GIT

GIT
Lec /2 Dr-Rajaa Ahmad

Autonomic control of GIT or Extrinsic innervations

The intestine receives a dual extrinsic innervations from the autonomic nervous system(A.N.S) . 1.parasympathetic nervous system(P.N.S). 2. sympathetic nervous system(S.N.S). Nerve fibers from both sympathetic postganglionic and parasympathetic preganglionic branches of autonomic N.S enter the GIT and synapse with nervous in both plexuses of enteric nervous system . A. parasympathetic innervations :The parasympathetic supply to the gut is divided the : 1.cranial outflow. 2. sacral outflow.

The parasympathetic division is called cranio-sacral 1.Cranial outflow : occulomotor ( III) , facial ( VII) , glossopharngeal ( 1X) and vagus nerve (X) .The parasympathetic system fibers leave the CNS through cranial nerves facial nerve ( VII) to submandbullary and sublingual salivary glands , glossopharngenl nerves (IX) to parotid salivary gland. About 75% of all parasympathetic nerves fibers are in the vagus nerve innervates esophagus , stomach , pancreas, liver , gallbladder , less to the small intestine , and proximal half of the colon.

2- sacral outflow: originated in the second , third , and forth sacral segments of spinal cord and pass through the pelvic nerves to the distal half of large intestine and all the way to the anus . These fibers function especially to execute the defecation reflexes . The parasymepathic fibers are preganglionic which is cholinergic (release acetylcholine) .so stimulation of parasympathetic nerves causes increase in the activity (motility) ,secretion and relaxation of sphincters GIT .

b. Sympathetic outflows The sympathetic fibers are postganglionic .The sympathetic fibers to the GIT originate in the spinal cord between T5 and L2 postganglionic sympathetic nerve endings secrete mainly norepinephrine but also small amounts of epinephrine. Stimulation of sympathetic system inhibits the activity of GIT such motility and secretion and can block the movement of food through the GIT. In general stimulation of the sympathetic N.S inhibits the activity of GIT in two ways : 1- to lesser extent by direct effect of secreted NE to inhibit intestine tract smooth muscle. 2.to a major extent by inhibitory effect of NE on the neurons of entire enteric NS

TYPES OF MOVEMENTS IN THE GIT

1.Propulsive Movements = Peristalsis the stretching of the gut wall stimulates the enteric nervous system to contract the gut wall 2 to 3 centimeters behind this point, and a contractile ring appears that initiates a peristaltic 2) Mixing movements. Are local intermittent constrictive contraction that occurs every few centimeters in the gut wall. These contractions usually last only 5-30 seconds then new constrictions at other point in the gut .. e.g .SEGMENTATION CONTRACTIONS movement

Peristaltic Reflex and the “Law of the Gut” The contractile ring causing the peristalsis normally begins on the orad side of the distended segment and moves toward the distended segment, pushing the intestinal contents in the anal direction for 5 to 10 centimeters before dying out. At the same time, the gut sometimes relaxes several centimeters downstream toward the anus, which is called “receptive relaxation,” thus allowing the food to be propelled more easily anally than orad. The complex is called the myenteric reflex or the peristaltic reflex. The peristaltic reflex plus the anal direction of movement of the peristalsis is called the “law of the gut.”

Gastrointestinal Circulation : Splanchnic Circulation

The blood from the intestine , pancreas and spleen --to--Hepatic Portal veins --to--liver and from the liver through hepatic veins to the inferior vena cava. This flow of blood through the liver, before it empties into the vena cava, allows the reticuloendothelial cells that line the liver sinusoids to remove bacteria andother particulate matter that might enter the blood from the gastrointestinal tract, thus preventing direct transport of potentially harmful agents into the remainder of the body.


Effect Of GIT Activity And Metabolic Factors On GI Blood Flow
The possible causes of the increased blood flow during GI activity are due to: 1. releasing of vasodilators, such as CCK, VIP , gastrin , secretin, bradykinins and kinins 2. also decreased O2 concentration( hypoxia)

Countercurrent” Blood Flow in the Villi. Blood oxygen diffuses out of the arterioles directly into the adjacent venules without ever being carried in the blood to the tips of the villi. Under normal conditions, this shunting of oxygen from the arterioles to the venules is not harmful to the villi, but in disease conditions in which blood flow to the gut becomes greatly curtailed, such as in circulatory shock, the oxygen deficit in the tips of the villi can become so great that the villus tip or even the whole villus suffers ischemic death and can disintegrate. Diseases---ischemic death-----diminished intestinal absorption.

Nervous Control of Gastrointestinal Blood Flow

Stimulation of the parasympathetic going to the stomach and lower colon increases local blood flow at the same time that it increases. Sympathetic stimulation cause vasoconstriction called “autoregulatory escape.” That is, the local metabolic vasodilator mechanisms that are elicited by ischemia become prepotent over the sympathetic vasoconstriction and, therefore, redilate the arterioles, thus causing return of necessary nutrient blood flow to the GI glands and muscle

Regulation of gastrointestinal tract 1.Hormonal Control 2. Neural control a. Enteric NS. b. extrinsic NS.

Hormonal Control

The stomach, small intestine, and colon have about 15 types of hormone-secreting enteroendocrine cells have been identified in the mucosa, these hormones are biologically active polypeptides and play a role in the regulation of gastrointestinal secretion and motility. Many chemical substances in the chyme stimulate the endocrine cells to release its hormones.

These hormones fall into one of two families: 1. gastrin family, the primary members of which are gastrin and cholecystokinin (CCK); 2. secretin family, the primary members of which are secretin, VIP, gastric inhibitory polypeptide (GIP), and glucagon,. There are other hormones that do not from these families such as substance p ,Gastrin Releasing Peptide(GRP),and glicentin(GLI).

1) GASTRIN produced by cells called G-cells in the antral portion of stomach , Brunner s glands of duodenum , pancreatic cell in the fetal life, pituitary gland , hypothalamus ,medulla oblongata , vagus and sciatic nerves Its action 1- stimulation of gastric acid and pepsin secretion. 2- stimulation of gastric motility . 3- stimulation of growth of gastric mucosa , small intestine and large intestine (trophic action ) 4- causes contraction of gastro- esophageal sphincter. 5- stimulation of insulin secretion only after a protein meal

Stimuli that increase gastrin secretion 1- distension of stomach. 2- amino acids in stomach which affect directly on G-cells . 3- gastrin releasing peptide (GRP) which released by vagal stimulation that innervate G-cells rather than Ach, so atropine dose not inhibit the gastrin release in response to a meal test in humans. 4- blood born factors such as calcium and epinephrine

2) cholecytokinin – pancreazymin (CCK – PZ) or cholecytokinin (CCK) is produced by I cells in the duodenum and upper jejunum , by endocrine cells , nerves in distal ileum ,colon , cerebral cortex , and nerves in many parts of the body.


Stimuli that inhibit gastrin secretion 1-Acid in the stomach gastrin secretion(-ve feedback mechanism). 2- secretion of somatostatin (growth hormone inhibitory hormone). 3- secretin, gastric inhibitory peptide (GIP) , VIP , glucagon and calcitonin in the blood

physiological actions : 1- strongly contracts the gallbladder. 2- inhibits stomach contraction moderately . 3- causing secretion of pancreatic juice rich in enzymes. 4- increases secretion of enterokinase . 5- enhance motility of the small intestine and colon. along with secretin it augments the contraction of pyloric sphincter thus preventing the reflex of duodenal contents into the stomach 6- relaxes sphincter of Oddi , Stimuli that increase CCK secretion are : amino acids , fatty acids in small intestine


3) Secretin: is the first GI hormone discovered and is secreted by the S -cells in the upper small intestine. Physiological actions 1- increases the secretion of bicarbonate by the duct cells of pancreas and biliary tract . 2- cause contraction of the pyloric sphincter . 3- has a mild effect on motility of the GIT . 4- increases biliary secretion rich in bicarbonate .

Stimuli that increase secretin secretion are: 1- acidic gastric juice secretin causes alkaline pancreatic juice to flood into the duodenum , neutralizing the acid from stomach .and thus stopping further secretion of the hormone 2- increased by amino acid in the small intestine .

Gastrointestinal Reflexes

Gastrointestinal reflexes that are essential to gastrointestinal control. They are: 1. Reflexes that are integrated entirely within the gut wall enteric nervous system. These include reflexes that control much gastrointestinal secretion, peristalsis, mixing contractions, local inhibitory effects

2. Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the gastrointestinal tract. These reflexes transmit signals long distances to other areas of the gastrointestinal tract, such as signals from the stomach to cause evacuation of the colon (the gastrocolic reflex), signals from the colon and small intestine to inhibit stomach motility and stomach secretion (the enterogastric reflexes), and reflexes from the colon to inhibit emptying of ileal contents into the colon (the colonoileal reflex)


3. Reflexes from the gut to the spinal cord or brain stem and then back to the gastrointestinal tract.These include especially (1) reflexes from the stomach and duodenum to the brain stem and back to the stomach—by way of the vagus nerves—to control gastric motor and secretary activity; (2) pain reflexes that cause general inhibition of the entire gastrointestinal tract; and(3) defecation reflexes that travel from the colon and rectum to the spinal cord and back again to produce the powerful colonic, rectal, and abdominal contractions required for defecation (the defecation reflexes).