THE MECHANISM OF THE EMETIC ACTION OF SODIUM SALICYLATE

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Abstract
In the dog, the emetic ED50 for sodium salicylate was 256 ± 113 mg/kg for the intravenous route with a mean latency of 10.4 ± 3.96 min, and for the oral route 228 ± 68 mg/kg with a mean latency of 18.2 ± 2.63 min. Values are means with standard errors. Ablation of the emetic chemoreceptor trigger‐zone gave complete protection against the emetic action of 300 mg of sodium salicylate intravenously but only partial protection against the emetic action of the same dose of sodium salicylate orally. Either the intravenous salicylate acted on the trigger‐zone or ablation of the trigger‐zone interfered with afferent nerves from peripheral receptors responding to intravenous salicylate and which were different from the receptors responding to oral salicylate. After supradiaphragmatic vagotomy, there was equal protection against intravenous and oral salicylate. Two explanations can be advanced. First, the receptors responding to intravenous and those responding to oral salicylate have a common path in the vagus nerves; or second, afferent fibres in the vagus nerve normally maintain the vomiting centre in a reactive state. When these fibres are cut any other afferent fibres become less effective in evoking vomiting. Spinal transection gave partial and spinal transection with vagotomy gave complete protection. It is concluded that further work is necessary to decide which of the two explanations obtained.