• short gastric SG - supplies area of the fundus
• left gastroepiploic LGE - supplies the left part of greater curvature of the stomach

• gastroduodenal GD
  • right gastric RG - supplies right side of lesser curvature of the stomach
  • right gastroepiploic RGE - supplies the right part of the greater curvature of the stomach

Venous Drainage of the Stomach

The stomach drains either directly or indirectly into the portal vein as follows:

• short gastric veins SGfrom the fundus to the splenic vein S
• left gastroepiploic LGE along greater curvature to superior mesenteric vein SM
• right gastroepiploic RGE from the right end of greater curvature to superior mesenteric vein SM
• left gastric vein LG from the lesser curvature of the stomach to the portal vein PV
• right gastric vein RG from the lesser curvature of the stomach to the portal vein PV

Lymphatic Drainage

Gastric Motility: Filling and Emptying

Contractions of gastric smooth muscle serves two basic functions:

• ingested food is crushed, ground and mixed, liquefying it to form what is called chyme.
• chyme is forced through the pyloric canal into the small intestine, a process called gastric emptying.

The stomach can be divided into two regions on the basis of motility pattern: an accordian-like reservoir that applies constant pressure on the lumen and a highly contractile grinder.

The upper stomach, composed of the fundus and upper body, shows low frequency, sustained contractions that are responsible for generating a basal pressure within the stomach. Importantly, these tonic contractions also generate a pressure gradient from the stomach to small intestine and are thus responsible for gastric emptrying. Interestingly, swallowing of food and consequent gastric distention inhibits contraction of this region of the stomach, allowing it to balloon out and form a large reservoir without a significant increase in pressure

The lower stomach, composed of the lower body and antrum, develops strong peristaltic waves of contraction that increase in amplitude as they propagate toward the pylorus. These powerful contractions constitute a very effective gastric grinder; they occur about 3 times per minute in people and 5 to 6 times per minute in dogs. Gastric distention strongly stimulates this type of contraction, accelerating liquefaction and hence, gastric emptying. The pylorus is functionally part of this region of the stomach - when the peristaltic contraction reaches the pylorus, its lumen is effectively obliterated - chyme is thus delivered to the small intestine in spurts

Gastric motility is controlled by a very complex set of neural and hormonal signals. Nervous control originates from the enteric nervous system as well as parasympathetic (predominantly vagus nerve) and sympathetic systems. A large battery of hormones have been shown to influence gastric motility - for example, both gastrin and cholecystokinin act to relax the proximal stomach and enhance contractions in the distal stomach. The bottom line is that the patterns of gastric motility likely are a result from smooth muscle cells integrating a large number of inhibitory and stimulatory signals.

Liquids readily pass through the pylorus in spurts, but solids must be reduced to a diameter of less than 1-2 mm before passing the pyloric gatekeeper. Larger solids are propelled by peristalsis toward the pylorus, but then refluxed backwards when they fail to pass through the pylorus - this continues until they are reduced in size sufficiently to flow through the pylorus.

Gastric Secretions

see befor in histoly of stomack to know type of cells

Mechanism of Acid Secretion

The hydrogen ion concentration in parietal cell secretions is roughly 3 million fold higher than in blood, and chloride is secreted against both a concentration and electric gradient. Thus, the ability of the partietal cell to secrete acid is dependent on active transport.

The key player in acid secretion is a H+/K+ ATPase or "proton pump" located in the cannalicular membrane. This ATPase is magnesium-dependent, and not inhibitable by ouabain. The current model for explaining acid secretion is as follows:

• Hydrogen ions are generated within the parietal cell from dissociation of water. The hydroxyl ions formed in this process rapidly combine with carbon dioxide to form bicarbonate ion, a reaction cataylzed by carbonic anhydrase.
• Bicarbonate is transported out of the basolateral membrane in exchange for chloride. The outflow of bicarbonate into blood results in a slight elevation of blood pH known as the "alkaline tide". This process serves to maintain intracellular pH in the parietal cell.
• Chloride and potassium ions are transported into the lumen of the cannaliculus by conductance channels, and such is necessary for secretion of acid.
• Hydrogen ion is pumped out of the cell, into the lumen, in exchange for potassium through the action of the proton pump; potassium is thus effectively recycled.
• Accumulation of osmotically-active hydrogen ion in the cannaliculus generates an osmotic gradient across the membrane that results in outward diffusion of water - the resulting gastric juice is 155 mM HCl and 15 mM KCl with a small amount of NaCl.

Control of Acid Secretion

Parietal cells bear receptors for three stimulators of acid secretion, reflecting a triumverate of neural, paracrine and endocrine control:

• Acetylcholine (muscarinic type receptor)
• Gastrin
• Histamine (H2 type receptor)

Histamine from enterochromaffin-like cells may well be the primary modulator, but the magnitude of the stimulus appears to result from a complex additive or multiplicative interaction of signals of each type. For example, the low amounts of histamine released constantly from mast cells in the gastric mucosa only weakly stimulate acid secretion, and similarly for low levels of gastrin or acetylcholine. However, when low levels of each are present, acid secretion is strongly forced. Additionally, pharmacologic antagonists of each of these molecules can block acid secretion.

Histamine’s effect on the parietal cell is to activate adenylate cyclase, leading to elevation of intracellular cyclic AMP concentrations and activation of protein kinase A (PKA). One effect of PKA activation is phosphorylation of cytoskeletal proteins involved in transport of the H+/K+ ATPase from cytoplasm to plasma membrane. Binding of acetylcholine and gastrin both result in elevation of intracellular calcium concentrations.

The animation below depicts acid secretion by the parietal cell. Even though many of the actors are unlabeled, you should be able to deduce the identity of all the components you see.

The Gastrointestinal Barrier

The gastrointestinal mucosa forms a barrier between the body and a lumenal environment which not only contains nutrients, but is laden with potentially hostile microorganisms and toxins

The gastrointestinal barrier is often discussed as having two components:

• The intrinsic barrier is composed of the epithelial cells lining the digestive tube and the tight junctions that tie them together.

• The extrinsic barrier consists of secretions and other influences that are not physically part of the epithelium, but which affect the epithelial cells and maintain their barrier function

Disruption of Barrier Function

Despite its robust and multi-faceted nature, the gastrointestinal barrier can be breached. Local infections by bacteria and virus, exposure to toxins or physical insults, and a variety of systemic diseases lead to its disruption. Such problems can be mild and readily repaired, or massive and fatal.

The micrographs below depict severe disruption of the barrier. On the left is mucosa from a normal canine small intestine, with large villi covered by intact epithelium extended into the lumen. The image on the right (same magnification) shows small intestinal mucosa from a dog that died of Salmonella enteritis - note the totally denuded epithelium and destruction of villi.

Ischemia and Reperfusion Injury

Damage to the gastrointestinal barrier due to ischemia and reperfusion injury is a common and serious condition. Ischemia occurs when blood flow is insufficient to deliver an amount of oxygen and nutrients necessary for maintenance of cell integrity. Reperfusion injury occurs when blood flow is restored to ischemic tissue.

Gastrointestinal ischemia results from two fundamental types of disorders, both of which can compromise the epithelial barrier:

• Non-occlusive ischemia results from systemic conditions such as circulatory shock, sepsis or cardiac insufficiency.
• Occlusive ischemia refers to conditions that directly disrupt gastrointestinal blood flow, such as strangulation, volvulus or thromboembolism

Neutrophils and Mucosal Injury

Diverse insults to the intestinal mucosa, including infectious processes, ischemia and damaging chemicals, promote infiltration of neutrophils. This common endpoint results because many types of injuries lead to local production of neutrophil chemoattractants such as leukotrienes, interleukins and activated complement components. In response to chemoattractants, neutrophils migrate out of capillaries, infiltrate the subepithelial mucosa and often transmigrate through the gastric or intestinal epithelium. In crossing the epithelium, neutrophils must break junctional complexes between epithelial cells. This "impalement" through tight junctions necessarily causes transient increases in permiability. When the insult is minor, the junctions reseal quickly, but transmigration of large numbers of neutrophils induces significant damage to barrier function.

Effects of Stress

Stress comes in a myriad of forms and is an integral part of all illness and trauma. The stress response involves modulation of literally dozens of hormones and cytokines, as well as significant effects on neurotransmission. However, the foremost effect of stress on the gastrointestinal tract is to decrease mucosal blood flow and thereby compromise the integrity of the mucosal barrier. Among other things, reduced mucosal blood flow suppresses production of mucus and limits the ability to remove back diffusing protons. As a consequence, significant stress is almost always associated with mucosal erosions, particularly in the stomach. A majority of these lesions are subclinical, but gastrointestinal hemorrhage and sepsis are not infrequent consequences.

Restitution and Healing After Injury

The critical first task following disruption of the gastrointestinal epithelium is to cover the denuded area and re-establish the intrinsic barrier. This rapid restoration of epithelium is accomplished by a process called restitution - epithelial cells adjacent to the defect flatten and migrate over the exposed basement membrane. In the small intestine, this process is aided by a rapid contraction and shortening of the affected villi, which reduces the area of basement membrane that must be covered.

Restitution provides a rapid mechanism for covering a defect in the barrier and does not involve proliferation of epithelial cells. It results in an area that, while protected, is not physiologically functional. Healing requires that the epithelial cells on the margins of the defect proliferate, differentiate and migrate into the damaged area to restore the normal cellular architecture and function.