Vol. 19, No.

6 June 1997 V

Continuing Education Article N E W ! C O N T I N U I N G E D U C AT I O N S E R I E S

Refereed Peer Review Successfully complete the quizzes at the end of each CE article in this series,
and receive a certificate indicating completion of a course of study in
Gastrointestinal Prokinetic Therapy. This is the fifth of five articles.

FOCAL POINT
Diagnosis and
★Disorders of gastrointestinal
motility are a common cause of
Management of
gastroenterologic disease in dogs
and cats.
Gastrointestinal
KEY FACTS
■ Motility disorders can be
Motility Disorders
mechanical or functional in
origin.
in Dogs and Cats
■ Examples of functional
motility disorders of the
esophagus include idiopathic University of Pennsylvania Oregon State University
megaesophagus, dysautonomia,
Robert J. Washabau, VMD, PhD Jean A. Hall, DVM, PhD
hiatal hernia, esophagitis, and
gastroesophageal reflux.

■ The following are functional

motility disorders of the stomach:
infection, inflammation, postgastric
dilatation–volvulus, ulcer, and
T he first four articles in this five-part series on gastrointestinal prokinetic
therapy discussed dopaminergic antagonist drugs, motilin-like drugs,
serotonergic drugs, and acetylcholinesterase inhibitors or parasympathet-
ic potentiating drugs, respectively. This article considers the diagnosis and man-
agement of esophageal, gastric, small intestinal, and colonic motility disorders.
idiopathic disease.
ESOPHAGEAL MOTILITY DISORDERS
■ Functional motility disorders of
Mechanical Obstruction
the intestine include infection,
Anatomic lesions of the esophagus (e.g., tumor, foreign body, stricture, vas-
inflammation, postoperative ileus,
cular ring anomaly, fistula, and gastroesophageal intussusception) impede
and idiopathic and inflammatory
esophageal peristalsis because of mechanical obstruction. Diagnosis of mechan-
bowel disease.
ical obstruction of the esophagus is usually straightforward and involves the use
of survey and contrast radiography, endoscopy, and occasionally ultrasonogra-
■ Examples of functional motility
phy. Mechanical obstruction should be treated as a primary disorder, which
disorders of the colon are feline
might require chemotherapy, surgical resection, endoscopic or surgical removal
idiopathic megacolon and
of foreign bodies, endoscopic or surgical reduction of intussusception, or bal-
inflammatory bowel disease.
loon dilation or bougienage (Figure 1).

Functional Obstruction
Cricopharyngeal Achalasia
Cricopharyngeal achalasia, a disorder of the cricopharyngeal sphincter, is
Small Animal The Compendium June 1997

ESOPHAGEAL MOTILITY DISORDER

Mechanical disorders Functional disorders

Tumor Foreign Stricture Vascular Esophagitis Gastroesophageal Idiopathic

Hiatal
body ring reflux megaesophagus
hernia
anomaly

1. Chemotherapy Endoscopic Surgical 1. Low-fat diet 1. Elevated oral

Balloon
2. Surgical correction 2. Chemical feedings
or dilation
resection diffusion barrier 2. Gastrostomy
surgical or (e.g., sucralfate) tube feedings
removal bougienage 3. H2 receptor 3. Antibiotics
antagonist (e.g., (pneumonia)
cimetidine or
ranitidine)
4. Prokinetic
therapy (e.g.,
cisapride or
metoclopramide)
Key 5. Surgical
correction—
Finding refractory hiatal
Therapy hernia

Figure 1—Management of esophageal motility disorders.

characterized by cricopharyngeal hypertension and in- is questionable, electromyography of the oropharyngeal

adequate relaxation during swallowing. Affected pup-
pies develop progressive dysphagia, and regurgitation is
observed shortly after weaning. Patients make repeated,
nonproductive attempts to swallow that culminate in
regurgitation of undigested food. Coughing develops as
a consequence of food aspiration; pulmonary crackles
may be detected in patients with aspiration pneumonia.
Diagnosis of cricopharyngeal achalasia is technically
difficult and requires videofluoroscopy and esophageal
manometry. Because of the inability to evaluate the
rapid, complex series of events that occurs during swal-
lowing, survey and static barium-contrast radiographs
are not useful in diagnosing the disorder. The videoflu-
oroscopic finding of multiple, nonproductive attempts
at swallowing barium liquid or paste only suggests a di-
agnosis of cricopharyngeal achalasia. Definitive diagno-
sis requires the manometric demonstration of elevated
basal pressures and inadequate relaxation during swal-
lowing.1,2 If manometry is unavailable and the diagnosis
musculature should be performed to exclude the pos-
sibility of a more proximal oropharyngeal motility dis-
order.
Cricopharyngeal achalasia is best treated by cricopha-
ryngeal myotomy. Most patients experience immediate
relief after surgery.3 Effective medical management of
the disorder has not been reported.
Idiopathic Megaesophagus
Congenital megaesophagus in puppies is usually
diagnosed by a history of regurgitation, weight loss,
and/or coughing associated with aspiration pneumonia
as well as by the radiographic finding of generalized
esophageal dilation. An increased incidence has been
reported in Irish setters, Great Danes, German shep-
herds, Labrador retrievers, Chinese shar-peis, and New-
foundlands; heritability has been demonstrated in
miniature schnauzers and wirehaired fox terriers. Al-
though the pathogenesis of the congenital form is not

PROGRESSIVE DYSPHAGIA ■ ELEVATED BASAL PRESSURES ■ REGURGITATION

The Compendium June 1997
completely understood, recent studies suggest a defect
in vagal afferent innervation to the esophagus.4–6 Treat-
ment consists of dietary management and supportive
care for aspiration pneumonia. Some patients exhibit
improvement or resolution of clinical signs with matu-
ration.
Congenital idiopathic megaesophagus has also been
reported in several cats.7,8 Megaesophagus may have
been secondary to pyloric dysfunction in one group of
cats.8
Acquired megaesophagus is a common cause of re-
gurgitation in adult dogs. Like the congenital form, the
disorder is characterized by ineffective esophageal peri-
stalsis and esophageal dilation. Acquired megaesoph-
agus may develop as a consequence of an underlying
disease process (e.g., myasthenia gravis, myositis or my-
opathy, esophagitis, adrenocortical insufficiency, lead
poisoning, distemper, brain stem disease, or dysautono-
mia).9 In most cases, there is no known cause and the
condition is referred to as idiopathic megaesophagus.
The morbidity and mortality of the disorder are un-
acceptably high. Many patients eventually succumb to
the effects of chronic malnutrition and repeated
episodes of aspiration pneumonia.
The minimal diagnostic investigation of acquired
megaesophagus should include complete blood count,
serum chemistry analysis, urinalysis, serology for nico-
tinic acetylcholine receptor antibodies, serum anti-
nuclear antibody titer, survey thoracic radiographs, and
esophageal videofluoroscopy. Additional tests that
might be considered are fecal examination for Spirocer-
ca lupi ova, serum lead concentration, thyroid function
assays, esophageal endoscopy, and electrophysiologic
evaluation (nerve conduction velocity and electromyog-
raphy). The additional medical investigation depends
on the individual case presentation.9,10
The pathogenesis of idiopathic megaesophagus is not
completely understood. The disorder has been com-
pared with esophageal achalasia in humans. Achalasia is
a failure of relaxation of the gastroesophageal sphincter
with secondary dilation of the esophageal body. A sim-
ilar disorder has not been rigorously documented in
dogs.11 Recent studies suggest several important differ-
ences between canine idiopathic megaesophagus and
human achalasia.
In dogs with idiopathic megaesophagus, (1) the re-
sponse of the cricopharyngeal sphincter and gastro-
esophageal sphincter to swallowing is intact and nor-
mal, (2) balloon distention in the proximal esophageal
body induces minimal increases in cricopharyngeal
sphincter pressure, and (3) balloon distention of the
distal esophageal body induces minimal relaxation of
the gastroesophageal sphincter. The diminished motor
DIETARY MANAGEMENT ■ THYROID FUNCTION ASSAYS ■ REFLUX ESOPHAGITIS
Small Animal
response of the cricopharyngeal and gastroesophageal
sphincters to intraluminal stimuli suggests a defect in
the afferent neural pathway,12 like the disturbance that
has been characterized in congenital canine megaesoph-
agus.5,6
Because the gastroesophageal sphincter is normoten-
sive and relaxes appropriately with swallowing in dogs
affected with idiopathic megaesophagus, gastroesoph-
ageal sphincter myotomy cannot be recommended in
treating this disorder. Instead, current therapeutic rec-
ommendations include elevated feedings, treatment for
reflux esophagitis in cases in which it can be demon-
strated, and antibiotic therapy for documented aspira-
tion pneumonia (Figure 1).
Affected animals should be fed a high-calorie diet, in
small, frequent feedings, from an elevated or upright
position to take advantage of gravity drainage through
a nonperistaltic esophagus. Dietary consistency should
be formulated to produce the fewest clinical signs.
Some patients handle liquid diets well; others do better
with solids. Patients that cannot maintain adequate
nutritional balance with oral intake should be fed by
temporary or permanent tube gastrostomy. Gastrosto-
my tubes can be placed surgically or percutaneously
with endoscopic guidance.
Esophagitis, if present, should be treated with oral
sucralfate suspensions (0.5 to 1.0 g three times daily)
and gastric acid secretory inhibitors (e.g., oral or intra-
venous cimetidine at 5 to 10 mg/kg three to four times
daily; oral or intravenous ranitidine at 1.0 to 2.0 mg/kg
two to three times daily; or oral omeprazole at 0.7
mg/kg once daily). Pulmonary infections should be
identified by culture and sensitivity, and an appropriate
antibiotic should be selected for the offending organ-
isms. This may be accomplished by transtracheal wash
or by bronchoalveolar lavage at the time of endoscopy.
It has been suggested that cisapride, a 5-HT4 seroton-
ergic agonist, might improve esophageal peristalsis in
dogs with idiopathic megaesophagus. This would not
seem to be a rational clinical application of the drug be-
cause a smooth muscle prokinetic agent would not be
expected to have much effect on striated muscle func-
tion. Indeed, the prokinetic effect of cisapride in the
esophagus of humans or cats is confined to the lower
esophageal body at the transition zone from striated
muscle to smooth muscle. Cisapride has no effect on
upper esophageal peristalsis in these species. Further-
more, 5-hydroxytryptamine (serotonin) stimulates con-
traction of the smooth muscle of the canine gastro-
esophageal sphincter but does not affect the striated
muscle of the canine esophageal body.13 Cisapride thus
cannot be recommended in treating idiopathic mega-
esophagus in dogs.14,15 A cisapride-induced increase in
Small Animal
gastroesophageal sphincter pressure could diminish
esophageal clearance and worsen clinical signs in dogs
with idiopathic megaesophagus. A preliminary report
suggests that cisapride actually decreases esophageal
transit rate in normal dogs.16
There are no other clinically useful drugs for improv-
ing esophageal peristalsis in dogs with acquired idio-
pathic megaesophagus. Bethanechol chloride, a cho-
linomimetic drug, reportedly increased esophageal
contraction amplitude in dogs with idiopathic mega-
esophagus but did not affect the frequency of motor
response to swallowing.17
Dysautonomia
Dysautonomia is a generalized autonomic neurop-
athy originally reported (as the Key-Gaskell syndrome)
in cats in the United Kingdom. The condition has now
been reported in dogs and cats from Western Europe
and the United States. The clinical signs reflect gen-
eralized autonomic dysfunction; megaesophagus,
esophageal hypomotility, and regurgitation are con-
sistent findings.18 Pathologically, degenerative lesions
are found in autonomic ganglia, intermediate gray
columns of the spinal cord, and some sympathetic ax-
ons. Despite an intensive search for genetic, toxic, nu-
tritional, and infectious causative agents, a definitive
cause has not been established.
The most frequently reported clinical signs are de-
pression, anorexia, constipation, and regurgitation or
vomiting. Fecal and urinary incontinence are reported
less commonly. Physical examination findings that are
consistent with dysautonomia include dry mucous
membranes, pupillary dilation, prolapsed nictitating
membranes, reduced or absent pupillary light reflex,
bradycardia, and areflexic anus. Paresis and conscious
proprioceptive deficits have been reported in a few pa-
tients.18
In most cases, a clinical diagnosis is based on the his-
tory and physical examination findings. Additional
findings that are consistent with the diagnosis include
esophageal dilation and hypomotility on survey and
barium-contrast radiographs, delayed gastric emptying
on barium-contrast radiographs, reduced tear produc-
tion in Schirmer’s tear tests, atropine-insensitive brady-
cardia, and bladder and colonic distention on survey
radiographs. There are few diagnostic differentials to
consider in a cat with the myriad of manifestations
characteristic of this syndrome. Early in the course of
the illness, however, other diagnostic differentials to
consider are colonic or intestinal obstruction, other
causes of megaesophagus, and feline lower urinary tract
disease.
Although supportive care (e.g., artificial tears, elevat-
ESOPHAGEAL PERISTALSIS ■ DEPRESSION ■ CHRONIC GASTRITIS
The Compendium June 1997
ed feedings, expressing the urinary bladder, and antibi-
otics) is the basis of therapy for this disorder, some cats
reportedly demonstrate improvement with parasym-
pathomimetic drugs (e.g., bethanechol or metoclo-
pramide). Gastrostomy tube feeding or total parenteral
nutrition may sustain some patients until they regain
neurologic function. In general, dysautonomia is associ-
ated with a guarded to poor prognosis for long-term
survival in dogs and cats. Although 20% to 40% of
affected cats are likely to recover, recovery may take 2
to 12 months. Complete recovery is uncommon; many
cats are left with residual impairment (e.g., intermittent
regurgitation, dilated pupils, and fecal or urinary in-
continence).
Esophagitis
Esophagitis is an acute or chronic inflammatory dis-
order of the esophageal mucosa that may involve the
underlying submucosa and muscularis. Regurgitation
is the most important sign in cats and dogs with
esophagitis. Severely affected patients may manifest ex-
cessive salivation, dysphagia, and painful swallowing
(odynophagia) with severe inflammation of the esopha-
gus.
Esophagitis most often results from chronic gastritis
with persistent vomiting or, less frequently, from reflux
of gastric juice during anesthetic episodes. Esophagitis
is more likely to develop after repeated episodes of gas-
tric reflux than after a single, long episode of acid expo-
sure.19 Esophageal endoscopy is the preferred method
of diagnosing esophagitis. After predisposing condi-
tions are corrected, therapy for the disorder is based on
drugs that form diffusion barriers (oral sucralfate at 0.5
to 1.0 g three times daily) and H2-receptor antagonists
(e.g., oral or intravenous cimetidine at 5 to 10 mg/kg
three to four times daily). Oral cisapride (0.1 to 0.5
mg/kg two to three times daily) or metoclopramide
(0.2 to 0.5 mg/kg three times daily) can be adminis-
tered to increase gastroesophageal sphincter tone and
reduce reflux (Figure 1).
Hiatal Hernia
Hiatal hernias may occur as congenital or acquired
lesions. Congenital hiatal hernias have been reported in
Chinese shar-peis, English bulldogs, and chow chows
and apparently result from incomplete closure of the
diaphragmatic hiatus during embryologic devel-
opment.20 Clinical signs include regurgitation, vomit-
ing, and dyspnea. Clinical signs result from mechanical
obstruction or the deleterious effects of gastric and in-
testinal juice (e.g., hydrogen ions, pepsins, and bile
salts) on esophageal mucosa. A clinical diagnosis may
be made if a gas-filled, soft tissue opacity is radiograph-
Small Animal
ically evident in the caudodorsal thorax. Affected pa-
tients often fail to respond to medical treatment and
subsequently require surgery (e.g., crural apposition,
gastropexy, and possibly esophagopexy).20
Although the pathogenesis of acquired hiatal hernia
is not completely understood, recent reports suggest
that hiatal hernia is likely to occur secondary to in-
creased intraabdominal pressure with chronic vomiting
disorders.21 Regurgitation is the most important clinical
sign observed in cats and dogs with acquired hiatal her-
nia.20,22 Patients with acquired hiatal hernia usually re-
spond to acid neutralization therapy (e.g., H2-receptor
antagonists and/or application of diffusion barriers)
and occasionally require restorative surgery22 (Figure 1).
Gastroesophageal Reflux
Gastroesophageal reflux has been poorly documented
in veterinary species but is more common than was
previously believed. Reflux is a disorder of the gastro-
esophageal sphincter that permits retrograde movement
of gastrointestinal fluids or ingesta into the esophagus.
Chronic vomiting, disorders of gastric emptying, hiatal
hernia, and anesthesia-induced decreases in gastro-
esophageal sphincter pressure are the major causes of
gastroesophageal reflux in dogs and cats. The normal
esophagus rapidly clears acid by secondary peristalsis;
remaining acid is neutralized by swallowed saliva.23
Anesthetic drugs can decrease gastroesophageal sphinc-
ter pressure,24 reduce peristalsis, and decrease salivation.
The frequency of reflux, the length of contact time,
and the composition of the refluxed material (gastric
acid, pepsin, trypsin, bile salts, and duodenal bicarbo-
nate) determine the severity of the esophagitis. Gastric
acid alone produces mild esophagitis; combinations of
acid and pepsin or trypsin, bicarbonate, and bile salts
produce severe esophagitis.25 The risk of reflux esoph-
agitis is greater with multiple episodes of acid exposure
than with a single, long episode.19
The clinical signs of gastroesophageal reflux are simi-
lar to those of esophagitis. In severe cases, patients may
exhibit regurgitation, salivation, odynophagia, exten-
sion of the head and neck during swallowing, and total
avoidance of food. In milder cases, patients may have
occasional episodes of regurgitation in the early morn-
ing. Such cases probably result from transient relax-
ation of the gastroesophageal sphincter during sleep.26
The history may suggest a diagnosis of gastroesoph-
ageal reflux. Survey thoracic radiographs are often nor-
mal. Videofluoroscopy may demonstrate intermittent
gastroesophageal reflux, but this finding may also be
observed in normal animals without esophagitis.27 En-
doscopy is currently the best means of documenting
mucosal inflammation in the distal esophagus, which is
CRURAL APPOSITION ■ ACQUIRED HIATAL HERNIA ■ CHRONIC VOMITING
The Compendium June 1997
consistent with reflux esophagitis. Definitive diagnosis
requires determinations of gastroesophageal sphincter
pressure and 24-hour intraluminal pH measurement;
these techniques are available only in major referral
centers.
Because dietary fat delays gastric emptying and re-
duces gastroesophageal sphincter pressure, patients
should be fed fat-restricted diets. Owners should avoid
late-night feedings, which tend to reduce gastroesoph-
ageal sphincter pressure during sleep. In addition to nu-
tritional considerations, rational medical therapy for
this disorder includes drugs that form diffusion barriers
(e.g., sucralfate), gastric acid secretory inhibitors (e.g.,
cimetidine, ranitidine, or omeprazole), and pro-
kinetic agents (e.g., cisapride or metoclopramide).
Drugs that form diffusion barriers may be the most
important medical therapy in patients with gastro-
esophageal reflux. Oral sucralfate (0.5 to 1.0 g three
times daily) protects against mucosal damage from gas-
troesophageal reflux and promotes healing of existing
esophagitis. 28 Dogs with refractory cases of gastro-
esophageal reflux should be medicated with acid secre-
tory inhibitors and/or prokinetic agents. The H2-his-
tamine receptor antagonists (e.g., oral or intravenous
cimetidine at 5 to 10 mg/kg three to four times daily
and ranitidine at 1.0 to 2.0 mg/kg two to three times
daily) inhibit gastric acid secretion and reduce the
amount of acid reflux. Omeprazole (0.7 mg/kg once
daily), an H+,K+-ATPase inhibitor, could also be used to
inhibit gastric acid secretion. Oral cisapride (0.1 to 1.0
mg/kg two to three times daily) and metoclopramide
(0.2 to 0.5 mg/kg three to four times daily) are useful
in treating gastroesophageal reflux because they pro-
mote gastric emptying and increase gastroesophageal
sphincter pressure (Figure 1 and Table I).
GASTRIC MOTILITY DISORDERS
Mechanical Obstruction
Anatomic lesions of the pylorus and adjacent duode-
nal segment (e.g., infiltrative pyloric neoplasia, chronic
hypertrophic pyloric gastropathy, chronic hypertrophic
gastritis, eosinophilic gastritis, gastric foreign bodies,
antral polyps, hepatic or pancreatic abscesses, and in-
traabdominal neoplasia) impede gastric emptying be-
cause of mechanical obstruction.29,30 Diagnosis of me-
chanical obstruction is usually straightforward and
involves survey and contrast radiography, ultrasono-
graphy, and/or gastroscopy. Mechanical obstruction
should be treated as a primary disorder (e.g., with en-
doscopic polypectomy, surgical pylorectomy, and gas-
troduodenostomy) (Figure 2). Surgical removal of the
foreign object or the affected area is the preferred thera-
py.29 Gastrointestinal prokinetic agents are contraindi-
The Compendium June 1997 Small Animal

TABLE I
Mechanisms, Sites of Activity, and Indications for Gastrointestinal Prokinetic Agents

Agent Mechanism of Action Sites of Activity Indications

Metoclopramide D2 dopaminergic antagonist LES, stomach, intestine, CRTZ Vomiting disorders,

α2-adrenergic antagonist Stomach gastroesophageal
β2-adrenergic antagonist Stomach reflux, delayed
5-HT4 serotonergic agonist LES, stomach, intestine gastric emptying,
5-HT3 serotonergic antagonist Stomach, intestine postoperative ileus,
intestinal pseudo-
obstruction
Domperidone D2 dopaminergic antagonist Stomach, CRTZ Vomiting disorders
α2-adrenergic antagonist Stomach
β2-adrenergic antagonist Stomach
Cisapride 5-HT4 serotonergic agonist LES, stomach, intestine Gastroesophageal reflux,
5-HT1 serotonergic antagonist Stomach, intestine, emetic center delayed gastric
5-HT3 serotonergic antagonist Stomach, intestine, CRTZ emptying,
5-HT2 serotonergic agonist Colon postoperative ileus,
Nonserotonergic mechanism Canine antrum intestinal pseudo-
obstruction,
constipation,
chemotherapy-induced
emesis
Erythromycin Motilin agonist (in cats) Stomach, intestine Delayed gastric emptying
5-HT3 serotonergic agonist Stomach, intestine (liquids more than
(in dogs) solids)
Ranitidine Acetylcholinesterase inhibitor Stomach, intestine, colon Delayed gastric
Possibly M3 muscarinic agonist Stomach emptying, intestinal
pseudo-obstruction,
constipation
Nizatidine Acetylcholinesterase inhibitor Stomach, intestine, colon Delayed gastric
Possibly M3 muscarinic agonist Stomach emptying, intestinal
pseudo-obstruction,
constipation

CRTZ = chemoreceptor trigger zone; 5-HT = 5-hydroxytryptamine; LES = lower esophageal sphincter.

cated in treating patients with mechanical obstruction.
Functional Obstruction
Functional disorders of gastric emptying (referred to
as delayed gastric emptying or gastroparesis) result from
abnormalities in myenteric neuronal or gastric smooth
muscle function or from abnormalities in antropyloro-
duodenal coordination. Delayed gastric emptying is
now recognized as an important cause of upper gastro-
intestinal tract signs (e.g., anorexia and vomiting).31
Delayed gastric emptying has been reported in animals
recovering from gastric dilatation–volvulus,32 infectious
and inflammatory gastric diseases,33 experimental gas-
tric ulcer,34 and radiation gastritis.35
Delayed gastric emptying has also been associated
with several secondary conditions, including electrolyte
disturbances, metabolic disorders, concurrent drug us-
age (anticholinergics, β-adrenergic agonists, and opi-
ates), acute stress, and acute abdominal inflammation.33
Gastric emptying disorders are usually diagnosed after
mechanical obstruction has been ruled out.
A gastric motility disorder should be considered
when there is a history of chronic vomiting. Vomiting
of undigested to partially digested food usually occurs
more than 10 hours after a meal, at a time when the
stomach should be empty. Other signs of a gastric
motility disorder include gastric distention, nausea,
anorexia, belching, polydipsia, pica, and weight loss.

FREQUENCY OF REFLUX ■ VIDEOFLUOROSCOPY ■ FAT-RESTRICTED DIETS

Small Animal The Compendium June 1997

GASTRIC MOTILITY DISORDER

Mechanical obstruction Functional obstruction

(delayed gastric emptying)

Polyp Tumor Foreign body Inflammation Infection Idiopathic

Polypectomy 1. Chemotherapy 1. Endoscopic Antiinflammatory Antibiotics Low-fat/low-

2. Partial removal drugs (e.g., protein diet:
gastrectomy 2. Surgical prednisone) neutral pH, low
removal
osmolality,
liquid
consistency

Resolution No improvement

Prokinetic therapy:
Key 1. Cisapride
2. Erythromycin
Finding 3. Ranitidine or
Therapy nizatidine

Figure 2—Management of gastric motility disorders.

The physical examination may be normal or reveal
findings associated with the underlying cause. There
may be increased bowel sounds with abdominal auscul-
tation or nonspecific pain on abdominal palpation.
Laboratory findings depend on the underlying cause.
Dogs with persistent vomiting may exhibit dehydra-
tion, electrolyte abnormalities, or acid–base imbalances.
Hypokalemia is the most common electrolyte abnor-
mality. Paradoxic aciduria is observed in some dogs
when vomiting occurs secondary to pyloric outflow
obstruction.
Methods that are available for evaluating gastric emp-
tying include oral administration of radioisotopes cou-
pled with external scanning, serial sampling of gastric
contents by intubation, ultrasonography, computed to-
mography, electrophysiology, and manometry. Radio-
graphic techniques are the most definitive means that
are generally available to practitioners for diagnosing
gastric motility disorders.
Liquid barium sulfate can be used to detect gross
abnormalities of gastric emptying in routine upper
gastrointestinal radiographic studies. However, such
studies provide inadequate information for assessing
emptying of the typical heterogeneous meal because
solids and liquids empty differently, as do large and
small particles, and lipids and carbohydrate solutions.
Barium mixed with food is believed to be better than
liquid barium for testing distal gastric motor function.
Small radiopaque particles mixed with food are also
used to assess gastric emptying. If available, radio-
isotopic methods are the most tolerable and clinically
accurate means of evaluating gastric emptying.
Because surgical procedures are often unsuccessful,
dietary management and gastric prokinetic agents are
used to treat patients with delayed gastric emptying dis-
orders (Figure 2). Dietary management is based on the
knowledge that liquids are emptied from the stomach
more rapidly than solids, carbohydrates are emptied
more rapidly than proteins, and proteins are emptied
more rapidly than lipids. A low-fat, low-protein diet of

GASTRIC EMPTYING ■ ELECTROLYTE DISTURBANCES ■ PARADOXIC ACIDURIA

The Compendium June 1997
liquid or semiliquid consistency thus should be fed at
frequent intervals to facilitate gastric emptying. Diets
should be selected for low acidity and low osmolality
and should be fed at warm temperatures (22˚ to 38˚C
[72˚ to 100˚F]).
Gastric prokinetic agents should be considered in pa-
tients that fail to respond to dietary management alone.
The 5-HT4 serotonergic agonists (e.g., cisapride and
metoclopramide), motilin-like drugs (e.g., erythro-
mycin), and acetylcholinesterase inhibitors (e.g., raniti-
dine and nizatidine) have been used to treat delayed gas-
tric emptying (Figure 2 and Table I). We currently
recommend cisapride as the initial gastric prokinetic
agent. Doses of cisapride from 0.05 to 0.20 mg/kg
enhance gastric emptying in dogs with normal empty-
ing.14,36 However, doses of 0.5 to 1.0 mg/kg are required
to enhance gastric emptying in dogs with delayed gastric
emptying induced by α2-adrenergic agonists, dopamine,
disopyramide, or antral tachygastria.14,15
Cisapride accelerates gastric emptying in dogs by
stimulating pyloric and duodenal motor activity, by
enhancing antropyloroduodenal coordination, and by
increasing the mean propagation distance of duodenal
contractions.36 In this regard, cisapride is apparently su-
perior to metoclopramide and domperidone in stimu-
lating gastric emptying.15,36,37 If oral cisapride (0.1 to
1.0 mg/kg two to three times daily) fails to improve
gastric emptying, we recommend the use of oral
erythromycin (0.5 to 1.0 mg/kg three times daily) or
one of the acetylcholinesterase inhibitors (e.g., oral ran-
itidine at 1.0 to 2.0 mg/kg twice daily or nizatidine at
2.5 to 5.0 mg/kg once daily) in place of cisapride.10,38,39
SMALL INTESTINAL MOTILITY DISORDERS
Mechanical Obstruction
Mechanical obstruction of the small intestine may be
associated with foreign body ingestion, neoplasia, stric-
tures, hematomas, or intussusceptions.40 Acute obstruc-
tion of the intestine is characterized by distention,
increased intraluminal pressure, and increased motor ac-
tivity in the segment of bowel proximal to the occlusion.
Distention of the bowel proximal to the obstruction re-
sults from fluid and gas accumulation. Intestinal secre-
tion is stimulated, absorption of fluid is decreased, and
aerophagia causes gas accumulation. As the small bowel
distends, neuromuscular activity increases.41 Distally, the
bowel becomes quiescent; nearly all motor activity
ceases.42,43 The increased motor activity of the proximal
segment tends to subside with chronic obstruction.
The diagnosis of obstruction can be confirmed via
radiography. Mechanical obstruction of the small intes-
tine should be treated as a primary disorder (e.g., by
enterectomy, foreign body removal, or reduction of in-
LOW ACIDITY ■ CISAPRIDE ■ ACETYLCHOLINESTERASE INHIBITORS
Small Animal
tussusception) (Figure 3). Gastrointestinal prokinetic
agents are contraindicated in treating patients with
these disorders.
Functional Obstruction
Functional disorders of small intestinal transit (in-
testinal pseudo-obstruction) have been associated with
parvoviral enteritis, postoperative ileus, nematode infes-
tation, intestinal sclerosis, and radiation enteritis.40,44,45
The clinical signs vary depending on the cause, the lo-
cation in the small intestine, and the duration. Chronic
diarrhea and weight loss are common. Vomiting is
common with more proximal obstructions. Over-
growth of small intestinal bacteria, a common compli-
cation of disordered motility, contributes to the patho-
physiology and clinical signs.
The medical investigation should be directed at iden-
tifying the underlying cause. In some cases, a primary
entity may not be obvious. Gastrointestinal prokinetic
therapy should be used to promote intestinal transit in
such cases (Figure 3). 5-HT4 serotonergic agonists (e.g.,
cisapride or metoclopramide) and motilin-like drugs
(e.g., erythromycin) have been recommended in the
therapy of patients with these disorders.15,37,38
In the treatment of small intestinal motility disor-
ders, the 5-HT4 serotonergic agonists apparently have
distinct advantages over other gastrointestinal prokinet-
ic agents. Cisapride, for example, stimulates jejunal
spike burst migration,46 jejunal propulsive motility,47
and antropyloroduodenal coordination48 after intestinal
lipid infusion in dogs. Cisapride thus apparently has a
rational place in the treatment of patients with post-
operative ileus and intestinal pseudo-obstruction. Well-
designed clinical trials are required to determine the
effectiveness of cisapride compared with that of other
prokinetic agents in treating patients with these dis-
orders.
Inflammatory Bowel Disease
Inflammatory bowel disease is a common disorder
of dogs and cats. The disorder may involve several
anatomic sites (e.g., the stomach, small intestine, and
colon). Clinical signs associated with inflammatory
bowel disease include vomiting, diarrhea, weight loss,
tenesmus, urgent defecation, hematochezia, and exces-
sive mucus in feces. The diarrhea of inflammatory bow-
el disease is associated with excessive secretion and mal-
absorption. Inflammation disrupts the tight junctions
between epithelial cells, which reduces absorption and
promotes loss of nutrients, electrolytes, and water.
Inflammatory mediators may also stimulate abnormal
motor activity. Inflammation produced by 95%
ethanol–20% acetic acid perfusion in the canine ileum,
Small Animal The Compendium June 1997

INTESTINAL MOTILITY DISORDER

Mechanical obstruction Functional obstruction

(pseudo-obstruction)

Tumor Intussusception Foreign body Inflammation Infection Idiopathic

1. Chemotherapy Surgical Surgical Antiinflammatory Antibiotics Low-fat diet,

2. Partial reduction removal drugs (e.g., antibiotics
gastrectomy prednisone)

Resolution No improvement

Prokinetic therapy:
Key cisapride or
metoclopramide
Finding
Therapy

Figure 3—Management of intestinal motility disorders.

for example, significantly increases the frequency of gi-
ant migrating contractions and decreases the frequency
of migrating motor complexes.49
In this canine model, diarrhea, urgent defecation,
hematochezia, and apparent abdominal discomfort are
related to the increased frequency of giant migrating con-
tractions.49 Inhibition of giant migrating contractions
by specific antagonists during inflammation thus may
minimize clinical signs and may alter the course of the
disease. Platelet-activating factor (PAF) is believed to be
one of the inflammatory cytokines that mediates the
increased frequency of giant migrating contractions.50
The PAF antagonist BN 50727 inhibits the contractile
response to PAF in the experimentally inflamed canine
ileum.50 Motor abnormalities (i.e., giant migrating con-
tractions) thus may be the major cause of clinical signs
in experimental inflammatory bowel disease. It remains
to be determined whether the same motor abnormali-
ties and inflammatory cytokines are involved in sponta-
neous canine inflammatory bowel disease.
COLONIC MOTILITY DISORDERS
Feline Idiopathic Megacolon
Colonic dilatation results in disruption of the coordi-
nated motility patterns of the distal colon and rectum
that permit receptive relaxation for fecal storage as well
as the giant migrating contractions associated with the
defecation reflex. This eventually leads to constipation,
obstipation, and idiopathic megacolon. Many cats pre-
sent with chronic histories of tenesmus and inability to
pass feces. Diagnosis is usually based on a history of ob-
stipation (dyschezia, depression, anorexia, and vomit-
ing) and abdominal palpation (colonic impaction). Ra-
diography is often necessary to rule out obstructive
causes.
Several researchers have emphasized the importance of
considering an extensive list of diagnostic differentials
(e.g., neuromuscular, mechanical, inflammatory,
metabolic–endocrine, pharmacologic, environmental,
and behavioral causes) for an obstipated cat. A recent re-
view, however, suggests that 96% of cases of obstipation

INCREASED INTRALUMINAL PRESSURE ■ INTESTINAL TRANSIT ■ DIARRHEA

Small Animal The Compendium June 1997

Resolution
Mild constipation Dietary fiber
Recurrence Dioctyl sodium
sulfosuccinate or petrolatum
and/or cisapride

Enemas and/or Dietary fiber, Resolution

Moderate or
manual extraction lactulose, Dietary fiber,
recurrent constipation
of feces cisapride Recurrence lactulose,
bisacodyl

< 6 mo Pelvic osteotomy or colectomy

Hypertrophy
Obstipation > 6 mo Colectomy
or megacolon
Dilation Colectomy
Key
Finding
Therapy
Time period

Figure 4—Management of feline idiopathic megacolon. (From Washabau RJ, Hasler AH: Constipation, obstipation, and
megacolon, in August JR [ed]: Consultations in Feline Internal Medicine. Philadelphia, WB Saunders Co, 1996, p 108.
Modified with permission.)

are accounted for by idiopathic megacolon (62%), pelvic
canal stenosis (23%), nerve injury (6%), or Manx sacral
spinal cord deformity (5%).51 Fewer cases are accounted
for by complications of colopexy (1%) and colonic neo-
plasia (1%). In another 2% of cases, colonic hypogan-
glionosis or aganglionosis was suspected but not proven.
Inflammatory, pharmacologic, and environmental–
behavioral causes were not cited as predisposing factors
in any of the original case reports. Endocrine factors
(obesity in five cases and hypothyroidism in one case)
were cited but were not necessarily implicated as part of
the pathogenesis of megacolon. Although it is important
to consider an extensive list of diagnostic differentials in
an individual animal, most cases are idiopathic, orthope-
dic, or neurologic in origin.51
The pathogenesis of idiopathic megacolon has been
variably attributed to a primary neurogenic or degener-
ative neuromuscular disorder. Although few cases
(11%) evidently result from neurologic disease, most
cases (more than 60%) have no evidence of neurologic
disease.51 These idiopathic cases may involve distur-
bances of colonic smooth muscle.
Recent studies suggest that colonic smooth muscle
function is impaired in cats with idiopathic mega-
colon.52 In vitro isometric stress measurements were
performed on colonic smooth muscle segments ob-
tained from cats with idiopathic dilated megacolon.
Compared with that of healthy controls, megacolonic
smooth muscle developed less isometric stress in re-
sponse to neurotransmitters (acetylcholine, substance P,
and cholecystokinin), membrane depolarization (potas-
sium chloride), and electrical field stimulation. These
differences were observed in longitudinal and circular
smooth muscle from the ascending and descending
colon. No significant abnormalities of smooth muscle
cells or myenteric neurons were observed on histologic
evaluation. These studies suggest that feline idiopathic
megacolon is a generalized dysfunction of colonic

OBSTIPATION ■ ENDOCRINE FACTORS ■ IDIOPATHIC MEGACOLON

Small Animal
smooth muscle and that treatments aimed at stimulat-
ing colonic smooth muscle contraction might improve
colonic motility.52
Traditional therapy for constipation and idiopathic
megacolon has been aimed at improving fecal hydra-
tion and bulk (Figure 4). Cat owners thus are advised
to encourage water consumption and to increase the
fiber content of the diet with bulk laxatives (e.g., psylli-
um). Warm-water enemas can be given intermittently
as needed. Thereafter, patients may be treated with
emollient laxatives (e.g., dioctyl sodium sulfosuccinate),
stimulant laxatives (e.g., bisacodyl), lubricant laxatives
(e.g., mineral oil or petrolatum), saline laxatives (e.g.,
magnesium citrate), hyperosmotic agents (e.g., lactu-
lose), or motility agents.51 Hyperosmotic agents that
contain sodium phosphate are contraindicated in cats
because these agents tend to induce severe hyperna-
tremia, hyperphosphatemia, and hypocalcemia in this
species.53
In several species, cisapride enhances colonic propul-
sive motility via activation of colonic smooth muscle 5-
HT2a receptors.14,15 Although in vitro studies demon-
strate that cisapride stimulates feline colonic smooth
muscle contraction,54 it has not yet been proven that
cisapride stimulates feline colonic propulsive motility in
vivo. Current anecdotal reports suggest that cisapride is
effective in stimulating colonic propulsive motility in
cats with mild to moderate idiopathic constipation; cats
with longstanding obstipation and megacolon are not
likely to demonstrate much improvement with cis-
apride therapy. The recommended dosage of oral cis-
apride for cats with mild to moderate idiopathic consti-
pation has been 0.1 to 0.5 mg/kg two to three times
daily. Higher doses (0.5 to 1.0 mg/kg) may be neces-
sary in cats with moderate to severe constipation. No
significant side effects have yet been observed or report-
ed in cats medicated with oral cisapride at dosages of
0.1 to 1.0 mg/kg two to three times daily.
Colectomy should be considered in cats that are re-
fractory to medical therapy (Figure 4). Cats have a gen-
erally favorable prognosis for recovery after colectomy.
Mild to moderate diarrhea occasionally persists for
weeks to months after surgery; constipation may recur
in some cats.
Inflammatory Bowel Disease
Experimental canine colitis is associated with an in-
creased incidence of giant migrating contractions that is
highly correlated with the clinical signs of tenesmus, di-
arrhea, hematochezia, and excessive mucus in feces.55,56
These findings are similar to those reported in experi-
mental canine ileitis49,50 and suggest that the diarrhea
produced in inflammatory bowel disease may be largely
The Compendium June 1997
attributable to the numerous giant migrating contrac-
tions that emerge during acute inflammation. Therapy
and resolution of disease may be facilitated by charac-
terizing the mechanisms that are involved in the regula-
tion of this abnormal motor pattern.
About the Authors
Dr. Washabau is affiliated with the Department of Clinical
Studies, School of Veterinary Medicine, University of
Pennsylvania, Philadelphia, Pennsylvania. Dr. Hall is affil-
iated with the college of Veterinary Medicine, Oregon
State University, Corvallis, Oregon. Drs. Washabau and
Hall are Diplomates of the American College of Veterinary
Internal Medicine.
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