CASE REPORT
drug reactions, phenylpropanolamine;
phenylpropanolamine, reactions to

Phenylpropanolamine: A Potentially
Hazardous Drug
Three cases of toxic reactions following relatively small doses of phenylpropanolamine are presented. One patient had a hypertensive crisis and seizures; the others had intracerebral hemorrhages culminating in death. A
discussion of the pharmacology of phenylpropanolamine and its previously
documented side effects and drug interactions is included. [Bernstein E,
Diskant BM: Phenylpropanolamine: A potentially hazardous drug. Ann
Ernerg Med 11:311-315, June 1982.]

INTRODUCTION
The availability of phenylpropanolamine (PPA) as a decongestant, anorectic, and as a component of "legal-stimulants," or "pic-me-ups" as they are
sometimes called, has increased dramatically in the United States over the
past five years. 1 With this increase in use has come an increase in the frequency of toxic reactions and overdoses in which PPA plays a role. Between
1975 and 1980, the frequency of PPA involvement in poison control case
reports increased tenfold 2 (Figure 1).
In the past few years there has been increased advertising of over-thecounter anorectic adjuncts, most of which contain PPA. 3 Despite the fact
that PPA has been k n o w n to be associated with hypertensive reactions, 4
seizures, s and intracerebral hemorrhage, 6 its use continues to grow. The recent appearance of "look-alike" stimulants (Figure 2) which are virtually indistinguishable from prescription amphetamines, and which generally conrain PPA along with caffeine and ephedrine in non-time-released capsules, is
especially worrisome.
We recently saw three patients who had severe cardiovascular and central
nervous system problems after taking relatively small doses of PPA.

Edward Bernstein, MD *t
Barry M. Diskant, MD*
Albuquerque, New Mexico
From St. Joseph Hospital* and the
Division of Emergency Medicine,
University of New Mexico School of
Medicine, t Albuquerque, New Mexico.
Address for reprints: Barry M. Diskant,
MD, Emergency Physicians, Inc, St.
Joseph Hospital, 400 Walter, NE,
Albuquerque, New Mexico 87102.

CASE REPORTS
Case Number One
An 18-year-old obese w o m a n with no prior history of medical illness presented with severe frontal headache, nausea, epigastric pain, blurred vision,
and shakiness 21/2 hours after taking two Comtrex ~ tablets for "congestion."
On initial examination in a physician's office her vital signs were as follows: temperature, 37 C; blood pressure, 210/130 m m Hg; pulse, 120 beats/
rain; and respirations, 24/rain. She was tremulous, anxious and restless, but
was noted to be oriented to person, place, and time. General examination
was unremarkable. Hydralazine 10 mg was administered intramuscularly
and the patient was transferred to a local hospital for further evaluation and
treatment. En route to the hospital she had a grand-mal seizure.
On arrival the patient was disoriented and lethargic. Shortly after arrival a
second grand-real seizure occurred. Diazepam 10 mg was administered intravenously, resulting in cessation of seizure activity. Vital signs immediately
after the second seizure were as follows: temperature, 37.1 C; blood pressure,
148/98 m m Hg; pulse, 134 beats/min; and respirations, 24/min. A repeat
physical examination was unremarkable except for the patient's post-ictal

11:6 June 1982

Annals of Emergency Medicine

311/43

PHENYLPROPANOLAMINE
Bernstein & Diskant

Fig. 1. Frequency of PPA product
mentions in poison control case reports, 1975-80. (From FDA Bulletin. 2)
Fig. 2. " L o o k - a l i k e " s t i m u l a n t s
which are virtually indistinguishable from prescription amphetamines.

15

co
cO

E
mental state. Funduscopic examination was within normal limits.
Laboratory data revealed a white
blood count of 12,000/cu m m with
54% segs, 17% bands, 24% lymphs,
and 3% monos. The hemoglobin was
16.8 g/dl, and the hematocrit was
48%. Serum electrolytes, creatinine,
glucose, urea nitrogen, urinalysis, and
chest and skull radiographs were entirely within normal limits. The electrocardiogram revealed sinus tachycardia at a rate of 120/min.
The patient was admitted to the intensive care unit, IV D5W was started
TKO, but no other drugs were administered. Her blood pressure gradually
returned to normotensive levels; it
was recorded as 118/80 m m Hg four
hours after admission. Her level of
consciousness gradually improved,
and within 12 hours she was alert and
oriented. The initial electroencephalogram {EEG), performed on the day following admission, was abnormal with
a basic dysrhythmia of sagittal origin.
Subsequent EEG, performed 48 hours
after admission, was within normal
limits. A radionuclide brain scan, CT
scan of the head, intravenous pyelogram, and CT scan of the abdomen
were all within normal limits. Twenty-four-hour urinalysis for catecholamines, metanephrines, 17-ketosteroids, creatinine, and protein was
within normal limits. Serum cortisol
and ACTH were also within the normal range. No drug screen was done.
The patient was discharged on the
16th hospital day. She Was free of residual neurologic deficits and required
no medication.

Case Number Two
A 26-year-old man drank three to
six ounces of whiskey eight hours
prior to presentation, and took two
black capsules three to four hours
prior to admission to the emergency
department. The capsules were later
identified as "legal-stimulants," each
containing caffeine 200 mg, ephedrine
25 rag, and PPA 50 mg. Approximately
one hour after ingestion of the capsules he went to sleep and was noted
44/312

1

AGE GROUP
ALL AGES
UNDER 5
5 AND OLDER . . . . . . .

/
i I

C~

Eb
~6
*d
'~ 0.5
13_

1975

1976

19'77

to be sober and without somatic complaints. Thirty minutes prior to presentation he began vomiting and was
said to be "having a lot of trouble
breathing," presumably because of
upper airway obstruction. A friend
cleared his upper airway manually and
brought him to the emergency department by private vehicle.
Examination revealed a slightly
cyanotic man in obvious respiratory
distress who was unresponsive to verbal and noxious stimuli. The vital
signs were as follows: temperature,
3Z2 C; blood pressure, 134/78 m m
Hg; pulse, 60 beats/min; and respirations, 40/min and of the KUssmaul
Annals of Emergency Medicine

19'78

19'79

1980

type. Stridor was present. The pupils
were symmetrically dilated, measuring 7 m m across, and were unreactive
to light. Funduscopic examination revealed a large subhyaloid hemorrhage
on the right and splinter hemorrhages
on the left. The oculocephalic reflex
was absent. Neurologic examination
revealed no evidence of reflex or motor activity. The patient was flaccid.
Laboratory data revealed a white
blood count of 21,000/cu m m with
68% segs, 19% bands, 7% lymphs, 5%
monos, and 1% eos. Hemoglobin and
hematocrit were 19.4 g/dl and 53.9%,
respectively. Initial arterial blood gas
determination with the patient on
11:6 June 1982

room air revealed a PO2 of 52 m m Hg;
PCO2, 36 m m Hg; and pH, 7.33. The
serum electrolytes and urea nitrogen
were normal; the serum glucose was
147 mg%. Urinalysis revealed a specific gravity of 1.021; pH of 5; 3 +
protein; trace occult blood; 50 to 75
white blood cells per high power field;
and no bacteria. Chest radiograph revealed diffuse areas of infiltration
bilaterally compatible with aspiration
pneumonitis.
Toxicology studies were drawn on
admission and the results were as follows: blood alcohol, 5 mg%; serum
ephedrine, 3 ~g/ml; negative screens
for tricyclic antidepressants, opiates,
glutethimide, and amphetamines.
Analysis for PPA was not ordered.
A nasotracheal airway was inserted
and an IV of D5LR was begun. The patient was admitted to the intensive
care unit. Two ampules of naloxone
were administered without noticeable
effect. The patient became apneic and
required mechanical respiratory assistance. A consulting neurosurgeon
thought the patient had suffered an intracranial hemorrhage with possible
brainstem herniation.
The patient's blood pressure rose to
156/110 m m Hg and later to 208/148
m m Hg. After several hours in the intensive care unit his blood pressure
fell to 80 m m Hg systolic and a dopamine infusion was administered. He
remained unresponsive. Approximately 11 hours after admission, he developed ventricular fibrillation and
died.
At autopsy, extensive subarachnoid
and intraventricular hemorrhage was
found. The site of hemorrhage could
not, however, be localized. No morphologic vascular abnormalities were
noted.
Case N u m b e r Three
A 17-year-old man ingested two
black capsules which were later identified as "pic-me-up" capsules containing caffeine 200 mg, ephedrine 25
mg, and PPA 50 mg. Shortly after ingestion he became tremulous and agitated, and was unable to sleep. He was
oriented, and alert during that time.
Approximately six hours after taking
the capsules there was an abrupt
change in his mental status, with
agitation giving way to somnolence,
confusion, and disorientation. His
speech became slurred and incomprehensible.
His family observed him at home,
and his brother repeatedly stated that
11:6 June 1982

he was "just crashing from speed,"
and that the effects would, in time,
wear off. The patient became very
drowsy and slept for periods of two to
three hours at a time. When aroused
he remained disoriented. Approximately 17 hours after ingestion, he
was brought to the emergency department.
E x a m i n a t i o n r e v e a l e d a welld e v e l o p e d w h i t e m a n w h o was
somnolent and disoriented to place,
person, and time. Vital signs were as
follows: temperature, 37 C; blood
pressure, 120/60 m m Hg; pulse, 60
beats/min; and respirations, 12/min.
His speech was slurred and could not
be understood. He could not follow
simple verbal c o m m a n d s . He responded to loud verbal stimuli by
s p e a k i n g n o n s e n s i c a l l y . He had
appropriate withdrawal responses to
painful stimuli. Pupils were 4 to 5
m m in diameter, round, equal, and
reactive to light. Funduscopic examination was unremarkable. Eye
movements were conjugate and the
oculocephalic reflex was intact. Deep
tendon reflexes were 2+ and equal
bilaterally. Babinski responses were
flexor bilaterally. Detailed neurologic
examination failed to reveal any focal
abnormality. Gait could not be tested.
Initial laboratory data were as follows: white blood count, 17,400/cu
m m with 67% segs, 25% bands, 4%
lymphs, 4% monos; hemoglobin, 16.2
g/dl; and hematocrit, 45.8%. The electrolytes, blood urea nitrogen, serum
glucose, and urinalysis were unremarkable, as was the room air arterial
blood gas determination. An SMA-20
blood chemistry profile done on the
day after admission was within normal limits. Chest and skull radiographs were unremarkable.
Toxicology studies drawn on admission were positive only for urinary
ephedrine, detected at 2 ~g/ml. No
ethanol, opiates, methaqualone, or
amphetamines were detected. Analysis for PPA was not ordered.
The patient was admitted to the intensive care unit for observation.
Throughout the first day and night he
was noted to be drowsy and intermittently combative. Approximately 15
hours after admission, the nurse noted
that the patient became deeply comatose. He was unarousable. Decerebrate
posturing was observed. Shortly thereafter he had a grand-mal seizure followed by respiratory arrest. Seizure
activity was controlled with diazepam
10 mg IV. Additionally phenobarbital
Annals of Emergency Medicine

60 mg was given IM. Endotracheal intubation was performed promptly but
the patient failed to resume spontaneous respiration. Mechanical ventilatory support was required.
Neurologic consultation was obtained. Pupils were mid-position and
unreactive. The oculocephalic reflex
was absent. Decerebrate posturing occurred with any stimulation. Babinski
responses were extensor bilaterally.
A CT scan of the brain revealed a
large intracerebral hemorrhage in the
left parieto-occipital area with a moderate mass effect and midline shift.
The intracerebral h e m a t o m a measured 4 cm in length and 2.5 cm in
width. Dexamethasone (10 mg IV followed by 6 mg IV qid) and mannitol
{500 cc of 20% solution m a single
dose) were given to reduce cerebral
edema. Brainstem auditory evoked responses (BAER) performed on the
second hospital day were indicative of
bilateral brainstem dysfunction.
Maximal supportive therapy was
continued. An EEG performed on the
fourth hospital day was isoelectric.
Repeat BAER s h o w e d no evoked
potentials. It was concluded that brain
death had occurred and mechanical
ventilatory support was discontinued.
The patient died shortly thereafter.
At autopsy the patient was found to
have a massive intracerebral hemorrhage in the left parieto-occipital area.
Intraventricular hemorrhage on the
left was also noted. No morphologic
vascular abnormalities of the intracranial vessels were seen.
DISCUSSION
These three cases raise the interesting and i m p o r t a n t question of
whether the severe reactions reported
were individual and idiosyncratic or
widespread and part of a continuum of
reactions to phenylpropanolaminecontaining drugs. There has been recent consumer interest and media
coverage of the problems of phenylpropanolamine-containing, over-thecounter, pic-me-up drugs and the diet
tablets. The medical c o m m u n i t y ' s
knowledge of phenylpropanolamine,
however, lags behind public interest.
Horowitz et al4 demonstrated m a
large group of young, healthy, normotensive adults an "important and
sometimes potentially dangerous rise
m blood pressure may occur even after
ingestion of a single capsule of a PPAcontaining preparation." The mean
supine diastolic blood pressure before
taking the capsule was 70 -+ 1.4 m m
313/45

PHENYLPROPANOLAMINE
Bernstein & Diskant

Fig. 3. Structures of phenylpropanol-

amine, metaraminol, ephedrine, and
amphetamine.
Hg; after taking a preparation containing 85 mg phenylpropanolamine, 12 of
37 subjects had a supine diastolic
blood pressure rise to 100 m m Hg or
more, and one had a rise to 190/142
m m Hg. Because of the very severe
effects with the 85-mg preparation,
the second half of the study was done
on Contac 500 * which contained only
50 mg PPA. On the lower dose, only 4
of 34 subjects had a comparable rise in
blood pressure. The authors concluded
that the response was dose related.
The results of this study are especially
significant in light of the fact that the
Food and Drug Administration has
been conducting hearings on whether
to allow the pharmaceutical industry
to continue incorporating higher dosages of PPA in these over-the-counter
anorectics. 3
In 1965, Livingston 7 reported the
cases of two young men who had transient BP rises of 180/110 m m Hg following ingestion of single capsules of
Contac ~. A number of cases in which
two or more capsules produced severe
hypertensive reactions have been reported. 842 One case reported by King6
describes a 37-year-old w o m a n who
developed right hemiparesis secondary
to a hemorrhage in the left internal
capsule following ingestion of two
diet capsules, each containing 85 mg
PPA.
In addition to hypertensive effects,
arrhythmias (premature ventricular
contractions, premature atrial contractions together with paroxyms of ventricular and atrial tachycardia) have
been reported. 13 The authors postulate
that the vasoconstrictive effect of PPA
causes h y p e r t e n s i o n w i t h a reflex
bradycardia which m a y allow the
ectopic pacemaker to assume control
of the ventricles.
Another important side effect of PPA
is its central nervous system stimulant properties. Although this is less
prominent than the stimulant properties of amphetamines, the effects are
well documented t'14 and are illustrated by our cases. They include restlessness, headache, dizziness, disorientation, confusion and agitation and
even hallucinations, and psychosis
(convulsions and visual hallucinations
were reported in a 4-year-old child
taking PPA-containing cold preparations5).
46/314

Phenylpropanolamine:

Aromatic Ring

CH
I
OH

OH3

B Carbon

Alpha Carbon

CH

CH

I

I

I

OH

OH3

H

CH

CH

NH

OH

CH3

OH 3

CH
I
OH

CH
I
OH3

NH
I
OH3

Metaraminol:
3-OH /
Ephedrine:

Amphetamine:
3

Our second and third cases are
dramatic examples of the effects of
PPA in combination with caffeine and
ephedrine. Although severe hypertensive reactions have been reported
when phenylpropanolamine was used
concomitantly with monoamine oxidase inhibitors, ts,~6 foods containing
t y r a m i n @ 7 anti-hypertensive drugs
such as methyldopa and oxprenolal, is
and indomethacin, 19 never before has
death resulting from intracerebral
bleed associated with the combination
with ephedrine and caffeine been reported. The combination and synergistic effect these drugs represent is a
new problem arising from the attempt
to find a substitute stimulant for the
discredited a m p h e t a m i n e preparations. These "look-alike" drugs contain as much as 50 mg PPA and 25 mg
ephedrine, and because they usually
do not give the user a high equivalent
to amphetamine, the user seems more
likely to take several pills at a time.
Because PPA and ephedrine have a
m u c h more pronounced peripheral
effect than do the amphetamines, the
hypertensive reactions from these
stimulants are much greater. These
preparations are sold legally in "picme-up" shops and mail order houses.
Their identification can be extremely
difficult for emergency physicians and
pharmacists.
Phenylpropanolamine is found in
more than 75 over-the-c0unter preparations, many of which are in widespread use. 2° In addition, PPA is contained in such common prescription
medicines as Omade ® and Novahistamine ®. Despite PPA's great popularity
Annals of Emergency Medicine

CH
I

NH
I
H
Amino Group
NH

for the past two decades, many physicians are not well versed in its biochemistry, structural similarities to
other potent vasoactive amines, and
interactions with other drugs.
PPA has been frequently compared
with ephedrine and amphetamine because of structural similarities.1 Comparison of the structural similarity
between PPA and metaraminol (Aramine ®) (Figure 3), is especially helpful
in understanding their pressor actions.
P h e n y l p r o p a n o l a m i n e has t w o
modes of action: 1) a direct alpha
adrenergic action, and 2) an indirect
action by virtue of its ability to release
norepinephrine from nerve ending
storage sites. 8A9 The OH on the beta
carbon enhances both alpha and beta
adreno-receptor activity, 21 while the
absence of substitution on the N H
amino group enhances the activity
and selectivity for alpha agonist action, 21 explaining the potent vasopressor properties of PPA as well as those
of metaraminol. The absence of the
OH group on the aromatic ring accounts for the enhanced CNS activity,
but also explains why PPA is less potent as an alpha and beta agonist than
is metaraminol.
In addition, the methyl CH3 group
on the alpha carbon prolongs and enhances this alpha agonist action. 21
The CH-CH3 methyl group blocks the
degradation of PPA by monoamine oxidase (MAO), allowing it to persist in
nerve terminals and enabling it to release norepinephrine from sites of
storage. The methyl group blocks the
MAO enzyme in the liver and intestines and prevents PPA's rapid deg11:6 June 1982

radation and detoxification. This permits oral administration with good
absorption and prolonged duration of
action, especially with respect to its
peripheral vasoconstrictive action. 21
PPA and ephedrine (from which PPA
is chemically derived) also share structural similarities. The difference between them lies in ephedrine's methylation at the terminal amino (NH)
group which increases its potency as a
primary amine, especially enhancing
its beta adrenergic activity. This explains ephedrine's ability to produce
bronchodilatationY The "look-alike"
stimulants that contain considerable
amounts of both PPA and ephedrine
have potent vasopressor and CNS
stimulant properties which could likely be enhanced in the presence of caffeine and alcohol. 22'23 The pharmacologic interaction of PPA, ephedrine,
and caffeine needs further study.
The ability of M A O - I n h i b i t o r s
(MAO-I) to potentiate the pressor
effects of PPA and to cause hypertensive crisis when these drugs are taken
together has been explained, x6 The
MAO-I, by preventing the degradation
of catecholamines, raises their concentration at nerve endings, and thus
more catecholamines are available for
release by the action of PPA. The interaction of PPA with foodstuffs high
in tyramine (such as aged cheese)
occurs because tyramine also releases
norepinephrine from nerve endings
and the synergistic action potentiates
the pressor effects of PPA.x7
The effects of indomethacin have
been explained. 19 Indomethacin inhibits prostaglandin production. Prostaglandins are k n o w n to control a
negative feedback loop which regulates the release of catecholamines at
the sympathetic nerve endings) 9 The
inhibition of prostaglandin formation
allows for the unopposed action of
PPA in releasing catecholamines.
Additionally, indomethacin suppresses
production of vasodilator prostaglandins. Because PPA has a direct effect
on small arterioles, the absence of
vasodilator prostaglandins allows PPA
to exert its vasoconstrictor effect unopposed. PPA's direct and indirect
modes of action are potentiated by indomethaein. Indomethacin and such
other nonsteroidal anti-inflammatory
drugs as aspirin are in widespread use,
and undoubtedly are used by persons
also taking PPA. Therefore, hypertensive episodes with indomethacin and
PPA present a greater threat to the
public than is generally recognized.
11:6 June 1982

CONCLUSIONS
Recently Blum 3 stated, "Clearly the
use of phenylpropanolamine poses a
danger to the public." His conclusions, though strongly worded, have
been voiced a number of times. In
1979, Tonks and Lloyd concluded that,
"The therapeutic and prophylactic
effects of PPA in upper respiratory
tract infections and in serious otitis
media have been questioned. Since
psychic disturbances including psychotic episodes seem to be a problem,
the prescribing of drugs containing
PPA should be restricted. ''is
Lee et a119 concluded that, "There is
little evidence that phenylpropanolamine produces sustained therapeutic
benefit as an appetite suppressant, and
its value in nasal decongestants or
cough {syrup) linctuses is questionable. In view of the risk of severe
hypertension caused by the interaction between phenylpropanolamine
and various commonly used drugs,
withdrawal of pharmaceutical preparations containing this substance should
be considered."
Because PPA is now widely marketed as a substitute for amphetamines as an anorectic, it is not likely
that this drug will be restricted or
taken off the market for some time.
For two decades phenylpropanolamine has been regarded by the public,
the medical community, and the Food
and Drug Administration as a relatively safe drug. Our three cases and other
cases in the literature give evidence to
the contrary. It is our hope that the
FDA will recognize that the risk to
benefit ratio of this drug is very high,
and that it will act in an expedient
and responsible manner in removing
the drug from all over-the-counter and
prescription medicines.

REFERENCES
1. Dietz AJ: Amphetamine-like reactions
to phenylpropanolamine. JAMA 245:601602, 1981.
2. Phenylpropanolamine Weight Control
Products. Bulletin, FDA National Clearinghouse for Poison Control Centers. 25:1620, 1981.
3. Blum A: Phenylpropanolamine: An
over-the-counter amphetamine. JAMA
245:1346-1347, 1981.
4. Horowitz JD, Lang WJ, Howes LG, et al:
Hypertensive responses induced by phenylpropanolamine in anorectic and decongestant preparation. Lancet 1:60-61, 1980.
5. Norvenius G, Widerlov E, Lonnerholm
G: Pl~enylpropanolamine and mental disturbance. Lancet 2:1367-1368, 1979.
Annals of Emergency Medicine

6. King J: Hypertension and cerebral
hemorrhage after Trimolets (85 mg PPAcontaining anorectic) ingestion. Med J Aust
2:258, 1979.
7. Livingston PH: Transient hypertension
and phenylpropanolamine. JAMA 196:1159,
1966.
8. Horowitz JD, McNeil JJ, Sweet B, et al:
Hypertensive and postural hypotension induced by phenylpropanolamine (Trimolets).
Med ] Aust 1:1975-1976, 1979.
9. Shapiro SR: Hypertension due to anorectic agent. N Engl J Med 280:1363, 1969.
10. WolfgangFC, Duvemoy MC: Positive
phenylpropanolamine test in hypertension
induced by a nasal decongestant. N EngI [
Med 280:877, 1969.
11. Ostem S, Dodson WH: Hypertension
following Omade ingestion. JAMA 194:472,
1965.
12. Salmon PR: Hypertensive crisis with
Eskomade. Br Med J 1:193, 1965.
13. Peterson RB, Vasquez LA: Phenylpropanolamine-induced arrhythmias. JAMA
223:324, 1973.
14. Schaffer CB, Pauli MW: Psychotic
reaction caused by proprietory oral diet
agents. Am J Psychol 137:10, 1256-1257,
1980.
15. Tonks CM, Lloyd AT: Hazards with
monamine oxidase inhibitor. Br Med J
1:589, 1965.
16. Cuthbert ME Greenberg MP, Morley
SW: Cough and cold remedies: A potential
danger to patients on monamine oxidase
inhibitors. Br Med J 1:404-406, 1969.
17. Gibson GJ, Warrell DA: Hypertensive
crisis and phenylpropanolamine. Lancet
2:492, 1972.
18. McLaren EH: Severe hypertension produced by interaction of phenylpropanolamine with methyldopa and oxprenolal. Br
Med J 2:283-284, 1976.
19. Lee KY, Beilin LJ, Vandongen R: Severe
hypertension after ingestion of appetite
suppressant (phenylpropanolamine) with
indomethacin. Lancet 2:1110-1111, 1979.
20. Physicians' Desk Reference, ed 34.
Oradell, NJ, Medical Economics Co, 1980,
p 311.
21. Weiner N: Norepinephrine, epinephrine, and the sympathomimetic amines, in
Goodman LS, Gilman A (eds): The Pharmacological Basis of Therapeutics, ed 6.
New York, MacMillan, 1980, p 142-143.
22. Rall TW: Xanthines, in Goodman LS,
Gilman A (eds): The Pharmacological
Basis of Therapeutics, ed 6. New York,
MacMillan, 1980, p 593-594.
23. Ritchie JM: The aliphatic alcohols, in
Goodman LS, Gilman A (eds): The Pharmacological Basis of Therapeutics, ed 6.
New York, MacMillan, 1980, pp 376, 377,
387.
315/47