Studies on the Emetic and Anti-Emetic Actions of Ergotamine

Abstract

Eggleston and Hatcher 1 showed that intravenous doses of 60.0 mg. of fluid extract of ergot (in terms of the dry drug) produced prompt emesis in the dog, whereas oral administration of even massive doses failed. Eviscerated dogs also showed emesis following intravenous doses. The authors concluded that ergot has a central emetic action. Hatcher and Weiss 2 apparently rejected this supposition, stating “that ergotoxin has no perceptible effect directly on the vomiting center, and that any inhibition by it of the emetic action of substances used in these experiments, must be due to its causing depression of some peripheral structure.”

These authors found that massive doses of ergotoxine prevented the emetic action of apomorphine, aconitin, digitalis, and pilocarpine by systemic administration, but not of large oral doses of mercuric chloride and tartar emetic. They concluded that the anti-emetic activity of ergotoxine is due to its depression of afferent sympathetic nerve ends.

Koppanyi 3 found a close parallelism to Hatcher and Weiss' results. His dogs, whose medullary vomiting centre was removed by ablation or depressed by local application of morphine, also failed to vomit following systemic administration of apomorphine, pilocarpine, digitalis, but vomited upon oral administration of tartar emetic, copper and zinc sulphate, and mercuric chloride.

The following experiments were performed to correlate the above findings. Doses are given in mg. × kilogram body weight. In dogs the intravenous administration of small doses (0.02-0.2 mg.) of ergotamine tartrate elicit repeated retching and vomiting, but large doses (0.5 mg. or higher) fail to produce retching or vomiting. In cats the minimum emetic doses are somewhat lower than in dogs (0.01-0.02 mg.) and doses of 0.3 mg. or higher fail to produce emesis.