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    Digestive system Physiology-Review & illustrations-GIT Motility

    Completion requirements

    Anatomy and Histology

    Layers of the Gastrointestinal Tract
    GIT layers-Questions & Answers
    Passage time from the time of food intake

    Electrical Potentials in the GI Tract (see figure):

    1. Slow waves are the resting membrane potential found in the smooth muscle of the GI tract. The undulating waves occur at regular intervals, and they are called the basic electrical rhythm (BER). Depolarization of the slow waves above threshold (-40 mV) stimulates action potentials, which cause contractions. Slow waves that act as pacemakers originate in a modified intestinal smooth muscle cells called the interstitial cells of Cajal. They are a feature of smooth muscle cells in the stomach, small intestine, and large intestine. Slow waves determine the basic frequency of contractions throughout the GI system by facilitating membrane depolarization at a particular rate. Slow-wave frequency is modified by neural or hormonal activity. These influence the amplitude of the oscillation more than the frequency. The rate of slow waves is lowest in the stomach (3/min) and highest in the duodenum (12/min). The mechanism of slow wave production is the cyclic opening of Ca2+ channels (depolarization) followed by opening of K+ channels (repolarization).

    2. Action or spike potentials are generated on the peaks of slow waves, when slow waves are depolarized above the electrical threshold (-40 mV). The action potential results from entry of calcium into the cells via voltage-gated Ca2+ channels, and Ca2+ flows into the cell down its electrochemical gradient, increasing the intracellular [Ca2+]. Calcium binds to calmodulin, which initiates cellular events leading to contraction.
    Comment: Depolarization of slow waves can be caused by stretch, ACh, or parasympathetic stimulation. The force of contraction increases with the number of action potentials generated. Thus, the stronger the stimulus (e.g., local stretch due to presence of chyme), the greater the depolarization and number of action potentials, and the stronger the contraction.
    I.e. The higher of stimulus intensity → the greater the depolarization and number of action potentials → the stronger the contraction

    Summary of GIT motility:

    Each part of the gastrointestinal tract has a unique function to perform in digestion, and as a result each part has a distinct type of motility. When the motility is not appropriate for its specific function in digestion, it can cause symptoms such as bloating, vomiting, constipation, or diarrhea which are associated with sensations such as pain, bloating, fullness, and urgency to have a bowel movement.

    Types of GIT motility:

    1. Peristalsis. This motility is mainly seen in the esophagus, stomach and to less extent in the small intestine and large intestine. See Peristalsis 1, Peristalsis 2, Peristalsis 3, Peristalsis 4. It moves food along the GIT in a proximal to distal direction.
    2. Receptive relaxation. This motility is seen in the stomach. See video. It allows food to pass from esophagus to the stomach, and allows the stomach to accommodate  greater and greater quantities of food .
    3. Segmentation. This type of motility is seen mainly in the small intestine, and to less extent in the colon. See video. It causes propelling and mixing food in the stomach and large intestine.
    4. Migrating motility complexes (MMC). This is a peristaltic type of motility seen in the stomach and small intestine. See video. It is observed in gastrointestinal smooth muscle during the periods between meals, and it is interrupted by feeding. It is thought to serve a "housekeeping" role and sweep residual undigested material through the digestive tube.
    5. Mass movements. This is a peristaltic type of motility seen in large intestine. See video. It ­forces the feces into the rectum.

     Regulation of the Gastrointestinal Tract Motility & Secretion

    1. Neural Control. 
    2. Hormonal Control (Endocrine Control, Paracrine Control & Neurocrine Control).

     1. Neural Control: The GI system is richly innervated by both extrinsic (autonomic nervous system, ANS) and intrinsic nerves (enteric nervous system, ENS). The enteric nervous system relays information from the ANS and is also able to directly and independently regulate many GI functions (see figure). Extrinsic Innervation (Autonomic Nervous System) provides for long reflexes, which coordinate activities at widely separated sites along the GI tract.The enteric nervous system possesses all the elements necessary for short reflex regulation of GI functions, that is, modification of motility and secretory activity by afferent and efferent nerves entirely within the GI tract. Submucosal plexus (Meissner plexus) principally controls GI secretions and blood flow. Myenteric plexus (Auerbach plexus) controls the motility of GI smooth muscle.

    [Hirschsprung’s disease is a congenital absence of the myenteric plexus, usually involving a portion of the distal colon. The pathologic aganglionic section of large bowel lacks peristalsis and undergoes continuous spasm, leading to a functional obstruction. The normally innervated proximal bowel dilates as a result of the obstruction and can lead to the most feared complication of Hirschsprung’s disease, toxic megacolon].

    2. Hormonal Control by GI peptides:

    A. Endocrine Control: GI hormones are released from endocrine cells in the mucosa of certain regions of the GI system, particularly the antrum of the stomach and the upper small intestine. The major hormones secreted by the GI system are gastrin, secretin, cholecystokinin (CCK), motilin,  glucagon-like peptide 1 (GLP-1), and gastric inhibitory peptide (GIP) (also called glucose-dependent insulinotropic peptide). Table shows the control of the release of these hormones  and their actions.

    [IN THE CLINIC: Glucagon-like peptide 1 (GLP-1) is a regulatory peptide released from EC cells in the gut wall in response to the presence of luminal carbohydrate and lipids. GLP-1 arises from differential processing of the glucagon gene, the same gene that is expressed in the pancreas and that gives rise to glucagon. GLP-1 is involved in regulation of the blood glucose level via stimulation of insulin secretion and also insulin biosynthesis. Agonists of the GLP-1 receptor improve insulin sensitivity in diabetic animal models and human subjects. Administration of GLP-1 also reduces appetite and
    food intake and delays gastric emptying, responses that may contribute to improving glucose tolerance. Long-acting agonists for the GLP-1 receptor, such as exanatide, have been approved for the treatment of type 2 diabetes].

    B. Paracrine Control: Paracrine substances are signaling molecules released by cells in the GI mucosa that diffuse through interstitial fluid to nearby target cells, where they exert their effects. The three key paracrine substances of the GI system are serotonin, histamine and somatostatin. The control of their release and their actions are summarized in Table. Serotonin is produced by enterochromaffin (EC) cells in the intestinal mucosa in response to distension of the gut wall. It exerts most of its effects indirectly through interactions with the ENS. The effects of serotonin are generally excitatory and result in increased intestinal motility and secretion.

    [Carcinoid tumors arise from the EC cells. Because these cells originate as neuroendocrine cells, they often secrete hormones, most commonly serotonin. Systemic release of serotonin results in carcinoid syndrome with clinical manifestations of flushing, diarrhea, bronchospasm, and cardiac valvular disease. When carcinoid  tumors arise in the gastrointestinal tract, they are most commonly seen in the ileum; the serotonin is secreted into the hepatic portal circulation, which undergoes fi rst-pass metabolism. Serotonin is rapidly metabolized in the liver, resulting in very little systemic serotonin. Carcinoid syndrome will manifest once the tumor has metastasized to the liver and can release serotonin directly into the systemic circulation].

    Somatostatin is a peptide produced by D cells and is a potent inhibitor substance in the gastrointestinal system. It may be released both into the blood to act in an endocrine fashion and also as a paracrine mediator. Somatostatin inhibits pancreatic and gastric secretion, relaxes the stomach and gallbladder, and decreases nutrient absorption in the small intestine. These actions result partly from inhibition of several other stimulatory gut hormones, including gastrin, secretin, gastric inhibitory peptide (GIP), and motilin.

    [Ruptured esophageal varices can cause severe bleeding into the gastrointestinal tract. Somatostatin analogues (e.g., octreotide) are used to reduce bleeding from ruptured esophageal varices, and are effective because somatostatin is a potent gastrointestinal vasoconstrictor].

    C., Neuroendocrine Control: Neurocrine substances are peptides synthesized by neurons of the GI tract. They are released from an axon following an action potential and diffuse synaptic cleft distant target cell to their target tissue. The three neurocrine substances in the GI tract are vasoactive intestinal peptide, gastrin-releasing peptide (GRP, or bombesin), and enkephalins. The control of their release and their actions are summarized in Table.

    • Gastrin:
    1. ↑ Gastric H+ secretion, 
    2. Stimulates growth of gastric mucosa. 
    3. Increases antral muscle mobility and promotes stomach contractions.
    4. Strengthens antral contractions against the pylorus, and relaxes the pyloric sphincter, which increases the rate of gastric emptying.
    5. Plays a role in the relaxation of the ileocecal valve.
    6. Induces pancreatic secretions and gallbladder emptying.
    7. May impact lower esophageal sphincter (LES) tone, causing it to contract, although pentagastrin, rather than endogenous gastrin, may be the cause.
    8. Gastrin contributes to the gastrocolic reflex.
    • CCK,
    1. Stimulates contraction of gallbladder and relaxation of sphincter of Oddi.
    2. ↑ Pancreatic enzyme and HCO3– secretion.
    3. ↑ Growth of exocrine pancreas/gallbladder.
    4. Inhibits gastric emptying
    5. It stimulates gallbladder contraction, and intestinal motility, while inhibits gastric emptying.
    • Secretin,
    1. inhibits gastric emptying.
    2. ↑ Pancreatic HCO3–, secretion,
    3. ↑ Biliary HCO3– secretion,
    4. ↓ Gastric H+ secretion
    • Motilin, It stimulates migrating motor complex.
    • Glucagon-Like Peptide I, Glucagon-like peptide 1 belongs to a family of hormones called the incretins, so-called because they enhance the secretion of insulin. Cells found in the lining of the small intestine (called L-cells) are the major source of glucagon-like peptide 1. Food is the main stimulus of glucagon-like peptide 1 release, with increased hormone levels detectable after 10 minutes of starting to eat and remaining raised in the blood circulation for several hours after that. The hormone somatostatin holds back the production of glucagon-like peptide 1. 
    1. Glucagon-like peptide 1 increases the feeling of fullness during and between meals by acting on appetite centres in the brain and by slowing the emptying of the stomach.
    2. It slows gastric emptying.
    3. Enhances the secretion of insulin
    • Glucose-dependent insulinotropic peptide (GIP) also called Gastric inhibitory polypeptide (GIP): It is released from duodenum and jejunum. The stimulus for secretion is the fatty acids and amino acids and the presence of oral glucose load. Thus, oral glucose is more effective than intravenous glucose in causing insulin release and, therefore, glucose utilization. GIP is the only GI hormone that is released in response to the three main food groups, i.e. fat, protein, and carbohydrate.
    1. ↑ Insulin secretion
    2. ↓ Gastric H+ secretion
    3. Inhibit the gastric and GI motility
    • Somatostatin:  is secreted by cells throughout the GI tract in response to H+ in the lumen. Its secretion is inhibited by vagal stimulation.
    1. Inhibits the release of all GI hormones.
    2. Inhibits gastric H+ secretion.
    • Histamine: is secreted by mast cells of the gastric mucosa. It increases gastric H+ secretion directly and by potentiating the effects of gastrin and vagal stimulation.
    • Neurocrines: Are synthesized in neurons of the GI tract, moved by axonal transport down the axon, and released by action potentials in the nerves. Neurocrines then diffuse across the synaptic cleft to a target cell. The GI neurocrines are vasoactive intestinal peptide (VIP), GRP (bombesin), and enkephalins.
    A. VIP: contains 28 amino acids and is homologous to secretin. is released from neurons in the mucosa and smooth muscle of the GI tract.
    1. Produces relaxation of GI smooth muscle, including the lower esophageal sphincter.
    2. stimulates pancreatic HCO3– secretion and inhibits gastric H+ secretion. In these actions, it resembles secretin.
    B. GRP:     is released from vagus nerves that innervate the G cells. It stimulates gastrin release from G cells.
    C. Enkephalins (met-enkephalin and leu-enkephalin)     are secreted from nerves in the mucosa and smooth muscle of the GI tract.
    1. Stimulate contraction of GI smooth muscle, particularly the lower esophageal, pyloric, and ileocecal sphincters.
    2. Inhibit intestinal secretion of fluid and electrolytes. This action forms the basis for the usefulness of opiates in the treatment of diarrhea.
    Chemical Signaling of GIT-Questions & Answers (see figure).

    GIT Motility

    Motility of mouth (Chewing): The mouth receives food into the GI tract. Chewing tears and grinds food, reducing lumps to a size that can be swallowed. Chewing also mixes ingested food with saliva, moistening it enough to be easily swallowed. Chewing is part voluntary and part reflex. The pattern and rhythm of chewing are set by cortex and brain stem centers. Pressure of food in the mouth elicits  chewing reflex actions. The presence of a bolus of food in the mouth at first initiates reflex inhibition of the muscles of mastication, which allows the lower jaw to drop → The drop in turn initiates a stretch reflex of the jaw muscles that leads to rebound contraction  → raises the jaw to cause closure of the teeth → compresses the bolus again against the linings of the mouth, which inhibits the jaw muscles once again.

    The mouth motility causes mechanical breakdown of food particles and mixing food with saliva. The tongue propels the bolus of food to the back of the oral cavity, initiating a swallowing reflex. The muscles of mastication are the masseter, the temporalis, and the medial and lateral pterygoids. They are innervated by the mandibular division of the trigeminal nerve (cranial nerve V).

    Motility of esophagus: The esophagus serves no digestive or absorptive functions. It is simply a conduit between the pharynx and stomach. Motility in the esophagus is peristalsis (integrated at swallowing center), a progressive wave of muscle contractions. The primary esophageal peristalsis (mediated by vagovagal long reflex) propel the bolus actively toward the lower esophageal sphincter. The force generated by peristaltic contractions varies with the size of the bolus. Stimuli from the distention of the esophagus wall are relayed to the CNS to modify the pressure generated by the esophageal muscles. Larger boluses produce greater forces If the bolus failed to move forward, the secondary esophageal peristalsis is initiated which is associated with distension or irritation of the smooth muscle portion of the esophageal body (mediated by short enteric reflex). In summary, motility in the esophagus is peristalsis, primary and secondary and its function is to propel a bolus of food to the stomach.

    Esophageal motility Monitoring is usually checked by measuring the pressure in the lumen, for example, during a peristaltic wave. The resting pressure within the lower esophageal sphincter (LES) is normally 20 to 25 mm Hg. During receptive relaxation, esophageal pressure drops to match the low pressure in the proximal stomach indicating opening of the LES. The LES opens due to a vagovagal reflex mediated through myenteric neurons (releasing VIP and nitric oxide).

    Peristalsis: Both mechanical and chemical stimulation can elicit motility in the GI tract. In Figure, identify the major neurotransmitters that are released during peristalsis from excitatory motor neurons (1) and inhibitory motor neurons (2). Describe whether stimulation of the respective motor neuron populations results in smooth muscle contraction or relaxation.

    Answer:

    1. Excitatory motor neurons in the GI tract can release acetylcholine (ACh) and substance P (tachykinin); these substances cause contraction of the smooth muscle.
    2. Inhibitory motor neurons release vasoactive intestinal peptide (VIP) or nitric oxide (NO); these substances cause relaxation of the smooth muscle.
    Comment: The oral constriction and aboral (away from the mouth) relaxation are the hallmark of peristalsis, allowing aboral movement of the chyme.

    Swallowing: The process of swallowing reflex almost entirely automatic and controlled by swallowing (or deglutition) center which is located at the medulla. The sequence of events of swallowing are as follow: Food is voluntarily squeezed posteriorly in the mouth to the oropharynx by pressure of the tongue upward and backward against the hard palate → automatic pharyngeal muscular contractions and inhibition of the respiratory center → The soft palate is pulled upward and the palatopharyngeal folds on either side of the pharynx are pulled medial ward to approximate each other → The glottis closed and pulled upward and anteriorly causing epiglottis to swing backward over the superior opening of the larynx → the upper esophageal sphincter is relaxed → bolus enters the esophagus and initiates primary peristalsis in the esophagus → Receptive relaxation of lower esophageal sphincter and the stomach. A typical swallow propels a bolus of food through the esophagus to the stomach in about 9 seconds. Liquids travel more rapidly than solids in the uptight human. Water travels down the esophagus to the LES in about 1 second. Water enters the stomach 5-8 seconds after the swallow, moved through the LES by the peristaltic wave.
    The upper esophageal sphincter (UES) is composed of striated muscle and is normally closed due to elasticity of the sphincter and tonic neural excitation. The lower esophageal sphincter (LES) is composed of smooth muscle. It is closed under resting conditions due in part to tonic myogenic contraction (i.e., the contraction is due to an intrinsic property of the myocyte cell, not due to neural stimulation). The LES relaxes at the start of the swallow, several seconds before the wave of peristalsis in the esophagus approaches the LES due to vagal (non-cholinergic) inhibition, allowing the bolus to pass into the stomach. It then closes to prevent reflux of gastric contents into the esophagus. Table lists the factors that modulate the tone of the LES.

    [Gastroesophageal reflux disease (GERD) occurs when stomach acid continuously refluxes into the esophagus. It may be caused by elevated intraabdominal pressure (e.g., due to obesity, big meals, or tight clothing), reduced LES tone (e.g., due to pregnancy, hiatus hernia, achalasia, fatty meals, and smoking), and by tricyclic and anticholinergic drugs. GERD causes pain, heartburn, and inflammation because the esophagus lacks the protective lining of the stomach. The pain of GERD radiates to the back and is worsened by stooping and ingesting hot drinks. Treatment is with antacids (e.g., calcium carbonate), H2-receptor antagonists (e.g., cimetidine), or proton pump inhibitors (e.g., omeprazole). Medication to strengthen the LES, known as prokinetic drugs (e.g., metoclopramide), may also be used. If medications alone do not control symptoms, surgery to tighten the LES may be necessary].

    In an upright posture, swallowed liquids can simply flow down the esophagus due to the force of gravity (although gravity is not essential for swallowing). The passage of semisolid food down the esophagus requires peristalsis. Peristalsis in the esophagus is coordinated by the extrinsic and intrinsic nervous systems.

    [Achalasia is a pathological condition caused by a deficiency of inhibitory myenteric neurons in the lower part of the esophagus. The LES fails to relax during swallowing, and peristalsis is absent. Food therefore accumulates above the LES, causing an increased risk of aspiration pneumonia. Symptoms of achalasia include regurgitation of food, chest pain, difficulty swallowing liquids and solids, cough, and weight loss. Drug treatment is aimed at reducing the tone of the LES. This may be achieved with Botox injections (temporary action) or by administration of long-acting nitrates or Ca2+ channel blockers. Surgical treatment includes esophagomyomectomy to reduce LES tone and dilation of the esophagus].

    Swallowing-Questions & Answers (see figure)

    Gastric Motility-Questions & Answers (see figure). The stomach has several functions: it stores food, mixes food with gastric juice for digestion, and empties chyme into the duodenum. Different movements serve each function. The movements reflect the muscular structure of the stomach wall.

         Receptive relaxation (accommodates a meal) occurs in the fundus and body of the stomach. Relaxation occurs with each swallow and permits the stomach to accommodate a volume of at least 1 liter with little increase in pressure. Receptive relaxation of the stomach is a vagovagal reflex that causes the muscles of the proximal stomach to relax, which facilitates entry of the bolus into the stomach. It allows the stomach to expand without increasing intragastric pressure. Receptive relaxation of the stomach fundus is associated with an increase in the peristaltic contraction of the body and antrum of it.  This property is known as accommodation.

         Gastric peristaltic contractions mix stomach contents and empty chyme into the duodenum. The frequency of gastric peristaltic contractions is 3-5/min. Peristaltic waves begin midstomach, ripple over the body, and become stronger over the muscular antrum and pylorus. Antral contractions force chyme toward the duodenum and smash small lumps. A small amount of chyme injects through the constantly contracted pyloric sphincter with each powerful antral contraction. As the contraction progresses, it closes the sphincter completely and most of the chyme is forced back into the stomach. This retropulsion effectively mixes food and gastric juice. Since frequency of peristaltic contractions is constant, the volume and contents of the stomach regulate the strength of contractions. In general, the greater the volume, the more rapidly the contents are emptied.

    • During cephalic phase of gastric secretion and motility, the gastric response is mediated by long reflex only without involvement of any hormone.
    • During gastric phase of gastric motility and secretion, gastric peristalsis is stimulated by long and short cholinergic reflexes initiated by distention and by elevated serum gastrin. Elevated serum gastrin not only stimulates contractions but also increases the frequency of slow-wave depolarizations.
    • During intestinal phase of gastric motility and secretion, the duodenum plays an equally important role in regulating gastric emptying. Fat, acid, and hypertonic solutions in the duodenum and duodenal distension, slow gastric emptying.

    Hunger contractions are the movements of empty stomach. These contractions are related to the sensations of hunger. Hunger contractions are the peristaltic waves superimposed over the contractions of gastric smooth muscle as a whole. This type of peristaltic waves is different from the digestive peristaltic contractions. The digestive peristaltic contractions usually occur in body and pyloric parts of the stomach. But, peristaltic contractions of empty stomach involve the entire stomach.

    [Belching is the process by which the gas accumulated in stomach is expelled through mouth. It is also called burping. It occurs because of inflation (distention) of stomach by swallowed air. The distention of the stomach causes abdominal discomfort and the belching expels the air and relieves the discomfort. Most of the gas accumulated in stomach is expelled through mouth. Only a small amount enters the intestine.
    Causes for Accumulation of Gases in Stomach:
    1. Aerophagia: Swallowing large amounts of air due to gulping the food or drink too rapidly
    2. Drinking carbonated beverages
    3. During some emotional conditions like anxiety lot of air enters the stomach through mouth.
    Act of Belching Belching is not a simple act and it requires the coordination of several activities such as:
    1. Closure of larynx, which prevents entry of liquid or food with the air from stomach into the lungs.
    2. Elevation of larynx and relaxation of upper esophageal sphincter. It allows exit of air through esophagus more easily.
    3. Opening of lower esophageal sphincter.
    4. Descent of diaphragm, which increases abdominal pressure and decreases intrathoracic pressure.
    All these activities are responsible for the expulsion of air from stomach to the exterior via esophagus].

    [Flatulence is the production of a mixture of intestinal gases. The mixture of gases is known as flatus. Expulsion of flatus through anus under pressure is called farting or passing gas. Farting is associated with disagreeable odor (due to odorous gases) and sound (due to vibration of anal sphincter).
    Quantity of Flatus: Average flatus released by human is about 500 to 1500 mL per day, with 10 to 25 episodes throughout the day.
    Source of Gases in Intestine: Flatulence is the mixture of gases present in the intestine.
    Flatulence by swallowed air is rare. Common sources of gases in flatulence are:
    1. Bacterial action on undigested sugars and polysaccharides (e.g. starch, cellulose)
    2. Digestion of some flatulence producing food stuffs such as cheese, yeast in bread, oats, onion, beans, cabbage, milk, etc.

    Constituents of Flatus: Major constituents of flatus:
    1. Swallowed non-odorous gases
    i. Nitrogen (major constituent)
    ii. Oxygen
    2. Non-odorous gases produced by microbes
    i. Methane
    ii. Carbon dioxide
    iii. Hydrogen
    3. Odorous materials such as
    i. Low molecular weight fatty acids like butyric acid
    ii. Reduced sulfur compounds (hydrogen sulfde and carbonyl sulfde)].

    Gastroileal reflex & gastrocolic reflex: Motility is increased due to the presence of food in the stomach, a long enteric reflex (gastroileal reflex) and gastrin hormone operate to increase the motility of ileum of small intestine and to relax the ileocecal sphincter. In addition, the gastroileal reflex also increases the mass movement (described later) of the colon. This is most evident in infants. Stimulation of mass movement upon ingestion of a meal is called the gastrocolic reflex and may be triggered by increased gastrin or by extrinsic neural reflexes. This reflex give the urge for defecation after meal.

    Control of Gastric Emptying:

    Stimulation of gastric emptying and secretion is achieved by gastric peristalsis which is enhanced mainly by the presence of food in the stomach (stomach distention) (short reflex by ENS) and to lesser extent by the release of hormone gastrin.

    Inhibition of gastric emptying and secretion: The mechanisms that inhibit gastric secretion and motility are an important counterbalance to stimulatory mechanisms and are necessary because of the corrosive nature of gastric juices. The main ways to inhibit gastric emptying are:

    1. The gastric acidity level: Gastric acid secretion is maximal about 1–2 hours after the ingestion of a balanced meal. The buffering capacity of the meal eventually becomes saturated, and the gastric pH begins to decrease; at this stage, a significant proportion of the meal has entered the small intestine. There are two ways in which a decreasing gastric pH inhibits gastrin secretion:

    1. Direct inhibition of G cells by H+ when the pH is reduced below 3.
    2. Paracrine inhibition of G cells by somatostatin; the secretion of somatostatin from D cells is stimulated by low gastric pH.

    2. Intestinal negative feedback from the small intestinal distension (through short and long enterogastric reflexes, see figure)  which activates duodenal stretch receptors and intestinal hormones. The intestinal negative feedback limits the amount of chyme that enters the duodenum at any one time so that digestion and absorption can proceed optimally. The hormones are collectively known as enterogastrones. The luminal factors that trigger the release of enterogastrones include H+, fatty acids, and hypertonicity. Secretin is the primary enterogastrone and is released in response to the low pH in the duodenum. The figure illustrates the enterogastrone concept and some mechanisms that are thought to be involved in this process. Duodenal hormones respond to the constituents in chyme and reduce gastric emptying.

    Question: See figure: Identify the hormones that respond to acid (1), fats (2), and amino acids/peptides (3) that decrease gastric emptying.

    Answer:

    1. Secretin is released in response to acidic chyme.

    2. Cholecystokinin (CCK) and gastric inhibitory peptide (GIP), vasoactive intestinal polypeptide (VIP) are released in response to fats in the chyme.

    3. Gastrin enhances gastric motility and secretion and is released in response to peptides and amino acids in the chyme.

    NOTES:     A meal of polysaccharide carbohydrates (starch and glycogen) is considered the best meal before engaging in a sporting activity. Polysaccharides help provide a steady source of glucose and have the fastest clearance time, typically 1 hour, from the stomach. For comparison, a meal containing both carbohydrates and proteins takes 3 hours to clear from the stomach, and a meal heavy with fats and proteins takes up to 6 hours. A major reason for the fast clearance of carbohydrates is that they do not increase cholecystokinin release, which is a major inhibitor of stomach emptying.

    Small intestine motility:

         During digestion, segmentation is the primary form of motility in the small intestine. Segmenting contractions are stationary, oscillatory, alternating contractions and relaxations. It is elicited by the distension of the small intestine (neural reflexes) due to the presence of chyme that stretch the wall of small intestine.

    Factors decrease the segmentation contraction of the small intestine:
    • Sympathetic stimulation,  
    • Epinephrine, 
    • Secretin, and 
    • Glucagon
    Factors increase the segmentation contraction of the small intestine:
    • Parasympathetic stimulation, 
    • Serotonin, 
    • Gastrin, 
    • Cholecystokinin, and 
    • Motilin
    They mix chyme with intestinal juices and bring it into repeated contact with the absorptive epithelium. Intestinal segmentation is slow. The frequency varies; it is greatest in the duodenum, about l2/min, and least in the ileum, about 9/min. segmentation contractions are very effective in mixing the contents of the gut. Because the frequency of segmenting contractions decreases from duodenum to ileum, there is a slow net movement of chyme along the small intestine.

         Small peristaltic waves that die out within a few centimeters also move chyme along.

    Slow passage of chyme through the small intestine permits maximum digestion and absorption of food. The volume and contents of the small intestine regulate the strength of segmenting contractions. In summary, Small intestine motility during digestion is mainly segmentation with limited peristalsis. The main functions are to mix the contents of the tract with intestinal secretions and bring chyme into contact with absorptive epithelium. 

    Migrating motility complexes: During fasting or during the interdigestive period , the stomach, and small intestine, exhibit regular contractile activity every 90 to 120 minutes called Migrating motility complexes (MMC). The contractions begin slowly and increase in strength, culminating in powerful peristaltic contractions. The pyloric sphincter remains open, allowing the contractions to remove large (> 1 mm) nondigestible solids left behind in the stomach and small intestine. MMC also removes mucus, sloughed cells, and bacteria from the small intestine, helping to prevent bacterial overgrowth. MMC is initiated by by intestinal hormone motilin and spread by the activity of the enteric nervous system. Activity of extrinsic neurons is not required for the complexes, but it can modify them.  It replaces segmenting contractions of small intestine that travel over successively more distal parts of the small intestine. Overnight, one may experience 6 to 8 of these complexes. The next complex of peristaltic waves sweeps across the duodenum and first part of the jejunum. The next complex sweeps across the rest of the jejunum. And so on, until the waves reach the terminal leum. Conversely, when a meal is ingested, secretion of motilin is suppressed and the MMC is abolished, until digestion and absorption are complete. The antibiotic erythromycin binds to motilin receptors, and derivatives of this compound may be of value in treating patients in whom gastrointestinal motility is decreased.

    Migrating motility complexes are a phenomenon of gastric and small intestine to sweep undigested contents of stomach and small intestine into the terminal ileum.

    [Paralytic ileus is a temporary cessation of gut motility that is most commonly caused  by abdominal surgery. Other common causes that result in an ileus are infection or inflammation in the abdominal cavity (e.g., appendicitis), electrolyte abnormalities (e.g., hypokalemia), and drug ingestion (e.g., narcotics). Signs and symptoms of paralytic ileus include nausea and vomiting, abdominal distension, and absent bowel sounds].

    Large intestine motility: Pressure in the terminal ileum opens the ileocecal sphincter. Typically 500 milliliters of chyme enters the large intestine per day. Slow, segmenting contractions, 1 to 5 per minute, knead the chyme and expose it to the epithelium so that water and salts can be absorbed. As the cecum fills, the sphincter closes, preventing the backward movement of chyme.

         Contractions of the transverse and descending colon (segmentation contractions) form haustra as contents are shuttled back and forth. Absorption of water and salts continues.

         During a meal, propulsive multihaustral contractions and a type of peristalsis called a mass movement occur. A mass movement is a rapidly spreading intense contraction that leaves the muscle contracted for some time. Contents progressing out of the ascending colon elicit the mass movement that often begins in the transverse colon. Fecal matter is moved ahead of the contraction filling the sigmoid colon and rectum by the end of a meal. When the rectum is distended, a person perceives the urge to defecate. The rectum contracts, the intemal anal sphincter relaxes, and tone in the external anal sphincter increases. Defeeation can be postponed because relaxation of the external anal sphincter is voluntary. Rectal contractions return the contents to the descending colon until the next mass movement. When a person voluntarily relaxes the external anal sphincter, defecation occurs. Contraction of the rectum and sigmoid colon expel the feces. Voluntary movements that increase intra-abdominal pressure may aid defecation. Of the 500 ml of chyme that entered the large intestine, about 150 ml become feces. Feces contain primarily undigested food stuffs and bacteria. Large intestine motility during the inter-digestive period is segmentation which promotes absorption of water and salts. Large intestine motility during a meal is mass movement which propels feces into rectum for evacuation.

    Control of gallbladder motility:
         During the cephalic phase, there is gradual rhythmic contraction of the gallbladder, mediated by the cholinergic vagal neurons.
         During the intestinal phase, the entry of a meal into the small intestine stimulates CCK and secretin secretion. CCK is the most powerful signal for gallbladder contraction and also mediates the relaxation of the sphincter of Oddi, allowing biliary and pancreatic secretions to enter the duodenum (see figure). Increasing levels of secretin stimulate cholangiocyte secretion, providing additional HCO3− to neutralize acidic chyme.

    Defecation reflex (see figure): Distension of the rectal wall then triggers the defecation reflex. This reflex involves two positive feedback loops.  Both loops are triggered by the stimulation of stretch receptors in the rectum.  Rectal stretch receptors also trigger two reflexes important to
    the voluntary control of defecation. One is a long reflex mediated by parasympathetic innervation within the pelvic nerves. This reflex causes the internal anal sphincter to relax. This smooth muscle sphincter controls the movement of feces into the anal canal. The second is a somatic reflex that stimulates the immediate contraction of the external anal sphincter, a skeletal muscle.

    Questions:
    Describe the main action(s) elicited in response to the reflexes listed below:
    1. Vomiting reflex
    2. Gastrocolic reflex
    3. Ileogastric reflex
    4. Enteroenteric reflex
    5. Defecation (rectosphincteric) reflex
    Answers:
    1. The vomiting reflex causes expulsion of upper intestinal and gastric contents via reverse peristalsis.
    2. The gastrocolic reflex stimulates colonic mass movements in response to food or chyme in the stomach.
    3. The ileogastric reflex reduces gastric emptying when there is chyme in the ileum.
    4. The enteroenteric reflex will relax an area of the intestines when an adjacent area is distended.
    5. The defecation reflex is initiated by feces entering and stretching the rectum. This elicits the relaxation of the internal anal sphincter (IAS) and the urge to defecate.
    Comment: These reflexes do not occur in an all-or-nothing manner, and many act in concert to promote efficient movement of the chyme. These represent only a few of the reflex actions present in the GI tract.

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