Abstract

The mechanism of digitalis-induced emesis was investigated in unanesthetized cats chronically prepared with indwelling catheters and cannulas. Ouabain, dihydroouabain, deslanoside and strophanthidin were injected intravenously, intraportally, intravertebrally, intracarotidly, intraventricularly, and intracisternally. Vertebral arterial injection proved to be the most effective means of eliciting emesis, whereas injections into the lateral and fourth ventricles of the brain were ineffective. Intraportal injection of the glycosides was no more effective than intravenous, and strophanthidin was even less effective by the intraportal route. Pretreatment with the microsomal inhibitor SKF-525A did not influence emetic effectiveness or toxicity of the drugs. Vomiting was not elicitable by intravenous or intravertebral injection after ablation of the medullary emetic chemoreceptor trigger zone. The cardiotonic steroids were more toxic when injected intraventricularly than intracisternally, and the central toxicity of the glycosides was more severe than that of the genin. The data support the contention that digitalis-induced emesis is mediated by direct action upon the chemoreceptor trigger zone, but the receptor site can be reached only through the blood stream.