organs after a physiologically relevant increase in body temperature induced by D-lysergic acid diethylamide.

A physiologically relevant increase in body temperature from 39.7 to 42.5 degrees C, which was generated after the intravenous injection of D-lysergic acid diethylamide (LSD), caused the induction of synthesis of a 74,000-dalton heat shock protein in the brain, heart, and kidney of the young adult rabbit. A marked increase in the relative labeling of a 74,000-dalton protein was noted after analysis of both in vivo labeled proteins and cell-free translation products of isolated polysomes. A temporal decrease in the synthesis of this protein was noted as LSD-induced hyperthermia subsided. The 74,000-dalton protein, which is induced in various organs of the intact animal at a body temperature similar to that attained during fever reactions, may play a role in homeostatic control mechanisms.

Animals↗
PubMedDate not supplied

Clinical pharmacology of lysergic acid diethylamide: case reports and review of the treatment of intoxication.

Intoxication and overdose are common presenting complaints to the emergency department. Acute intoxication with lysergic acid diethylamide (LSD) has become a relatively rare event, especially when compared with the incidence of ethanol and cocaine intoxication. We recently had an outbreak of presumed LSD intoxications occurring over one weekend. All patients had attended a performance by the musical group The Grateful Dead. At present, LSD intoxication or overdose can only be suspected based on clinical findings because there are no readily available rapid laboratory tests for detecting either the parent compound or the metabolites of the drug. The clinical findings and outcomes of five patients with suspected LSD intoxication are presented. The pharmacological effects of LSD and treatment modalities of intoxication are reviewed. All patients were treated conservatively based on clinical signs and symptoms. Only one patient required hospital admission for combative behavior that was initially refractory to pharmacological restraint.

Adult↗
PubMed1992

Determination of lysergic acid diethylamide (LSD), iso-LSD, and N-demethyl-LSD in body fluids by gas chromatography/tandem mass spectrometry.

Procedures for detection and quantitation of lysergic acid diethylamide (LSD), iso-LSD, and N-demethyl-LSD by capillary chromatography/tandem mass spectrometry (GC/MS/MS) are presented. Several methods for derivatization, sample introduction, and ionization, in combination with mass spectrometry/mass spectrometry (MS/MS), have been evaluated for overall ionization efficiency and product-ion sensitivity and specificity. Fragmentation pathways derived from low-energy collision-induced dissociation (CID) spectra of protonated LSD, and the protonated trimethylsllyl derivatives of LSD (LSD-TMS) and deuterium-labeled analogs of LSD, have been proposed. Principal dissociations primarily involve the amide and piperidine-ring moieties in which losses of CH3 radical, CH3NH2, CH3NCH2, diethylamine, diethylformamide, and N,N-diethylpropenamide from MH+ are observed. Positive-ion ammonia chemical ionization and subsequent MS/MS analysis of the protonated molecules (MH+) of the trimethylsilyl (TMS) derivatives of LSD, iso-LSD, and N-demethyl-LSD provide a high degree of specificity for identification of these compounds in urine or blood at low-pg/mL concentrations. Negative-ion chemical ionization and GC/MS/MS analysis of the molecular anion (M-) of the trifluoroacetyl (TFA) derivative is well suited for trace-level identification of N-demethyl-LSD, a metabolite of LSD.

Body Fluids↗
PubMed1984

Differences in d-[3H]lysergic acid diethylamide binding in mouse cortex and hippocampus in vivo and in vitro revealed by radioautography and rapid filtration studies.

The localization of d-[3H]lysergic acid diethylamide ([3H]LSD) binding sites in mouse brain was compared in vivo and in vitro. Radioautography of brain sections incubated with 6 nM [3H]LSD in vitro revealed substantial specific binding in cortex (CTX), especially in layers III to IV and anterior cingulate gyrus, and in areas CA1 and dentate gyrus of hippocampus (HIP). In sections of brains from mice that received 100 nmol of [3H]LSD per kg and were killed 10, 15 or 30 min later, specific [3H]LSD binding in CTX had a pattern of distribution similar to that observed in vitro. In contrast, the pattern of specific [3H]LSD binding in HIP in vivo differed from the results obtained in vitro, in that it was sparse and lacked differential subregional distribution. The low specific [3H]LSD binding in vivo in HIP but not in CTX was confirmed by homogenate filtration studies of brain areas from mice that received 100 nmol of [3H]LSD per kg. The levels of free [3H]LSD, obtained after correction for time-dependent metabolism of [3H]LSD, did not vary among regions, but [3H]LSD specifically bound in HIP was 30 to 50% of that in CTX. In contrast, steady-state binding studies in vitro in membrane preparations from CTX and HIP demonstrated a similar density and affinity of [3H]LSD binding sites in the two regions. Comparison of [3H]LSD binding characteristics in vivo and in vitro suggests possible mechanisms causing the lower specific binding in HIP in vivo, including modulation of the binding sites that differ in CTX and HIP.

Animals↗
PubMed2003

Determination of lysergic acid diethylamide (LSD) in mouse blood by capillary electrophoresis/ fluorescence spectroscopy with sweeping techniques in micellar electrokinetic chromatography.

The separation and on-line concentration of lysergic acid diethylamide (LSD) in mouse blood was achieved by means of capillary electrophoresis/fluorescence spectroscopy using sodium dodecyl sulfate (SDS) as the surfactant. Techniques involving on-line sample concentration, including sweeping micellar electrokinetic chromatography (sweeping-MEKC) and cation-selective exhaustive injection-sweep-micellar electrokinetic chromatography (CSEI-sweep-MEKC) were applied; the optimum on-line concentration and separation conditions were determined. In the analysis of an actual sample, LSD was found in a blood sample from a test mouse (0.1 mg LSD fed to a 20 g mouse; approximately 1/10 to the value of LD(50)). As a result, 120 and 30 ng/mL of LSD was detected at 20 and 60 min, respectively, after ingestion of the doses.

Animals↗
PubMed1999

Detection of metabolites of lysergic acid diethylamide (LSD) in human urine specimens: 2-oxo-3-hydroxy-LSD, a prevalent metabolite of LSD.

Seventy-four urine specimens previously found to contain lysergic acid diethylamide (LSD) by gas chromatography-mass spectrometry (GC-MS) were analyzed by a new procedure for the LSD metabolite 2-oxo-3-hydroxy-LSD (O-H-LSD) using a Finnigan LC-MS-MS system. This procedure proved to be less complex, shorter to perform and provides cleaner chromatographic characteristics than the method currently utilized by the Navy Drug Screening Laboratories for the extraction of LSD from urine by GC-MS. All of the specimens used in the study screened positive for LSD by radioimmunoassay (Roche Abuscreen). Analysis by GC-MS revealed detectable amounts of LSD in all of the specimens. In addition, isolysergic diethylamide (iso-LSD), a byproduct of LSD synthesis, was quantitated in 64 of the specimens. Utilizing the new LC-MS-MS method, low levels of N-desmethyl-LSD (nor-LSD), another identified LSD metabolite, were detected in some of the specimens. However, all 74 specimens contained O-H-LSD at significantly higher concentrations than LSD, iso-LSD, or nor-LSD alone. The O-H-LSD concentration ranged from 732 to 112 831 pg/ml (mean, 16340 pg/ml) by quantification with an internal standard. The ratio of O-H-LSD to LSD ranged from 1.1 to 778.1 (mean, 42.9). The presence of O-H-LSD at substantially higher concentrations than LSD suggests that the analysis for O-H-LSD as the target analyte by employing LC-MS-MS will provide a much longer window of detection for the use of LSD than the analysis of the parent compound, LSD.

Chromatography, Liquid↗
PubMed1998

Analysis of lysergic acid diethylamide: comparison of capillary electrophoresis with laser-induced fluorescence (CE-LIF) with conventional techniques.

The increasing use of the potent hallucinogenic drug D-lysergic acid diethylamide (LSD) makes the application of highly sensitive analytical techniques necessary. For an effective analysis of biological specimens a limit of detection in the sub-ng/ml range is required. Using capillary electrophoresis (CE), with laser-induced fluorescence detection it was possible to determine 0.1-0.2 ng LSD/ml blood. The conventionally used immunoassays and gas and high-performance liquid chromatographic methods have cut-off values and limit of detection, respectively, in the same range. Only tandem mass spectrometry techniques can be more sensitive. Therefore, CE can be considered a good complementary method to conventional immunological and chromatographic techniques for the forensic analysis of biofluids.

Blood Chemical Analysis↗
PubMed1998

Lysergic acid diethylamide (LSD) is a partial agonist of D2 dopaminergic receptors and it potentiates dopamine-mediated prolactin secretion in lactotrophs in vitro.

The hallucinogenic effects of lysergic acid diethylamide (LSD) have mainly been attributed to the interaction of this drug with the serotoninergic system, but it seems more likely that they are the result of the complex interactions of the drug with both the serotoninergic and dopaminergic systems. The aim of the present study was to investigate the functional actions of LSD at dopaminergic receptors using prolactin secretion by primary cultures of rat pituitary cells as a model. LSD produced a dose-dependent inhibition of prolactin secretion in vitro with an IC50 at 1.7x10(-9) M. This action was antagonized by spiperone but not by SKF83566 or cyproheptadine, which indicates that LSD has a specific effect on D2 dopaminergic receptors. The maximum inhibition of prolactin secretion achieved by LSD was lower than that by dopamine (60% versus 80%). Moreover, the fact that LSD at 10(-8)-10(-6) M antagonized the inhibitory effect of dopamine (10(-7) M) and bromocriptine (10(-11) M) suggests that LSD acts as a partial agonist at D2 receptors on lactotrophs in vitro. Interestingly, LSD at 10(-13)-10(-10) M, the concentrations which are 10-1000-fold lower than those required to induce direct inhibition on pituitary prolactin secretion, potentiated the dopamine (10(-10)-2.5x10(-9) M)-mediated prolactin secretion by pituitary cells in vitro. These results suggest that LSD not only interacts with dopaminergic receptors but also has a unique capacity for modulating dopaminergic transmission. These findings may offer new insights into the hallucinogenic effect of LSD.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1982

Lysergic acid diethylamide (LSD) and lisuride: differentiation of their neuropharmacological actions.

The nonhallucinogenic ergot derivative lisuride exerts many pharmacological effects that are similar to those of its hallucinogenic congener, lysergic acid diethylamide (LSD). Animals trained to discriminate between the presence of one drug and the other can be used to differentiate the actions of these compounds on a neuronal level. The discriminative stimulus effect of LSD (the LSD cue) is similar to that of the serotonin agonist quipazine, whereas the lisuride cue is similar to that of the dopamine agonist apomorphine. These data support the hypothesis that serotonin is intricately involved in the hallucinogenic effects of LSD.

Animals↗