Gastric Physiology

Mototrik stomach has four functions, among others

A. Filling
When the stomach is empty, the stomach volume of about 50 ml, but can be increased to 1000 ml when eating. This occurs because the structure of the gastric mucosa has indentations and the hull has a mechanism called receptive relaxation. Receptive relaxation occurs when the stomach contains food. At that time the gastric mucosa to shrink the depth of the pleats so that the volume of the stomach can be increased.

B. Storage
Storage of food in the stomach is at the fundus and gastric corpus. This happens because the muscles in the lining thinner than the layer of muscles in the gastric antrum areas. This will have an impact on the strength of peristalsis in these areas. In the fundus and corpus motion peristaltiknya weaker compared with that at the antrum peristalsis at the fundus and corpus are not overly affect the gastric contents.

C. Mixing
Food mixing occurs in the muscle layer of the antrum due antrum thick enough to produce a strong peristalsis. Peristalsis stimulated by pacemaker cells located at the fundus. When the cells undergo depolarization, the stimulus will spread from the fundus to the pylorus. Stimulus is sometimes followed by muscle contractions and gastric peristalsis form but may also not be followed by stomach muscle contraction due to depolarization of pacemaker cells do not reach the threshold. Peristalsis will push toward eating pyloric sphincter. When the food reaches the pyloric sphincter, some food will go into the duodenum in the form kimus. When peristalsis was reached pyloric sphincter, the sphincter will close and the food can not pass through. As a result, food moves into the sphincter sphincter will hit and bounced toward the pylorus causing foods can be mixed with gastric secretions.

D. Evacuation
Gastric emptying occurred on a piecemeal basis as openings in the pyloric sphincter is very small. Gastric emptying depends on the strength of peristalsis produced by the stomach. Peristalsis kimus forced to pass through the pyloric sphincter openings are very small heading into the duodenum.
Gastric emptying is influenced by several factors such as lipids in the duodenum, acidity, hipertonus and distension of the duodenum due to accumulation kimus in the duodenum.

The volume of food into the stomach affect gastric emptying rate. The more food that enters the stomach, the faster gastric emptying occurs. In addition, the hormone gastrin can also increase the speed of gastric emptying. Both of these are factors that affect the rate of gastric emptying of the stomach from the duodenum while the factors that affect the speed of gastric emptying, among others

a. The inhibitory effect by reflex nerve enterogastric of the duodenum.
When kimus (chime) enters the duodenum, the various nerves in reflex stimulated duodenal wall and then gave orders to the emptying of the stomach to reduce speed if the number is in the duodenum kimus too much. This reflex can be via three routes, among others, (1) directly from the stomach through the duodenum leading to the enteric nervous system in the gut wall, (2) through extrinsic nerves leading to the prevertebral sympathetic ganglion and then into the stomach through the nerve fibers simpais inhibitor and (3) possible stimulation propagates through n. vagus to the brain stem and then back again to the hull form of stimulation to slow gastric emptying.

b. The inhibitory effect by hormones from duodenum
Lipids to stimulate the release of hormones that can inhibit gastric emptying. When lipids enter the duodenum, stimulates duodenal lipid to secrete the hormone cholecystokinin (CCK) by binding to receptors or by other means. The hormone then be carried by the blood and will mestimulasi gastric peristalsis to reduce power and increase the speed of contraction of the pyloric sphincter to gastric emptying will decrease.
Besides cholecystokinin, and gastric inhibitoy sekretin hormone peptide (GIP) are secreted by the duodenum can also inhibit gastric emptying. Sekretin hormone secretion is stimulated by the presence of acid in the duodenum