Gastric phase

Gastric phase 60 to 70% of gastric secretory response to a meal... 

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. 

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. 

The gastric phase, which occurs when food actually enters the stomach. The presence of food and the composition of gastric contents stimulate local reflexes involving intrinsic nerve plexuses and stretch receptors and initiate release of gastrin from G cells to further enhance secretion. 

Gastric secretion and motility are controlled by both nervous and hormonal mechanisms. The vagus initiates the cephalic phase of secretion in response to the sight or smell of food, before food is eaten. The gastric phase occurs when food enters the stomach and is controlled both by intrinsic nerve reflexes in the stomach wall and released gastrin. The third, or intestinal, phase of secretion is coordinated by nervous and hormonal mechanisms to limit the release of the chyme from the stomach into the duodenum and reduces further acid secretion. 

The gastric phase of protein digestion is not absolutely required for health. Patients lacking gastric function because of a gastrectomy (surgical removal of the... 

The basal rate of hydrochloric acid secretion varies diurnally, being highest in the evening and lowest in the morning. After ingestion of a meal, the rate of acid secretion in the stomach increases. The three phases of increased acid secretion in response to food are the cephalic phase (before food reaches the stomach), the gastric phase (elicited by the presence of food in the stomach), and the intestinal phase (elicited by input from the duodenum and upper jejunum). 

Gastric Phase. Gastrin is the main mediator of acid secretion. Acid secretion occurs h response to both the presence of nutrients and the physical distension produced by food entering the stomach. Distension-induced gas.-trie acid secretion, relative to the total amount of acid released, is species dependent (human = 20% dog = 50% rat = 38%). The chemical constituents of a meal are the strongest stimulant of gastrin release and acid output during... 

Results of the IVG gastric phase were linearly correlated (r = 0.92) with in vivo bioavailable As P <0.01) (Fig. 3). The IVG intestinal phase was also linearly correlated with in vivo As with an r value of 0.91 (P < 0.01). The PBET... 

These experiments convincingly established that direct contact of food with the mucosa also stimulates gastric secretion. Direct stimulation of secretion by contact with the mucosa is referred to as the gastric phase. Pavlov was the first to show that when food is introduced directly into the intestine, avoiding contact with the stomach, gastric juice is secreted. 

Although earlier physiological experiments suggested that the mechanism of stimulation of gastric secretion was different in the cephalic and gastric phases of secretion, it now appears that known physiological mechanisms for the cephalic and gastric phases involve only acetylcholine as a mediator. 

A number of factors are concerned with the stimulation of the glands to secrete gastric juice. Initially, in the cephahc phase, stimuli such as the sight and smell of food act via the vagus nerve. Then, in the gastric phase, secretion is maintained by chemical sensors and distension of the stomach. Finally, the presence of digesta in the duodenmn ehdts secretion by neural and hormonal messages. 

Hydrolysis of esterified lipids is essential in order for lipid absorption to occur. Anatomically, lipolysis begins in the stomach where a limited amount of partial hydrolysis of triglycerides provides more polar lipids (fatty acids and partial glycerides) to assist in emulsification. A lingual lipase is thought to be involved in this process. The net result of this gastric phase of fat digestion is the initiation of lipolysis and the preparation of a stable emulsion on which the major pancreatic lipolytic enzymes can act in the milieu of the small intestine. 

Dietary retinyl esters, retinol, and provitamin A carotenoids are dispersed and emulsified in the stomach during the gastric phase of lipid digestion. They then enter the lumen of the duodenum where extensive hydrolysis of retinyl esters takes place. In infants, the bile salt-stimulated lipase in human milk may play a role in retinyl ester hydrolysis in the duodenum (Fredrikzon et al., 1978). The major retinyl ester hydrolase activity that acts in the intestines is, however, derived from the pancreas. 

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