Noxious stimulation of emesis

Abstract

This review will focus on the mechanisms of emesis initiated or inhibited from receptors located in the periphery or activated by a peripherally released humoral factor. Excitatory and inhibitory receptors have been found in the thorax. Nausea and vomiting sometimes occur after coronary artery occlusion or with vasovagal syncope, and the receptors of this emetic response are probably tension receptors of the left ventricle. The thorax is also source of antiemetic receptors. Vagal section above the level of the heart causes an intractable vomiting syndrome and central cervical vagal stimulation inhibits vomiting. In addition, respiratory maneuvers that decrease activation of pulmonary afferents enhance the sensitivity to motion sickness. Therefore, pulmonary vagal afferent fibers may tonically inhibit retching and vomiting. Abdominal stimulation by irritants or toxins can activate nausea and vomiting through mechano- or chemoreceptors. Mechanoreceptors have been found in the stomach, jejunum and ileum, but the location of these receptors in the gut wall or the type of mechanical stimuli most effective in exciting these receptors is unknown. The chemoreceptors have a similar distribution and are probably located in the mucosa and respond to a variety of noxious agents, eg, CuSO4. CuSO4-induced vomiting is mediated by peripheral 5-HT4 receptors. Two clinically relevant toxic stimuli, x-irradiation and chemotherapeutic agents, have been found to activate vomiting through 5-HT3 receptors in the digestive tract. Regardless of the stimulus, the afferent neural pathways mediating emesis from the abdomen may be the same. The noxious stimulus may cause release of serotonin from enterochromaffin cells of the digestive tract, which activates visceral afferents. The vagus nerves mediate responses from the stomach and proximal small intestine and the splanchnic nerves and spinal cord mediate responses from the entire small intestine. Emesis-related afferents from the periphery terminate primarily in the nucleus tractus solitarius and area postrema. The area postrema contains the chemoreceptive trigger zone that can be activated by endogenous agents released into the circulation from the periphery. The role of peripheral receptors or peripherally released agents in the etiology of cyclic vomiting is unknown, but multiple pathways have been identified that can form a brain-gut interaction to provide a possible mechanism of cyclic vomiting.