ABSTRACT
The mechanisms and mechanics of emesis (nausea, retching and vomiting) have been reviewed extensively.1,5 In summary, the autonomic (e.g. vagus nerve) and somatic (e.g. phrenic nerve) motor outputs are co-ordinated by brainstem nuclei (especially the parvicellular reticular formation, the Botzinger complex and the nucleus tractus solitarius), which affect gastric, cardiac, respiratory and other functions. The nuclei coordinating emesis have previously been referred to as the ‘vomiting centre’. While this is still a useful concept for modelling it is no longer thought to be represented by a single anatomical substrate. Emesis can be evoked or inhibited by drugs, which are assumed to act on pathways projecting to these areas (e.g. via opiate, histamine H1, cannabinoid receptors), but there are many parallel pathways that lead to these brainstem nuclei and hence, other ways of inducing retching and vomiting. This complexity means that to make a ‘universal’ anti-emetic drug that blocks emesis whatever the cause is exceedingly difficult. Nevertheless, preclinical studies have identified several potential approaches, including opioid receptor activation,6 5HT1A receptor antagonism7 but the most promising of which is NK1 receptor antago-
is currently under investigation but, irrespective of the outcome, the preclinical studies have illustrated that it is possible to make such agents.
