Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 28

Gastrointestinal Motility 473

AEROPHAGIA & INTESTINAL GAS

Some air is unavoidably swallowed in the process of eating and
drinking
(aerophagia).
Some of the swallowed air is regurgi-
tated (belching), and some of the gases it contains are ab-
sorbed, but much of it passes on to the colon. Here, some of
the oxygen is absorbed, and hydrogen, hydrogen sulfide, car-
bon dioxide, and methane formed by the colonic bacteria
from carbohydrates and other substances are added to it. It is
then expelled as
flatus.
The smell is largely due to sulfides. The
volume of gas normally found in the human gastrointestinal
tract is about 200 mL, and the daily production is 500 to 1500
mL. In some individuals, gas in the intestines causes cramps,
borborygmi
(rumbling noises), and abdominal discomfort.

STOMACH

Food is stored in the stomach; mixed with acid, mucus, and
pepsin; and released at a controlled, steady rate into the
duodenum.

GASTRIC MOTILITY & EMPTYING

When food enters the stomach, the fundus and upper portion

of the body relax and accommodate the food with little if any

increase in pressure

(receptive relaxation).

Peristalsis then

begins in the lower portion of the body, mixing and grinding

the food and permitting small, semiliquid portions of it to pass

through the pylorus and enter the duodenum.

Receptive relaxation is vagally mediated and triggered by

movement of the pharynx and esophagus. Peristaltic waves

controlled by the gastric BER begin soon thereafter and sweep

toward the pylorus. The contraction of the distal stomach

caused by each wave is sometimes called

antral systole

and

can last up to 10 s. Waves occur three to four times per minute.

In the regulation of gastric emptying, the antrum, pylorus,

and upper duodenum apparently function as a unit. Contrac-

tion of the antrum is followed by sequential contraction of the

pyloric region and the duodenum. In the antrum, partial con-

traction ahead of the advancing gastric contents prevents

solid masses from entering the duodenum, and they are

mixed and crushed instead. The more liquid gastric contents

are squirted a bit at a time into the small intestine. Normally,

regurgitation from the duodenum does not occur, because the

contraction of the pyloric segment tends to persist slightly

longer than that of the duodenum. The prevention of regurgi-

tation may also be due to the stimulating action of cholecysto-

kinin (CCK) and secretin on the pyloric sphincter.

REGULATION OF GASTRIC

MOTILITY & EMPTYING

The rate at which the stomach empties into the duodenum de-

pends on the type of food ingested. Food rich in carbohydrate

leaves the stomach in a few hours. Protein-rich food leaves

more slowly, and emptying is slowest after a meal containing

fat (Figure 28–5). The rate of emptying also depends on the os-

motic pressure of the material entering the duodenum. Hy-

perosmolality of the duodenal contents is sensed by “duodenal

osmoreceptors” that initiate a decrease in gastric emptying

which is probably neural in origin.

Fats, carbohydrates, and acid in the duodenum inhibit gas-

tric acid and pepsin secretion and gastric motility via neural

and hormonal mechanisms. The hormone involved is proba-

bly peptide YY. CCK has also been implicated as an inhibitor

of gastric emptying (Clinical Box 28–2).

VOMITING

Vomiting is an example of central regulation of gut motility

functions. Vomiting starts with salivation and the sensation of

nausea. Reverse peristalsis empties material from the upper

part of the small intestine into the stomach. The glottis closes,

preventing aspiration of vomitus into the trachea. The breath

is held in mid inspiration. The muscles of the abdominal wall

contract, and because the chest is held in a fixed position, the

CLINICAL BOX 28–1

Motor Disorders of the Esophagus

Achalasia

(literally, failure to relax) is a condition in which

food accumulates in the esophagus and the organ be-

comes massively dilated. It is due to increased resting LES

tone and incomplete relaxation on swallowing. The myen-

teric plexus of the esophagus is deficient at the LES in this

condition and the release of NO and VIP is defective. It can

be treated by pneumatic dilation of the sphincter or inci-

sion of the esophageal muscle (myotomy). Inhibition of

acetylcholine release by injection of botulinum toxin into

the LES is also effective and produces relief that lasts for

several months. The opposite condition is LES incompe-

tence, which permits reflux of acid gastric contents into the

esophagus

(gastroesophageal reflux disease).

This com-

mon condition causes heartburn and esophagitis and can

lead to ulceration and stricture of the esophagus due to

scarring. In severe cases, the intrinsic sphincter, the extrin-

sic sphincter, and sometimes both are weak, but less severe

cases are caused by intermittent periods of poorly under-

stood decreases in the neural drive to both sphincters. The

condition can be treated by inhibition of acid secretion

with H

2

receptor blockers or omeprazole (see Chapter 26).

Surgical treatment in which a portion of the fundus of the

stomach is wrapped around the lower esophagus so that

the LES is inside a short tunnel of stomach

(fundoplica-

tion)

can also be tried, although in many patients who un-

dergo this procedure the symptoms eventually return.