Abstract

Dhawan et al. (1961) reported that d-lysergic acid diethylamide (LSD-25) was one of the most effective antagonists of apornorphine-induced pecking in pigeons (Dhawan and Saxena, 1960a). It was further seen that many drugs influenced the pecking (in pigeon) and emetic (in dog and cat) responses to apomorphine in an identical manner. Since no reports regarding the effects of LSD-25 on apomorphine-induced emesis were available, we decided to investigate this problem. In addition, we undertook (a) to determine whether the structurally related compound 2 d-bromolysergic acid diethylamide (BOL-180), which is devoid of central nervous system stimu-lant properties (Rothlin, 1957), had a similar effect and (b) to elucidate the site of antiemetic effect of LSD-25 by studying its interaction with emetic agents acting at various sites. METHODS. These results were obtained in 56 mongrel dogs of either sex. The dogs were used twice a week. They were fed and, after about 30 minutes, a dose of LSD-25 or BOL-1802 was given. Fifteen minutes after this they were given one of the following emetic agents: apomorphine hydro-chloride, 50 per kg (100 % emetic dose in 26 dogs); emetine hydrochloride, 3.0 mg per kg (Hatcher and Weiss, 1923); Hydergine, 30 /hg per kg (Wang and Glaviano, 1954); ouabain, 50 g per kg (Hatcher and Weiss, 1923); morphine hydrochloride, 1.0mg per kg (Wang and Glaviano, 1953) and protoveratrine, 10 ig per kg (100% emetic dose in 16 trials). All the agents were given intravenously except morphine which was given intramuscularly (Wang and Glaviano, 1954). All the dosage levels chosen represent the 100% effective emetic dose or greater. In all tests the dogs were observed for at least 1 hour after they ‘Presented in part at the annual meeting of the Association of Physiologists and Pharma-