Ganong's Review of Medical Physiology, 23rd Edition

474
SECTION V
Gastrointestinal Physiology

contraction increases intra-abdominal pressure. The lower
esophageal sphincter and the esophagus relax, and the gastric
contents are ejected. The “vomiting center” in the reticular
formation of the medulla (Figure 28–6) consists of various
scattered groups of neurons in this region that control the dif-
ferent components of the vomiting act.

Irritation of the mucosa of the upper gastrointestinal tract is

one trigger for vomiting. Impulses are relayed from the

mucosa to the medulla over visceral afferent pathways in the

sympathetic nerves and vagi. Other causes of vomiting can

FIGURE 28–5
Effect of protein and fat on the rate of
emptying of the human stomach.
Subjects were fed 300-mL liquid
meals.
(Reproduced with permission from Brooks FP: Integrative lecture. Response
of the GI tract to a meal.
Undergraduate Teaching Project.
American
Gastroenterological Association, 1974.)

Mean

± S.E.

300

200

100

0

20 60 100

Protein Protein

+ lipid

Standard meal

(inert pectin)

Time after feeding (min)

(300-mL liquid meals)

Volume of test meal emptied (mL)

CLINICAL BOX 28–2

Consequences of Gastric Bypass Surgery

Patients who are morbidly obese often undergo a surgical

procedure in which the stomach is stapled so that most of it

is bypassed, and thus the reservoir function of the stomach is

lost. As a result, such patients must eat frequent small meals.

If larger meals are taken, because of rapid absorption of glu-

cose from the intestine and the resultant hyperglycemia and

abrupt rise in insulin secretion, gastrectomized patients

sometimes develop hypoglycemic symptoms about 2 h after

meals. Weakness, dizziness, and sweating after meals, due in

part to hypoglycemia, are part of the picture of the

“dump-

ing syndrome,”

a distressing syndrome that develops in pa-

tients in whom portions of the stomach have been removed

or the jejunum has been anastomosed to the stomach. An-

other cause of the symptoms is rapid entry of hypertonic

meals into the intestine; this provokes the movement of so

much water into the gut that significant hypovolemia and

hypotension are produced.

FIGURE 28–6
Neural pathways leading to the initiation of vomiting in response to various stimuli.

Pain

Sights

Anticipation

Motion

Vertigo

Drugs

eg, opiates, chemotherapy

Hormones

eg, pregnancy

Ipecac

Cytotoxic drugs

Irritants

Vagus nerve

Higher

centers

Gastric

mucosa

Nucleus

tractus solitarius

Pharyngeal

stimulation

Glossopharyngeal

nerve

Brain stem

vomiting center

Area postrema

chemoreceptor

trigger zone

Cerebellum

Labyrinth

Programmed

vomiting

response