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Hollister LE, Moore F. 
“Urinary catecholamine excretion following lysergic acid diethylamide in man”. 
Psychopharmcologia. 1967;11:270-5.
Lysergic acid diethylamide (LSD) evokes symptoms and signs of sympathetic stimulation. Prominent clinical phenomena from the drug include feelings of anxiety and tension, blurred vision, dilated pupils, tremors, nausea and increased deep tendon reflexes. (Hollister and Sjorber, 1964). Some have considered LSD a phenylethylamine derivate capable of stimulating central adrenergic sites (Brodie, 1958). Thus LSD might be excepted to release catecholamines as part of its action. Previous data in humans on this point have been somewhat confusing. One study found no change in plasma concentration of epinephrine and norepinephrine following 50 mcg oral doses of LSD (Liddell and Weilmalherbe, 1953). Such doses are rather small and technical advances in measurement have accurred over the past decade. Another study of mental patients given 40 to 60 mcg doses of LSD intraveneously described an initial rise in plasma epinephrine followed by a fall below the starting level and then a late rise (Manger et al, 1956). Fragmentary data from psychiatric patients given 150 to 300 mcg orally indicated that those patients who developed a psychiatric reaction to the drugs tended to show a constant increase in epinephrine excretion with a variable effect on norepinephrine (Elmadjian et al, 1958). Two experiments were conducted in the present study, one comparing the effects of LSD and epinephrine in the same subjects following a control period, the other comparing a separate control period with a similar period during which LSD was given.
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