Friday, 18 May 2012

The Monogastric Stomach

Hello :) In this post we’ll be taking a look at the structure and functions of the monogastric stomach. We’ll discuss the species differences in the composition of gastric mucosa, the motility patterns that occur in the stomach and how these assist the processing of digesta. In addition, I’ll explain the neurohormonal regulation of gastric emptying and the passage of digesta into the duodenum as well as the mechanism and regulation of acid and pepsin secretion. We’ll finish off by discussing the main mechanisms that protect the gastric lining from damage by the gastric secretions. If you have any questions please don’t forget to ask in the comments section of this post.

Structure and Functions of the Monogastric Stomach

The stomach functions in the storage and mixing of digesta with gastric secretions. It is also involved in the mechanical and chemical break down of food as well as the delivery of digesta to the small intestine at a rate optimal for digestion and absorption.

The stomach of a monogastric animal (such as a dog, pig or human) contains four regions:
  • Cardia 
  • Fundus: this section receives and stores food. 
  • Corpus (body): this acts as a mixing chamber.
  • Pyloric (antrum): this region is involved with emptying, trituration (grinding) and mixing. The wall of the stomach is thickest in the pyloric region because this is where most of the movement occurs.
There may be differences in the mucosa between species. For example, the oesophageal portion occupies about 30% of the equine stomach but much less in other species.  

The proximal region of the stomach acts as a reservoir to store food and its wall undergoes receptive relaxation and adaptive relaxation to accommodate the meal. The tonic contractions of the proximal gastric wall push the digesta towards the antrum. These tonic contractions are gentle and create a low pressure.

Motility Patterns in the Stomach

As mentioned earlier, the proximal region of the stomach undergoes receptive and adaptive relaxation. Receptive relaxation is triggered by swallowing and the stimulation of pharyngeal mechanoreceptors. Afferent nerve fibres carry impulses to the central nervous system and efferent vagal fibres innervate the inhibitory nerves in the gastric wall. During adaptive relaxation distension of the gastric wall activates stretch receptors which initiate a vagovagal reflex. Here, the efferent fibres also innervate the inhibitory nerves in the gastric wall. 

Motility also occurs in the distal stomach. Emptying of the stomach involves 3 steps:
1.       Contraction waves start in the corpus
2.       When this wave reaches the antrum, the pyloric sphincter opens and the pressure in the antrum moves the chyme into the duodenum.
3.       When the wave reaches the pyloric sphincter it closes. Antral contraction then propels the chyme back into the gastric body and this mixes the contents.

Sieving and trituration also occur in the stomach. Antral contractions grind large particles and moves them back into the gastric body where they are digested further. The antrum also acts like a sieve and prevents larger particles from passing into the duodenum.

In the stomach, slow waves of contraction are generated by the interstitial cells of Cajal which lie between the circular and longitudinal layers of muscle. These cells act as pacemaker cells for the stomach.


Gastric emptying is regulated by several factors. Emptying will be stimulated by:
  • Dilation of the stomach: this increases the activity of the stretch-sensitive sensory cells which leads to increased contraction of smooth muscle cells and the secretion of gastrin and emptying of the stomach increases. 
  • Peptides in the stomach: This also increases the secretion of gastrin which causes more smooth muscle cells to contract and causes the stomach to empty more.
When there is a high concentration of peptides, high pressure, and high osmolarity in the duodenal lumen, and a low pH the activity of the sensory cells in the duodenum increase. This is detected by the central nervous system which stimulates the sympathetic and inhibits the parasympathetic nerve fibres to the stomach. This results in less emptying of the stomach. In addition, a high fat content will cause the release of hormones from the duodenal epithelium (mainly CCK) and this produces the same effect.

Acid and Pepsin Secretion in the Stomach

Hydrochloric acid is generated by the parietal (aka. Oxyntic) cells in the wall of the fundus and body of the stomach. It is generated by the action of the enzyme carbonic anhydrase which is located inside the cell. This enzyme produces H+ and HCO3- from carbon dioxide and water. The H+ ions which are produced are secreted via the K+/H+ ATPase counter-transporter (this is often called a ‘proton pump’). The H+ is transported against a steep concentration gradient and so this process requires energy. The HCO3- which is produced diffuses into the extracellular fluid and blood plasma, increasing the pH of the blood. Some of this bicarbonate also diffuses into the mucosal capillary in exchange for a Cl- ion. It then diffuses into the mucosal cell and helps protect the cells from acid damage. The main role of gastric acid is to facilitate the conversion of pepsinogen to pepsin.

Gastric acid secretion is regulated by three substances:
  • 1.  Gastrin (which binds with a CCK-2 receptor) 
  • 2.       Histamine (which binds with a H-2 receptor) 
  • 3.       Acetylcholine (which binds to a M3 receptor)
The stimulation of all three receptors is necessary for the maximal secretion of acid. The blocking of any one of these receptors will greatly reduce the response of the other two.

Mechanisms That Protect the Gastric Lining

Mucus is continually secreted onto the surface of mucosal epithelial cells and acts as a physical barrier which ‘sticks’ to the epithelium. Bicarbonate, which is produced by parietal cells during acid secretion, reaches the mucosal epithelial cells via the blood stream. It is then secreted into the mucus layer and this produces a neutral pH next to the epithelial cells. The bicarbonate acts to neutralise the hydrogen ions that penetrate the mucus layer.

Glycoproteins and phospholipids are secreted by gastric epithelial cells and also help to protect the epithelial cells. The glycoproteins form a barrier which prevents pepsin from diffusing while the phospholipids provide a hydrophobic layer at the base of the mucus layer. This provides extra protection against water-soluble acids.

The cell membranes of the gastric epithelial cells also act as a barrier to acid damage. These cells also contain intracellular amounts of HCO3- and this protects the cell from acid that back-diffuses into the cell.

Another mechanism which protects the mucosa is the fact that the epithelial cells are continually being renewed. The surface mucus cells are replaced by new cells every three days. This cell renewal is mainly controlled by gastrin but other growth factors may be involved.

In addition, all defence mechanisms depend on the maintenance of mucosal blood flow. The actions of prostaglandins (PGs) have an important role here. Factors that compromise blood flow, such as shock or the production of PG’s predispose animal to ulcers.  

 That's all for this post, see you next time :)

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