1. Gastrointestinal Motility, Propulsion and Digestion

2. Learning Objectives
GIT anatomy and the movement of food through the alimentary tract.
Know the basic anatomy of the GI tract, including the circulation and structure of the intestinal wall.
Understand how peristalsis provides GI motility and mixes food.
Understand neuronal control of the GI tract and the types of electrical signals used by those neurons.
Know the basic processes of digestion as food passes from the beginning to the end of the alimentary tracts.

3. Alimentary Tract
The general purpose of the alimentary tract is to absorb H2O, electrolytes and nutrients from ingested food and liquid.
This requires:
- Propelling of contents
- Digestion of contents
- Absorption of nutrients
- Large supply of blood flow (~ 25% of total)

4. Alimentary Tract Anatomy
From beginning to end:
Mouth
Esophagus
Stomach
Small intestine
Duodenum (26 cm = 9.8’’)
Jejunum (2.5 m = 8.2 ft)
Ileum (3.5 m = 11.5 ft)
Large intestine (1.5 m = 4.9 ft)
Cecum
Ascending colon
Transverse colon
Descending colon
Anus

5. Overview of GI Blood Flow

6. Arterial Blood Supply to the Intestines
As you would expect, there is extensive blood flow for nutrient absorption
We will revisit the GI circulation and absorption of nutrients.

7. Microvasculature of Intestines

8. Intestinal Wall

9. GI Motility 2 Types of movement in the GI tract.
Propulsive movement of food forward at an appropriate rate for digestion and absorptiion.
Mixing movements – caused by peristalsis and local intermittent contractions.

10. Peristalsis
The propulsive movement in the GI is achieved by peristalsis.

11. Muscle Contraction for Peristalsis
The smooth muscle of the gut is a syncytium.
Thus, stimulation at 1 point spreads to adjacent areas, creating a peristaltic spread.
Peristalsis also occurs in the bile ducts, glandular ducts, and ureters.

12. Stimulation of Peristalsis
Stretching of the gut wall, such as occurs with a large amount of food, stimulates contraction 2-3 cm behind the stretched wall.
This initiates the peristalsis that propels the food forward.
Other stimuli include parasympathetic signals and physical or chemical irritation of the epithelial lining.

13. Neurons Controlling Peristalsis
The myenteric plexus primarily controls peristalsis. It is an interconnected chain of neurons
between the longitudinal and circular layers of muscle that extends the entire length of the
GI tract.
The submucosal plexus mainly controls GI secretion and local blood flow.

14. Myenteric Plexus Stimulation of the myenteric plexus causes:
- Increased tonic contractions
- Increased intensity of contractions
- Slight increase in rhythm of contractions
- Increased velocity of excitatory waves along the gut wall
Blocking the myenteric plexus or its parasympathetic stimulation greatly decreases peristalsis.

15. Directional Movement in GI Tract
The forward movement of food is achieved by:
- The initiation or peristalsis 2-3 cm behind the distended wall.
- Relaxation of the gut wall in from of the distended wall.
This pattern requires the myenteric plexus and is called the meyenteric or peristaltic reflex.

16. Electrical Activity in GI Smooth Muscle
Excited by fairly constant, slow electrical activity that consists of 2 types of electrical activity:
Slow waves
Spikes
Note: the resting membrane potential can be adjusted. This is important, as spikes occur once a threshold resting membrane potential is reached.

17. Slow Waves
Slow waves are undulating changes in the resting membrane potential caused by the entry of Na+.
The frequency of the slow waves sets the rhythm of contractions.
However, the slow waves themselves do not usually cause the contractions. They drive the membrane to threshold, which causes spikes to occur.
Spikes cause the contraction

18. Spikes
Spikes are APs, caused by the influx of primarily Ca2+ and some Na+.
They occur once the resting membrane potential depolarizes to ~ 40 mV.
The more depolarized the resting membrane potential becomes during the slow waves, the greater the frequency of spikes.
The Ca2+ that enters the muscle during the spike causes the contraction.

19. Changes in Resting Membrane Potential (RMP)
Factors that depolarize the RMP and increase the excitability are:
- Stretching
- Parasympathetic stimulation (acetylcholine)
- Some GI hormones.
The RMP hyperpolarizes and becomes less excitable by sympathetic stimulation (norepinephrine and epinephrine).

20. Tonic Contractions
Tonic contractions are continuous instead of rhythmical and last several minutes-to-hours.
They are caused by:
- Repetitive spikes
- Continuous depolarization
- Continuous entry of Ca2+

21. Transition Slide
So far, we have discussed the general anatomy of the alimentary tract and how food is propelled via peristaltic contractions.
Now, we will describe broadly the events that occur as food passes through the alimentary tract.

22. Chewing and Swallowing
Briefly,
Mastication breaks apart indigestible components and greatly increase the surface area exposed to digestive enzymes.
During swallowing, the trachea closes, the esophagus opens, and a peristaltic wave moves the food into the upper esophagus.
In the esophagus, peristaltic waves propel the food into the stomach.

23. Stomach
The stomach has a capacity of L and is divided into 2 sections: the body (upper 2/3) and the antrum (lower 1/3).
Food processed in the stomach is ultimately forced through the pyloris into the duodenum.
The stomach performs 3 functions:
Storage of food
Mixing with gastric secretions to form a semifluid mixture called chyme.
Emptying of chyme at suitable rate for digestion.

24. Mixing and Propulsion in the Stomach
When food is present, peristaltic constrictor waves or mixing waves begin in the body and move toward the antrum. The rhythm of the constrictor waves is set by the slow waves.
In addition, the constrictor waves dig deep into the food contents of the antrum. This mixes the food and exposes more food to digestive juices that are secreted by the walls of the stomach.
At the pyloris, some of the processed food (chyme) is passed into the duodenum; however, most of it is pushed back upstream by strong contractions (increasing the mixing).

25. Stomach Emptying
Most of the stomach contractions mix the food with gastric juices.
Strong contractions occur ~ 20% of the time. These propel larger amounts of chyme through the pyloris (pyloric pump).
The pyloris is tonically contracted to a point where fluid easily passes, but unprocessed food does not.

26. Regulation of Stomach Emptying by the Stomach
Stomach emptying is regulated somewhat by the stomach itself. Stretching stimulates myenteric reflexes that enhance the pylorc pump, relaxes the pyloris and stimulates the release of the hormone, gastrin.
Gastrin causes the secretion of acidic gastric juices and moderately stimulates the pyloric pump.
The digestive products of meat also stimulate gastrin release.

27. Regulation of Stomach Emptying by the Duodenum
A more important regulator of stomach emptying is the duodenum.
Control by the duodenum prevents the movement of excess food into intestines. Too much food would limit the ability to reabsorb nutrients.
The inhibition of stomach emptying by the duodenum is mediated by nervous reflexes and hormones.

28. Inhibition of Stomach Emptying by the Duodenum Nerve Reflexes
Factors that inhibit stomach emptying by the duodenum are:
- Distension of the duodenum
- High acidity of the chyme
- Hypertonic and hypotonic chyme (particularly hypertonic)
- Breakdown products of proteins and to a lesser extent, fat
- Irritation of the duodenum

29. Inhibition of Stomach emptying by the Duodenum Hormones
Fats in the duodenum inhibit stomach emptying by extracting hormones from the epithelium.
One important hormone is cholecystokinin (CCK). Other hormones will be discussed later.
CCK inhibits stomach motility induced by gastrin.

30. Movement in the Small Intestine
Stretching of the intestine causes peristaltic contractions that cause forward movement and mixing.
Movement is slow to allow greater absorption of nutrients (1 cm/min). At this rate, it takes 3-5 hr for food to pass through the small intestine.
Hormones that increase peristaltic activity are gastrin, CCK, insulin, motilin, and serotonin.
Hormones that inhibit intestinal motility are secretin and glucagon.

31. Peristatic Rush
Normally, peristalsis in the small intestine is weak. As indicated by the slow movement of food.
However, irritation, as occurs with infectious diarrhea, causes rapid and powerful peristalsis.
This involves the autonomic nervous system and intrinsic control of the myenteric plexus.

32. Movements in the Colon
The colon absorbs water and nutrients, progressively making solid feces.
It also stores the solid feces until it can be expelled.
Movement is slow, requiring 8-15 hr to move material through the colon.
Movement and mixing are achieved by peristaltic-like contractions.

33. Haustrations
The combination of constricted and relaxed portions of the colon create haustrations (bag-like pouches).
Haustrations mix the chyme or fecal material and provide slow persistent forward movement.

34. Propulsive (Mass) Movements
Occasionally (1-3 times/day), a modified contraction will propel the contents forward en masse.
This occurs by a peristaltic contraction pushing the contents through 20 cm or more of colon in which the haustrations are relaxed.
A series of mass movements persist for min; then cease. They may recur ~ 12 hr later.
Irritation can cause mass movements.

35. Defecation
Feces entering the rectum stretches the walls and stimulates the myenteric plexus to initiate peristaltic contractions in the descending colon downward.
The myenteric plexus relaxes the internal sphincter.
If the external sphincter is voluntarily relaxed, defecation occurs.
This is augmented by parasympathetic activity.