Drugs Used for Emesis Induction in Dogs

Vomiting is coordinated by the emetic center in the medulla oblongata of the brain stem, leading to an efflux of gastric and proximal duodenal content.³ The emetic center receives afferents from both the CNS and the periphery, particularly the GI tract and vestibular apparatus, but can also include viscera (eg, urinary and reproductive tracts).

The chemoreceptor trigger zone (CRTZ) is located in the medulla oblongata and contains dopamine 2 (D2), neurokinin-1 (NK-1), 5-hydroxytryptamine, acetylcholine, and histamine receptors that respond to substances circulating in the blood. Unlike dogs, cats have a significant number of alpha-2–adrenergic receptors in the CRTZ, making alpha-2–adrenergic agonists more likely to cause emesis.⁴ The forebrain can also provide input to the CRTZ in response to noxious stimuli (eg, pain, repulsive smells or sights).³

Peripheral input from the GI tract acts via NK-1 and serotonin receptors and transmits signals into the emetic center through vagal and other afferents.⁵ The vestibular system can also induce vomiting through histamine and acetylcholine receptors. Knowledge of these receptors is helpful when considering drugs that induce emesis in dogs and cats.

Complications associated with emesis induction can include aspiration pneumonia, ineffective recovery of ingested substances, sedation, and gastroesophageal intussusception (rare).⁶

Administration of an antiemetic (maropitant, 1 mg/kg IV or SC; metoclopramide, 0.4-0.6 mg/kg SC or 2 mg/kg/day IV CRI; ondansetron, 0.5-1 mg/kg IV) should be considered after successful emesis induction to prevent protracted nausea and/or retching.^7-9

Emetic drugs can act via peripheral or central mechanisms.

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