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Given the importance of clinical phenomena such as nausea, vomiting, and alterations in bowel and bladder function associated with anesthesia, it is surprising how little is understood about the third branch of the ANS. The enteric nervous system is the system of neurons and their supporting cells found within the walls of the gastrointestinal tract, including the neurons within the pancreas and gallbladder. [19] The history of this system is as rich as its innervation: Meissner (1829–1903) and Auerbach (1828–1897) first described the ganglionated plexus of the system; Dogiel (1852–1922) recognized and classified the unique morphologies of enteric neurons and correctly predicted that differences in shape would indicate differences in function; Bayliss (1860–1924) and Starling (1866–1927) showed the existence of polarized reflexes operating in the intestine independent of extrinsic influences; and John Langley defined the unusual features of the enteric nervous system and classified it as the "third division of the autonomic nervous system." The enteric nervous system contains as many nerve cells as the spinal cord. It is derived from neuroblasts of the neural crest that migrate to the gastrointestinal tract along the vagus nerve.
One major difference between the enteric nervous system and the sympathetic and parasympathetic branches of the ANS is its extraordinary degree of local autonomy. Digestion and peristalsis occur after spinal cord transection or during spinal anesthesia, although sphincter function may be impaired.
Although functionally discrete, the gut is influenced by sympathetic and parasympathetic activity. The sympathetic preganglionic fibers from T5 through L1 inhibit gut action; a spinal or epidural anesthetic to the midthoracic levels removes this inhibition, yielding a contracted small intestine that may afford superior surgical conditions in combination with the profound muscle relaxation of a spinal anesthetic.[20] The sphincters are relaxed, and peristalsis is normally active.
Norepinephrine within the gut is the transmitter of postganglionic sympathetic neurons to the gut. For example, if the contents of the upper intestine become overly acidic or hypertonic, an adrenergically mediated enterogastric reflex reduces the rate of gastric emptying. The adrenergic neurons, which run to the myenteric ganglia of the gastrointestinal tract from the thoracic and lumbar spinal segments, are usually inactive in the resting individual. Reflex pathways within and external to the alimentary tract cause discharge of these neurons. During abdominal surgery, when the viscera are handled, a reflex firing of the adrenergic inhibitory nerves inhibits the motor activity of the intestine for an extended period. This adrenergic inhibition is thought to be the basis of the common condition known as postoperative ileus. Loss of parasympathetic nervous control usually decreases bowel tone and peristalsis, but over time, the increased activity of the enteric plexus compensates for the loss. Spinal cord lesions may remove sacral parasympathetic input, but cranial parasympathetics may still be carried by the branches of the vagus nerve down to the end-organ ganglia; colonic dilation and fecal impaction (which may precipitate hypertension in autonomic dysreflexia) occur more often than small intestinal dysfunction.
Enteric neurons can be sensory, monitoring tension in the wall of the intestine or its chemical contents; associative, acting like interneurons; or motor, contracting intestinal muscles, dilating vessels, or transporting water and electrolytes. The motor neurons in the enteric nervous system may be excitatory or inhibitory.
Certain plexuses play important roles in the enteric nervous system. The myenteric plexus, also called the Auerbach plexus, is a network of nerve strands and small ganglia lying in the plane between the external longitudinal and circular muscle coats of the intestine. The submucous plexus (Meissner plexus) consists of nerve cell bodies, glial cells, and glial and neuronal processes, but it does not contain connective tissue or blood vessels. Within the ganglia, many neuronal processes contain vesicles that store neurotransmitters.
What is the organizational pattern of these neurons, which can contain up to a dozen neurotransmitters? Unlike the sympathetic and parasympathetic nervous systems, in which geographic location can confer selective action, this is anatomically impossible in the gut, and an alternative pattern of chemical coding for function assumes an important organizational role. The combination of amines and peptides within the enteric neuron is thought to code for its function.
Acetylcholine is the principal excitatory trigger of the nonsphincteric portion of the enteric nervous system, causing muscle contraction. Cholinergic neurons have several roles in the enteric nervous system, including excitation of external muscle, activation of motor neurons augmenting water and electrolyte secretion, and stimulation of gastric cells. Neural control of gastrointestinal motility is mediated through two types of motor neurons: excitatory and inhibitory. These neurons act in concert on the circular smooth muscle layer on sphincteric and nonsphincteric regions throughout the digestive tract, and they supply the muscle of the biliary tree and the muscularis mucosae. Although excitatory motor neurons supply the external longitudinal muscle, it is not well established that all regions of the longitudinal muscle are supplied by inhibitory motor neurons. Enteric motor neurons to the circular muscle of the small and large intestine are activated by local reflex pathways contained within the wall of the intestine. Distention evokes polarized reflexes, including contraction orally and relaxation anally, which in synchrony constitute peristalsis. Nicotinic antagonists abolish enteric reflexes, suggesting that the sensory neurons or interneurons in the pathway are cholinergic. In cases of cholinergic overload, such as insecticide poisoning or "overreversal" of muscle relaxants, there is a tendency for the gut (in which cholinesterase is inhibited) to become hyperreactive.
There are, however, many other compounds that participate in intestinal function, including substance P, a variety of opiate peptides, VIP, and a growing population of peptide hormones. There is evidence for nonadrenergic, noncholinergic (NANC) neurons in the small intestine and for similar cells that mediate gastrin release. Evidence also indicates that nitric oxide (NO), the same compound that
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