Abstract

The emetic action of nicotine and lobeline was studied in cats and dogs. The minimum uniformly effective emetic doses were found to be 1.5 mgm./kgm. of i.m. nicotine bitartrate and 0.5 mgm./kgm. of i.m. lobeline sulfate for both species. In terms of alkaloid base, the emetic dose-response curves of the two drugs are almost identical. Sixty-eight cats and 17 dogs were used to establish the locus of emetic action of the alkaloids. In dogs, ablation of the medullary emetic chemoreceptor trigger zone (CT zone) sufficed for protection against the emetic effect of nicotine and lobeline. In cats, however, it was found that the alkaloids act at a peripheral locus as well as at the CT zone. Thus, in order to eliminate the vomiting response in cats, it became necessary to perform the combined procedures of spinal deafferentation, midcervical vagotomy, and CT-zone ablation. This combination was accomplished either by interrupting peripheral nerves directly, along with ablating the CT zone, or by making a broad medullary lesion which appeared to destroy concomitantly both the CT zone and centripetal emetic pathways. Antiemetic drug studies demonstrated that tetraethylammonium (TEA) was effective in preventing emesis in response to nicotine in both cats and dogs, but it was not effective against lobeline in dogs. Hexamethonium (C6) protected both species against nicotine and lobeline. Neither atropine nor chlorpromazine prevented the vomiting response.