Emesis is composed of 3 independent digestive tract correlates that are individually organized by a brainstem neural network and all 3 hierarchically organized by a central pattern generator. The central pattern generator may be in the Bötzinger nucleus of the brain stem. The digestive tract sensory mechanisms that activate vomiting are the digestive tract mucosa or chemoreceptive trigger zone of the area postrema. Regardless of the initial stimulus, the area postrema may be activated in order to inhibit orthograde digestive tract motility and reflux blocking reflexes that would interfere with anterograde movement, which is the basic purpose of vomiting. The digestive tract correlates are (1) relaxation of the upper stomach and contraction of the lower pharynx, (2) retrograde giant contraction, and (3) the pharyngo-esophageal responses during retching and vomitus expulsion. The proximal gastric response allows gastroesophageal reflux, the lower pharyngeal response prevents supra-esophageal reflux, and both last the duration of the vomit process. The retrograde giant contraction empties the proximal digestive tract of noxious agents and supplies the stomach with fluids to neutralize the gastric acid which protect the esophagus from damage during expulsion. The retch mixes the gastric contents with acid neutralizer and gives momentum to the expelled bolus. During vomitus expulsion the esophagus is maximally stretched longitudinally which stiffens its wall to allow rapid transport as the suprahyoid muscles and diaphragmatic dome contract, and the hiatal fibers relax.

BACKGROUND/AIMS: The role of the enteric (ENS) and central (CNS) nervous systems in the control of the retrograde giant contraction (RGC) associated with vomiting is unknown. METHODS: The effects of myotomy or mesenteric nerve transection (MNT) on apomorphine-induced emesis were investigated in 18 chronically instrumented dogs RESULTS: Neither surgery affected the RGC orad of the surgical site or the velocity of the RGC over the entire small intestine. Myotomy blocked the RGC for 17 ± 5 cm aborad of the myotomy, and the velocity of the RGC from 100 to 70 cm from the pylorus slowed (18.1 ± 3.0 to 9.0 ± 0.8 cm/sec) such that the RGC orad and aborad of the myotomy occurred simultaneously. After MNT, the RGC was unchanged up to 66 ± 6 cm from the pylorus, and the sequence of the RGC across the denervated intestine was unaltered. The velocity of the RGC from 100 to 70 cm from the pylorus increased from 12.8 ± 1.6 to 196 ± 116 cm/sec. After myotomy or MNT, the percent occurrence and magnitude of the RGC across the intestine 100 to 70 cm from the pylorus decreased. CONCLUSIONS: The CNS activates the RGC 10 to 20 cm aborad of its innervation of the intestine and controls the RGC sequence. On the other hand, the ENS plays a role in initiation and generation of the RGC.
Animals ; Central Nervous System ; Dogs ; Enteric Nervous System* ; Hand ; Intestine, Small ; Intestines ; Nervous System ; Pylorus ; Vomiting