lysergic acid/fever

In free moving rats trained to press a bar to escape from radiant heat, lysergic acid diethylamide (LSD, 8-16 micrograms) produced a significant and dose-dependent increase of the bar-pressing rate when injected intraperitoneally. During the increase in the bar-pressing rate, the rectal temperature

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

Eight patients were seen within 15 min of intranasal self-administration of large amounts of pure D-lysergic acid diethylamide (LSD) tartrate powder. Emesis and collapse occurred along with sign of sympathetic overactivity, hyperthermia, coma, and respiratory arrest. Mild generalized bleeding

In pigs, the serotonin-2 (5-HT2) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), 0.8 mg/kg, induced "psychotic" behaviour (e.g., grimacing, backward locomotion, blank stare) and a muscular syndrome, which is known as malignant hyperthermia (MH) in pigs and humans. This syndrome

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

Eight patients were seen within 15 minutes of intranasal self-administration of large amounts of pure D-lysergic acid diethylamide (LSD) tartrate powder. Emesis and collapse occurred along with signs of sympathetic overactivity, hyperthermia, coma and respiratory arrest. Mild generalized bleeding

Intravenous administration of bacterial endotoxins in dogs is followed within 2 hours by the appearance of a fever-producing substance in the blood. This endogenous pyrogen differs from the endotoxins originally administered by its ability to produce fever in tolerant recipients and failure to

An initiating cell-free protein synthesis system derived from brain was utilized to demonstrate that the intravenous injection of d-lysergic acid diethylamide (LSD) to rabbits induced a transient inhibition of translation following a brief stimulatory period. Subfractionation of the brain cell-free

A detailed pathological description of the muscle findings in a case of the neuroleptic malignant syndrome (NMS) following ingestion of lysergic acid diethylamide (LSD) is given, including the first ultrastructural analysis. Focal necrosis, oedema, and hypercontraction of fibres with glycogen and

Hyperthermia (temperature of at least 40.5 degrees C for at least one hour) associated with drug intoxication was identified in 12 patients over a 5-yr period. Intoxication was due to anticholinergic drugs (tricyclic antidepressants, antipsychotics, antihistamines), CNS stimulants (phencyclidine,

The intravenous administration of LSD to young adult rabbits resulted in the disaggregation of both free and membrane-bound classes of brain polysomes. Based on the analysis of LSD dosage and the time course of the LSD-induced brain polysome shift, it was found that free polysomes were more

Free and membrane-bound polysomes and polyadenylated mRNA isolated from rabbit brain were translated in an mRNA-dependent rabbit reticulocyte lysate system. Electrophoretic analysis of the cell-free translation products demonstrated that although most of the nascent proteins were common to both free

Rabbits treated with LSD 25 exhibit characteristic signs of hyper-excitability, increased peripheral sympathetic activity, and hyperthermia. When the rabbits received prior treatment with DL-(alpha)-methyl-p-tyrosine, the excitation and sympathetic actions of LSD 25 were abolished or attenuated, but