Receptors on the floor of the fourth ventricle of the brain represent a chemoreceptor trigger zone, known as the area postrema, stimulation of which can lead to vomiting. The area postrema is a circumventricular organ and as such lies outside the blood-brain barrier; it can therefore be stimulated by blood-borne drugs that can stimulate vomiting or inhibit it.
There are various sources of input to the vomiting center:
- The chemoreceptor trigger zone at the base of the fourth ventricle has numerous dopamine D2 receptors, serotonin 5-HT3 receptors, opioid receptors, acetylcholine receptors, and receptors for substance P. Stimulation of different receptors are involved in different pathways leading to emesis, in the final common pathway substance P appears to be involved.
- The vestibular system which sends information to the brain via cranial nerve VIII (vestibulocochlear nerve). It plays a major role in motion sickness and is rich in muscarinic receptors and histamine H1 receptors.
- Cranial nerve X (vagus nerve), which is activated when the pharynx is irritated, leading to a gag reflex.
- Vagal and enteric nervous system inputs that transmit information regarding the state of the gastrointestinal system. Irritation of the GI mucosa by chemotherapy, radiation, distention, or acute infectious gastroenteritis activates the 5-HT3 receptors of these inputs.
- The CNS mediates vomiting arising from psychiatric disorders and stress from higher brain centers.
The vomiting act encompasses three types of outputs initiated by the chemoreceptor trigger zone: Motor, parasympathetic nervous system (PNS), and sympathetic nervous system (SNS). They are as follows:
- Increased salivation to protect the enamel of teeth from stomach acids (excessive vomiting leads to dental erosion). This is part of the PNS output.
- A deep breath is taken to avoid aspiration of vomit.
- Retroperistalsis, starting from the middle of the small intestine, sweeping up the contents of the digestive tract into the stomach, through the relaxed pyloric sphincter.
- A lowering of intrathoracic pressure (by inspiration against a closed glottis), coupled with an increase in abdominal pressure as the abdominal muscles contract, propels stomach contents into the esophagus as the lower esophageal sphincter relaxes. The stomach itself does not contract in the process of vomiting except for at the angular notch, nor is there any retroperistalsis in the esophagus.
- Vomiting is ordinarily preceded by retching.
- Vomiting also initiates an SNS response causing both sweating and increased heart rate.
The neurotransmitters that regulate vomiting are poorly understood, but inhibitors of dopamine, histamine, and serotonin are all used to suppress vomiting, suggesting that these play a role in the initiation or maintenance of a vomiting cycle. Vasopressin and neurokinin may also participate.
The vomiting act has two phases. In the retching phase, the abdominal muscles undergo a few rounds of coordinated contractions together with the diaphragm and the muscles used in respiratory inspiration. For this reason, an individual may confuse this phase with an episode of violent hiccups. In this retching phase nothing has yet been expelled. In the next phase, also termed the expulsive phase, intense pressure is formed in the stomach brought about by enormous shifts in both the diaphragm and the abdomen. These shifts are, in essence, vigorous contractions of these muscles that last for extended periods of time - much longer than a normal period of muscular contraction. The pressure is then suddenly released when the upper esophageal sphincter relaxes resulting in the expulsion of gastric contents. For people not in the habit of exercising the abdominal muscles, they may be painful for the next few days. The relief of pressure and the release of endorphins into the bloodstream after the expulsion causes the vomiter to feel better.
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