Printed in U.S.A. CENTRAL EMETIC ACTION AND TOXIC EFFECTS OF DIGITALIS IN CATS’2

The mechanism of digitalis-induced emesis has been extensively investigated (see Borison and Wang, 1953). Hatcher and Weiss (1922) and Dresbach and Waddell ( 1926) failed to elicit emesis in cats by topical application of cardiac glycosides to the floor of the fourth ventricle. On the other hand, it was shown by Dresbach (1947) that digitalis was capable of evoking emesis even after extensive chronic denervation of the abdominal viscera and heart. Borison and Wang (1951) abolished emesis to intravenously administered digitalis in dogs by ablation of the medullary emetic chemoreceptor trigger zone (CTZ). Borison (1952) extended this observa-tion to cats and demonstrated further that oral digitalis was just as effective in causing emesis after gut denervation as before, but that CTZ ablation reduced the incidence of vomiting. Thus, in spite of convincing evidence for a direct ac-tion of digitalis on the CTZ, two features of the emetic process required explanation, namely: 1) the reported failure of topical application to produce vomiting, and 2) the consistent de-lay in emetic response after intravenous ad-ministration. Recent experiments of Share et al. (1964) indicate that, in contrast to the in-effectiveness of local application, intracerebro-ventricular injection of deslanoside in dogs is an effective means of eliciting emesis. It is evident from the experiments presented herein, however, that cats respond differently from dogs. Indeed, Melville and Shister (1957) at no time observed vomiting in cats following lethal doses of lanatoside C, digoxin, and digitoxin in-jeeted into the lateral ventricle of the brain. Received for publication September 4, 1964.1This investigation was supported by NI