EMESIS INDUCED BY INTRACEREBROVENTRICULAR INJECTIONS OF APOMORPHINE AND DESLANOSIDE IN NORMAL AND CHEMORECEPTIVE TRIGGER ZONE ABLATED DOGS

¹ Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, N. Y.

Emetic responses were determined by the administration of apomorphine or digitalis glycosides into the lateral, third and fourth ventricles of chronically cannulated dogs. For apomorphine, the estimated emetic ED50 was significantly (P < .05) largest for the lateral, smaller for the third, and smallest for the fourth ventricle site of administration. The mean emetic latency was also significantly less (P < .05) for the latter route. Furthermore, chronic CT zone ablation rendered animals refractory to doses up to 10,000 times the ED50 of intraventricular apomorphine. For deslanoside, the estimated emetic ED50 was determined and found to be approximately 35 times less than the intravenous ED50 for a similar glycoside, lanatoside C. A lack of dose-relationship between the various sites of intraventricular administration, unlike apomorphine, was observed. With the lower doses of deslanoside employed, it was observed that, similar to apomorphine, the range and mean latencies for emesis were largest for the lateral, smaller for the third and smallest for the fourth ventricle injections. Furthermore, chronic CT zone ablation also rendered animals refractory to almost 4 times the emetic ED50 for intraventricular deslanoside.

From these results it was concluded that both apomorphine and digitalis glycosides directly activate the CT zone to induce emesis. Furthermore, there appear to be no sensitive emetic receptor sites for these drugs in other ventricular ependymal linings.