Copper Sulphate Emesis: A Study of Afferent Pathways from the Gastrointestinal Tract

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Abstract
The emetic threshold of intragastric CuSO4 was 40 mg. for 11 normal dogs. In causing emesis, CuSO4 has a central as well as peripheral effect. Interruption of the vagi has a profound effect on the threshold and latency of vomiting while sympathectomy causes no discernible change; however, both pathways transmit impulses from the peripheral emetic receptors. In animals with both abdominal sympathectomy and vagotomy, the threshold to CUSO4 was increased 8-fold, but its latency was greatly prolonged. There was no evidence that interference in the cardiac sphincter caused this phenomenon. The residual delayed response to intragastric CUSO4 was not eliminated by sectioning the intrinsic vagal fibers in the esophageal wall or interrupting the sacral innervation to the large bowel. The remaining possibility is that Cu is absorbed and acts as a central emetic to produce the delayed emesis. Ablation of a central "trigger" zone in addition to gut denervation totally eliminates the emetic response to a lethal dose of intragastric CUSO4.

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