Vomiting in cats

Question 1

How can you summarize the pathophysiological mechanisms and neurohormonal control of vomiting in cats

Answer 1

The vomiting centre in the brainstem can be stimulated by:
- toxins via the CRTZ
- abdominal viscera (e.g., distension, inflammation) via vagosympathetic stimulation
- cerebral cortex and limbic system (e.g., stress; fear, raised intracranial pressure)
- vestibular disease, otitis interna via the vestibular apparatus of inner ear

Question 2

Explain why apomorphine (a D2 agonist) is a poor inducer of vomiting in cats

Answer 2

D2 receptors are of relatively low importance in cats, and consequently the lack of effect of apomorphine to induce emesis and the limited value of anti-emetics such as metoclopramide (D2 antagonist)

Question 3

What is the main neurohormonal mediator implicated in motion sickness

Answer 3

Acetylcholine stimulation of M1 receptors in the vestibular apparatus has been demonstrated to be of importance in motion sickness
- thus mixed M1 and M2 antagonists such as atropine or pure M1 antagonists such as pirenzepine have been shown to be effective anti-emetics for this type of vomiting in cats
- conversely, there is evidence that the H1 receptors have relatively little importance in feline motion sickness