Vagus nerves

In the gastrointestinal tract, drugs or toxins, as well as mechanical stimulation, induce emesis by activation of sensory receptors on afferent neurons in the vagus and sympathetic nerves. Information is relayed to the vomiting centre via the nucleus tractus solitarius... 

The most widely used emetic is syrup of ipecac, containing the alkaloids, emetine and cq haeline. Emetine induces vomiting by activation of sensory neurons in the vagus and sympathetic nerves to the stomach and centrally in the medulla, possibly at the CTZ. The release of serotonin and SP may be involved as 5-HT3 and NKi receptor antagonists prevent emesis induced... 

Vagus nerve stimulation (VNS) may be used for adult patients with treatment-resistant depression. A pulse generator is surgically implanted under the skin of the left chest, and an electrical lead connects the generator to the left vagus nerve. Stimulation of this nerve sends signals to the brain. This therapy is intended to be used along with traditional therapies, such as pharmacotherapy and ECT.20... 

Parasympathetic stimulation decreases heart rate. Acetylcholine, the neurotransmitter released from the vagus nerve (the parasympathetic nerve to the heart), binds to muscarinic receptors and causes the following effects ... 

The effects of the autonomic nervous system on MAP are summarized in Figure 15.4. The parasympathetic system innervates the SA node and the AV node of the heart. The major cardiovascular effect of parasympathetic stimulation, by way of the vagus nerves, is to decrease HR, which decreases CO and MAP. 

Pulmonary stretch receptors are responsible for initiating the Hering-Breuer reflex. These stretch receptors are located within the smooth muscle of large and small airways. They are stimulated when the tidal volume exceeds 1 1. Nerve impulses are transmitted by the vagus nerve to the medullary respiratory center and inhibit the inspiratory neurons. The primary function of these receptors and the Hering-Breuer reflex is to prevent overinflation of the lungs. 

The major gastric factor that affects motility and the rate of emptying is the volume of chyme in the stomach. As the volume of chyme increases, the wall of the stomach becomes distended and mechanoreceptors are stimulated. This elicits reflexes that enhance gastric motility by way of the intrinsic and vagus nerves. The release of the hormone gastrin from the antral region of the stomach further contributes to enhanced motility. 

As the volume of the chyme in the duodenum increases, it causes distension of the duodenal wall and stimulation of mechanoreceptors. This receptor stimulation elicits reflex inhibition of gastric motility mediated through the intrinsic and vagus nerves. Distension also causes release of gastric inhibitory peptide from the duodenum, which contributes to inhibition of gastric contractions. 

The gastric phase is elicited by the presence of food in the stomach. Distension of the stomach wall, as well as the presence of protein, caffeine, and alcohol, enhances gastric secretion. This phase is mediated by the intrinsic nerves, the vagus nerve, and gastrin. Each of these mechanisms promotes secretion of HC1 and pepsinogen. 

The return of the bile salts to the liver from the small intestine is the most potent stimulus of bile secretion. In fact, these bile salts may cycle two to five times during each meal. The intestinal hormone secretin, which is released in response to acid in the duodenum, enhances aqueous alkaline secretion by the liver. Secretin has no effect on the secretion of bile salts. During the cephalic phase of digestion, before food even reaches the stomach or intestine, parasympathetic stimulation, by way of the vagus nerve, promotes bile secretion from the liver. 

As with gastric secretion, nervous stimulation and hormones regulate secretion from the pancreas. During the cephalic phase and gastric phase, the pancreas secretes a low-volume, enzyme-rich fluid mediated by the vagus nerve. 

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