Introduction
Different hormones, neurotransmitters and reflexes are involved in the complicated process of feeding in animals. Secretions and motility of the gastrointestinal tract are stimulated and carefully regulated by numerous factors, including environmental stimuli and the presence of food in different parts of the gastrointestinal tract from the oral cavity right through to the intestines.
When a harmful substance is ingested the body acts to eliminate it in different ways to prevent the animal becoming ill, for example, through vomiting and diarrhoea.
If one or more of the pathways in controlling feeding is damaged or inhibited, then problems such as obesity occurs.
Feeding Methods
- Absorption over body surface
- Fluid feeding
- Piercing and sucking
- Cutting and biting
- Herbivores and grazing
- Invertebrates
- Vertebrates- bony plates or teeth
Functions of the GIT
The main function of the GIT is to efficently breakdown feed to the essential nutrients that can then be absorbed. The GIT then acts to propell the waste fed material out of the body. The following functions constitute this main function;
- Secretion of enzymes and co-factors for digestion including water, ions and mucous
- Motility for forward propulsion, mechanical breakdown, mixing of ingesta and sphincter tone
- Migrating myoelectric complex to prevent debris accumulation
- Peristalsis
- Haustration
- Segmental motility
- Blood flow to muscles, submucosa and epithelial surfaces to sustain secretion, motility and the uptake of products of digestion
Control of the GIT
- Endocrine hormones released into the circulation by cells within the GIT or an accessory organ
- Paracrine mediators released by cells within the tract and diffuse locally to act on neighbouring target cells
- Neurotransmitters from nerves and other cells
- Autonomic nervous system superimposed over the local control
Control of Motility
- Intrinsic
- Muscle pacemaker cells (Cajal cells)
- Set a basic electric rhythm (BER) of 3-20 per minute
- Passes through gap junctions
- Action potential created producing a slow wave of contraction
- Likelihood of an action potential is increased through the stretch of food in the lumen and chemical food stimulation
- Endocrine, paracrine or neural enter the enteric nervous system via sensory neurones
- Neurons interact with plexuses in the GIT wall
- Myenteric plexus controls muscle movement
- Submucosa plexus controls secretion and blood flow
- 2 plexuses connected by interneurones to co-ordinate control
- Autonomic nervous system superimposed
- Excitatory neurotransmitters are parasympathomimetic
- ACh (muscarinic M1 and M2)
- Serotonin
- Substance P
- Inhibitory neurotransmitters are sympathomimetic
- Vasoactive intestinal polypeptide (VIP)
- Nitric oxide (NO)
- ATP
- Enkephalins
- Extrinsic - Autonomic nervous system (ANS)
- Sympathetic via norepinephrine (A1 and B2)
- Thoraco-lumbar innervation
- Parasympathetic via ACh (M1 and M2)
- Cranio-sacral innervation
Control of GIT Secretions
- Presence of food in the GIT is detected by open chemoreceptors
- Signals to the endocrine cells or via the ANS releases gastrointestinal peptide hormones
- These hormones act to promote secretion, provide negative feedback or affect motility
- Closed mechanoreceptors also act to alter secretions
- Conditioned (associative) and unconditioned responses act via the ANS
| Control Method
|
Neural
|
Endocrine
|
| Saliva
|
Yes
|
No
|
| Stomach
|
Yes
|
Yes
|
| Small Intestine
|
No
|
Yes
|
Phases of Gastric Secretion
Cephalic
Cephalic phase of secretion - Copyright RVC 2008
- Sight, smell, taste of food
- Vagus nerve (CN X)
- Parasympathetic fibres
- Synapse in submucosal plexus
- Gastrin secreted from endocrine cells in pyloric mucosa
- Postganglionic fibres activate chief, parietal, mucous and G cells
- Histamine secreted from paracrine action
- Increase stomach motility by release of hydrochloric acid and pepsinogen
- Overlaps with gastric phase of secretion
- Inhibited by stress, increased by aggression
Gastric control of secretion - Copyright RVC 2008
Gastric
- Chemical and mechanical receptors in stomach respond to stretch and chemical stimulation
- Increase in pH of gastric contents
- Response to undigested materials, especially proteins
- Negative feedback loop by sympathomimetic somatostatin released by paracrine method to inhibit gastrin secretion (when pH falls below 3)
- Submucosal and myenteric plexuses activated in vagus reflex arcs
- Postganglionic release of ACh at parietal cells
- Neural response and presence of peptides in chyme stimulate gastrin release
- Parietal and chief cells stimulate via gastrin acting in the bloodstream
Intestinal control of secretion - Copyright RVC 2008
Intestinal
- Chyme in the duodenum inhibits acid secretion and motility by decreasing the stomach distension and increasing the stretch of the duodenum leading to the enterogastric reflex
- A drop in pH below 4.5 causes release of secretin which inhibits parietal and chief cells and stimulate buffer release from the pancreas
- Chyme causes release of secretin, GIP and CCK decreasing gastric sectreions and motility
Pancretic control of secretion - Copyright RVC 2008
Pancreatic
- Parasympathetic stimulation during cephalic and gastric phases
- Negative feedback from paracrine sympathomimetics (somatostatin and enkephalins)
Biliary
- Secretin stimulates hydrogencarbonate ions from bile duct
Small Intestinal
- Vagal tone and parasympathomimetic reflex
Neuroendocrine Regulation of Feeding
- Major hypothalamic nuclei involved:
Gut Peptides
| Peptide
|
Site of Release
|
Effect on Feeding
|
| CCK
|
Duodenum
|
Reduces food intake
|
| Ghrelin
|
Gastric fundus
|
Increases food intake
|
| GLP-2
|
Intestine
|
Reduces food intake
|
| Motilin
|
Small intestine
|
Indirectly inhibits food intake
|
| Oxyntomodulin
|
large intestine
|
Inhibits food intake
|
| Pancreatic Polypeptide
|
Pancreas
|
Inhibits food intake
|
| PYY3-36
|
Intestine
|
Inhibits food intake
|
| Somatostatin
|
Pancreas
|
Inhibits food intake
|
Other Peptides
The Vomit Reflex
The Vomit Reflex - Copyright nabrown RVC
- Emesis is the process of vomiting
- Persistent vomiting can be exhausting and can lead to metabolic alkalosis, dehydration and electrolyte inbalances which may require fluid therapy
- Extreme cases of persistent vomiting can lead to shock
- Retching involves the abdominal and chest walls contracting
- Vomiting includes retching and the action of the diaphragm
- Diaphragm moves caudal to open the cardia
- Gastrointestinal tract have protective stimuli to recognise harmful products ingested. The mechanoreceptors and chemoreceptors respond using viscerent afferent pathways.
- Medulla co-ordinates process
- Chemoreceptive trigger zone in the 4th ventricle responds to blood and CSF
- Inputs also from inner ear and higher centres
- Emetic agents can be used in cases of gastric obstruction and to remove non-corrosive poisons from the stomach (for corrosive poisons charcoal can be used which will help adsorb the substance and decrease its absorbtion into the GIT)
- For more information on emetic and anti-emetic drugs click here
Emetic agents
- Drugs cause emesis by irritating the gastric mucosa
- Histamine
- ACh
- Dopamine
- Catecholamines
- 5-hydroxytryptamine
- Substance P
- Enkephalins
- NK1 receptor agonists
Anti-emetic agents
- Anti-emetic agents can be used to treat motion sickness and to treat or prevent vomiting
- Dopamine (D2) receptor antagonists
- 5-hydroxytryptamine antagonists
- NK1 receptor antagonists
- Muscarinic receptor antagonists
- Histamine (H1) receptor antagonists
- Gastroprotective agents
Species Differences
Equine
The anatomy of the equine stomach, the close proximity of the exiting duodenum and the entering oesophagus along with the well developed cardiac sphincter, make it difficult for the horse to vomit. However on rare occasions it does occur.
