This document summarizes the physiological effects of heat and cold on the human body. It discusses how the body regulates its core temperature through compensatory mechanisms like vasoconstriction, sweating, and shivering in response to temperature changes. Both local skin receptors and central receptors in the hypothalamus detect changes in temperature and trigger these thermoregulatory responses through efferent pathways in the nervous system. Local application of heat or cold also causes vasodilation or vasoconstriction in the skin as an immediate reflex, while more prolonged or intense exposure can impact deeper tissues like muscles as well. Maintaining thermal balance requires both local tissue responses and coordinated whole-body regulation.

1. Physiological
Effects
Of Heat and Cold
JOHN A. DOWNEY, M.D., D.Phil.
MAN AND WARM-BLOODED ani­
mals respond to changes in temperature by both
local and general circulatory and metabolic
changes. In man the temperature of the central
or deep body tissues, as reflected at those sites
where temperature is traditionally measured, e.g.,
rectum, tongue, axilla, is closely regulated with a
coefficient of variation that is one of the smallest
of available human data.1 When exposed to heat
or cold, a local vasomotor and metabolic effect
and a more widespread compensatory mechanism
tend to restore and maintain thermal balance.
This regulation of thermal balance at or near a
constant temperature requires temperature-sensi­
tive receptors in both the peripheral and the central
parts of the body and effector mechanisms which
can adjust heat production conservation or loss,
e.g., vasomotor tone, shivering, and sweating.
In addition to initiating the general thermo­
regulatory response, heating or cooling have local
effects on metabolism, blood vessels, local sensa-
Dr. Downey is in the Department of Physical Medicine
and Rehabilitation, Columbia-Presbyterian Medical Center,
New York, New York.
tion, and possibly on muscle tone. To this end, it
is proposed to review the mechanisms of regula­
tion of body temperature and discuss how these
as well as the responses to localized temperature
change can be modified.
NORMAL TEMPERATURE REGULATION
When exposed to a change in temperature, man
responds by adjusting his heat balance so as to
maintain his central temperature at or near its
constant level. When the trunk is exposed to heat,
the blood flow to the skin of the trunk and ex­
tremities is increased and sweating is started;
when exposed to cold, the circulation to the skin
is reduced and if this does not conserve enough
heat to maintain the central temperature, the heat
production of the body is increased. These re­
sponses, in the first instance, are initiated by re­
flexes from the temperature receptors in the skin.
Reflexes from the Skin
The thermosensitive structures in the skin are
probably a network of free nerve endings rather
than those special endings classically described.2
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2. These nerve endings have best been characterized
by Hensel, Iggo, and Witt.3 Both the warm and
the cold receptors have an electrical discharge
with a frequency dependent on the absolute tem­
perature of the skin. When change in tempera­
ture occurs, there is a sudden change in activity.
A cold receptor responds to cooling by a propor­
tionate, sharp but transient increase in discharge,
and to warming by an inhibition of discharge. A
warm receptor acts in the opposite direction. This
combination of electrical activity, relayed to the
central nervous system, indicates both the absolute
temperature and change in temperature of the skin.
The afferent nerve impulses from these receptors
in the skin pass to the central nervous system
through the peripheral sensory nerves, especially
along the C fibres, and probably in part along the
sympathetic nerves.4
Central Temperature Receptors
Some would attribute the whole of temperature
regulation to receptors in the skin5-6-7; however,
there is excellent experimental evidence that deep
or central receptors are present in both animals and
man.8-9-10 Heating of the anterior hypothalamus
of dogs causes an increased rate of respiration,
cutaneous vasodilation, and a fall in rectal tem­
perature.11-12 Recently, it has been shown that
cooling the blood to the brains of rabbits 13 or
directly cooling the anterior hypothalamus of
dogs 11 produces vasoconstriction and shivering.
It is not always possible to translate experimental
evidence from animals to man but in this instance
the translation is probably correct. The central
receptors are sensitive to changes of temperature
of less than 0.2 degrees centigrade.14
Experimental evidence suggests that there may
also be thermosensitive structures in other deep
parts of the body, particularly in the great veins,
heart, or lungs.13-15>16
The Efferent Nervous Pathways
The blood flow to the skin of the hand is
controlled largely by sympathetic vasoconstrictor
nerves and thus increased blood flow in the hand
occurs only as a result of release of vasoconstrictor
tone.17
In contrast, in the skin of the forearm there
are vasodilator fibers in addition to vasoconstrictor
nerves.18-19 The blood vessels of the muscles of
the forearm are supplied by vasoconstrictor nerves,
and they are normally subject to an appreciable
sympathetic vasoconstrictor tone. It is probable
that cholinergic vasodilator nerves are present to
the blood vessels in muscle of man but they do
not seem to enter into the changes in the fore­
arm blood flow that occur in response to heat­
ing.20-21 They do, however, take part in emo­
tional and postural reflex changes.
Shivering. Shivering is a rhythmic, involuntary
muscular activity. It is dependent on an intact
nervous system; the efferent pathways of its action
from the central nervous system include a pathway
in the anterolateral columns of the spinal cord and
the lower motor neurones. When there is disease
of the nervous system, temperature regulation may
be impaired; for example, shivering does not oc­
cur below the level of a spinal cord transection.
The Sweat Glands. The onset and rate of sweat­
ing has been closely correlated with changes in the
temperature of the blood flowing to the brain,22
but sweating can be initiated by reflexes from the
skin.23 Thermal sweating occurs below the level
of spinal cord transection, but is impaired.24
There is an important relationship between
sweat gland activity and vasodilatation of the skin.
The sweat glands are under the cholinergic sym­
pathetic nervous system. When sweat glands are
activated, they produce a polypeptide (brady-
kinin) which is a potent vasodilator and which dif­
fuses into the blood vessels in the neighborhood
of the sweating. There is a definite increase in the
degree of vasodilitation of the forearm blood ves­
sels during heating that usually occurs about the
time of onset of sweating.25
Reflex Effects of Application
Of Heat or Cold
When cold is applied to one part of the body,
vasoconstriction occurs within a few seconds in
the skin of other areas. This immediate response
is due to a nervous reflex mediated by the skin
temperature receptors and is dependent on an in­
tact nervous system. As the sensation of cold
diminishes the vasoconstriction will decrease. If,
however, the cooling is adequate to cool the blood
flowing into the central receptors, vasoconstriction
will be sustained as long as the cooling persists.9
If the vasoconstriction is not sufficient to prevent
a further fall in central temperature, shivering will
start.
Similarly with heating, consensual vasodilation
will occur as a reflex to heating the skin, although
to produce the initial response a large area of the
body (e.g., trunk) must be heated.26 With a rise
of central temperature the dilation continues and is
proportional to the rise.10 The reflex blood flow
increase through the forearm can be as much as
400 to 500 per cent, a change that occurs in the
skin with no change or even a decrease in muscle
flow.27-28
There are also secondary cardiovascular adjust­
ments to the circulatory changes such as increased
heart rate, increased cardiac output, shifts of blood
from some visceral organ, e.g., the kidney.
LOCAL EFFECTS OF
TEMPERATURE CHANGE
The direct local effect of the heating or cooling
also depends in part on an intact vasomotor inner-
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3. vation. In addition, there is an interaction between
the changes that occur in local tissues upon heat­
ing or cooling and the over-all thermal state of the
individual. For example, when a subject is lying
in a cool room and his peripheral circulation is
constricted to conserve heat, the local effect of
heating the skin will be considerably reduced.29
When heat or cold applications are made onto an
extremity, the greatest effect will be on the blood
vessels of the skin. The underlying muscles will be
effected only when application of heat or cold is
prolonged and vigorous and here, too, the prior
temperature of the local tissues will effect the re­
sponse. When the applied heat or cold stimulus is
a mild one, the response will be such as to assist the
body in maintaining its regulation of temperature.
This would be vasoconstriction to a cold stimulus
and vasodilatation to a warm one. However, when
the stimulus is very severe, the reaction in the local
tissues may be of a nature so as to reduce the po­
tential damage from the irritation. For example,
severe cooling of the hands may cause vasodilata­
tion, a response that tends to prevent the tissues
from freezing.
Heating
Local heating leads to vasodilation of the ves­
sels of the skin and possibly of muscles although
the reactions are not as simple as expected.30 Local
heating of an arm in water at 42 degrees centigrade
causes increased blood flow up to four or five times
that of resting level and this occurs almost, if not
entirely, in the skin of the arm. If the heating is
prolonged at temperatures of 39-42 degrees cen­
tigrade, the flow reaches a plateau in one hour
and then slowly declines. This "fall away" re­
sponse does not occur in water at 45 degrees cen­
tigrade at which temperature the vasodilation is
continuous. There is little good evidence that
local heating, either superficial or deep, can change
muscle blood flow. Abramson et al. reported a
modest increase in blood flow of the forearm with
heating by diathermy.31 However, they did not
show a consistent increase in the oxygen content
of blood draining the forearm muscle so it would
appear that the dilatation was largely in the skin.
The rate of metabolism of tissues is dependent
in part on temperature. The metabolism of skin
or muscle is increased an average of 13 per cent
for each rise in degree centigrade.32 Conversely,
metabolism is reduced when temperature falls.
Heating beyond 45 degrees centigrade causes ir­
reversible damage of tissue proteins and death of
the tissues.
Local dilatation can occur in the skin in re­
sponse to heating independently of the nervous
system and may be propagated away from the
local area of stimulation by a nonneural pathway,
possibly by a wave of relaxation conducted in the
smooth muscles of the subarterial plexus. A simi­
lar response occurs in reaction to a rubefacient
or ultraviolet light.33-34
Cooling
Cooling of the hand in water or air causes a
local decrease in blood flow. If the cooling is in
water below 10 degrees centigrade there is ini­
tially an intense vasoconstriction followed by pe­
riods of vasodilation. This cold vasodilation oc­
curs even in denervated fingers,35 but is greater
when the nerve supply is intact. The mechanism
of cold vasodilation is not fully understood.
Cooling of the forearm causes a decrease in
blood flow. Upon cooling of the skin in water
below 20 degrees centigrade no further reduction
takes place. There is no good evidence for vaso­
constriction in muscle with cooling although the
increased blood flow after ischemia or exercise is
reduced by cooling.30
When heat or cold is applied over a knee joint,
the blood flow through the tissues around the
joint, as measured by venous occlusion plethysmo­
graphy with the cuff above and below the knee,
is increased or decreased as expected.36 How­
ever, this does not necessarily mean that the blood
flow to the bony structures of the knee is changed.
In fact, the temperature of the knee joint may
actually be reduced when a superficial form of
heating such as hot packs is applied to the joint
or increased with a cold application.37 However,
with deep heating (diathermy or microwave) the
knee-joint temperature is increased37 and this
probably indicates an increased blood flow as the
clearance of Na24 from the knee joint is increased
up to 100 per cent by diathermy.38
RATIONALE FOR THERAPEUTIC
HEAT OR COLD
It is not difficult to understand and predict the
benefit of increasing or decreasing the blood flow
to an area when there is ischemia, inflammation,
or congestion. However, changes in circulation
through the skin and other tissues either locally
or generally do not in themselves explain all the
beneficial effect that seems to occur when these
applications are made as part of a therapeutic
regime.
The experimental evidence on which the ra­
tionale for thermotherapy to reduce pain or mus­
cle spasm is based is not wholly adequate. It is
suggested that when there is more than one form
of sensory stimulation—for example, heat plus
pain—the perception of either is reduced.39 In
support of this is the observation that local heating
of the skin reduces the sensation of pain to pulling
a hair.40 Conversely, when an area of the skin
is anesthetized, the pain arising from stimulation
of a nerve ending, e.g., tooth, is increased.41 It
is also possible that the nerve ending sensitivity
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4. to pain may be less when at other than a neutral
temperature.
Changing of the local temperature both in the
skin and in the subcutaneous tissues may decrease
the sensitivity of the muscle spindles to stretch.42
The muscle spindles and their reflex response to
stretch are an important element in the develop­
ment of increased muscle tone that occurs in some
diseases. In addition, it has been shown that
when the temperature of the central nervous sys­
tem is raised, the gamma efferent activity (that
activity which tends to increase the sensitivity of
the stretch receptors in muscle) is reduced.43
This may reflect one aspect of the observed bene­
ficial effect of general body heating above and
beyond that found with local temperature change
alone. In like manner, cooling has been used to
reduce muscular spasm. Here, too, it has been
reported that the tendon organ endings fire more
slowly when cooled.44 It has also been suggested
that there is an increased sympathetic activity
possibly with excess secretion of adrenaline when
there is cooling of the body and that this may in
some way change the nervous responses to stretch
and pressure.45 It is obvious that these results are
somewhat paradoxical and do not in any way per­
mit a clear and cohesive principle on which to base
the use of thermotherapy. The rational use of
these modalities will improve on further investi­
gation of the basic physiological effects.
REFERENCES
1. Pearl, R.: Introduction to Medical Biometry and Statis­
tics, Third Edition. London: W. B. Saunders Co.,
1940, p. 359.
2. Waddell, G.: Advances in Biology of Skin, Volume 1.
New York and Oxford: Pergamon Press, 1960, pp.
112-160.
3. Hensel, H., Iggo, A., and Witt, I.: A quantitative
study of sensitive cutaneous thermo receptors with C
afferent fibres, J. Physiol. (London), 153:113-126,
1960.
4. Cooper, K. E., and Kerslake, D. McK.: Abolition of
nervous reflex vasodilatation by sympathectomy of the
heated area, J. Physiol. (London), 119:18-29, 1953.
5. Burton, A. C., and Edholm, O. G.: Man in a Cold
Environment. London: Edward Arnold, Ltd., 1955,
p. 100.
6. Hensel, H.: Physiologie der Thermoreception, Ergebn.
Physiol., 47:166-368, 1952.
7. Thauer, R.: Mecanismes peripheriques et centraux de
la regulation de la temperature, Arch. Sci. Physiol.
(Paris), 15:95-123, 1961.
8. Sherrington, C. S.: Notes on temperature after spinal
transection, with some observations on shivering, J.
Physiol. (London), 58:405-424, 1924.
9. Pickering, G. W.: The vasomotor regulation of heat
loss from the skin in relation to external temperature,
Heat, 16:115-135, 1932.
10. Gerbrandy, J., Snell, E. S., and Cranston, W. I.: Oral,
rectal and oesphageal temperatures in relation to cen­
tral temperature control in man, Clin. Sci., 13:615-624,
1954.
11.Fusco, M. M., Hardy, J. D.. and Hamel, H. T.: Inter­
action of central and peripheral factors in physiological
temperature regulation, Amer. J. Physiol., 200:572-
580, 1961.
12. Fusco, M. M.: Calorimetric measurements by physio­
logical responses of the conscious dog to local heating
of the anterior hypothalamus, Physiologist, 1:25-26,
1958.
13. Downey, J. A.: Studies Relating to the Regulation of
Body Temperature. D.Phil. Thesis, Bodleian Library,
Oxford, 1962.
14. Pickering, G. W.: Regulation of body temperature in
health and disease, Lancet, 1:1-64, 1958.
15. Bligh, J.: Possible temperature-sensitive elements in or
near the vena cava of sheep, J. Physiol. (London),
159:85P, 1961.
16. Hallwach, O., Hupfer, H., and Thauer, R.: Die beden-
tungder Tiefen Korpertemperatur fur die Auslosung
der Chemischen Temperatur regulation, Pflueger. Arch.
Ges. Physiol., 274:97-114, 1961.
17. Fox, R. H., and Edholm, O. G.: Nervous control of
the cutaneous circulation, Brit. Med. Bull., 19:110—
114, 1963.
18. Edholm, O. G., Fox, R. H., and Macpherson, R. K.:
The effect of cutaneous anaesthesia on skin blood flow,
J. Physiol. (London), 132:15P, 1956.
19. Edholm, O. G., Fox, R. H., and Macpherson, R. K.:
Vasomotor control of the cutaneous blood vessels in
the human forearm, J. Physiol. (London), 139:455-
465, 1957.
20. Barcroft, H., Bock, K. D., Henschel, H., and Kitchen,
A. H.: Die Muskeldurchblutung des menschen bei in-
direkter erwarmung und abkulung. Pflueger Arch. Ges.
Physiol., 261:199-210, 1955.
21. Edholm, O. G., Fox, R. H., and Macpherson, R. K.:
The effect of body heating on the circulation in skin
and muscle, J. Physiol. (London), 134:612-619, 1956.
22. Benzinger, T. H.: The thermostatic regulation of hu­
man heat production and heat loss. In Proceedings of
the International Union of Physiological Sciences, Vol­
ume 1, 1962, pp. 415-438.
23. Brebner, D. F., and Kerslake, D. M.: The effects of
cyclical heating of the front of the trunk on the rate
of sweat production from the forearm, J. Physiol.
(London), 156:4P, 1961.
24. Seckendorf, R. C., and Randall, W. C.: Thermal re­
flex sweating in paraplegic man, Fed. Proc., 17:144,
1958.
25. Blair, D. A., Glover, W. E., and Roddie, I. C.: Vaso­
motor fibres to skin in the upper arm, calf and thigh,
J. Physiol. (London), 153:232-238, 1960.
26. Kerslake, D. McK., and Cooper, K. E.: Vasodilata­
tion in the hand in response to heating the skin else­
where, Clin. Sci., 9:31-47, 1950.
27. Clarke, R. S. J., and Hellon, R. F.: Venous collection
in forearm and hand measured by the strain-gauge and
volume plethysmograph, Clin. Sci., 16:103, 1957.
28. McGirr, E. M.: The rate of removal of radioactive
sodium following its injection into muscle and skin,
Clin. Sci., 11:91-99, 1952.
29. Hellon, R. F.: Personal communication.
30. Hellon, R. F.: Local effects of temperature, Brit. Med.
Bull., 19:141-144, 1962.
31. Abramson, D. I., Bell, Y., Rejal, H., Tuck, S. Jr., Bur­
nett, C., and Fleischer, C. J.: Changes in blood flow,
oxygen uptake and tissue temperature produced by
therapeutic physical agents, Amer. J. Phys. Med., 39:
87-95, 1960.
32. Du Bois, E. F.: The basal metabolism in fever, JAMA,
77:352, 1921.
33. Crockford, G. W., Hellon, R. F., and Parkhouse, J.:
Thermal vasomotor responses in human skin mediated
by local mechanisms, J. Physiol. (London), 161:10-20,
1962.
34. Crockford, G. W., Hellon, R. F., and Heyman, A.:
Local vasomotor responses to rubefacients and ultra­
violet radiation, J. Physiol. (London), 161:21-29,
1962.
35. Greenfield, A. D. M., Shepherd, J. T., and Whelan,
R. F.: Circulatory response to cold in fingers infiltra­
ted with anesthetic solution, J. Appl. Physiol., 4:785-
787, 1952.
36. Bonney, G. L. W., Hughes, R. A., and Janus, O.: Blood
flow through the normal human knee segment, Clin.
Sci., 11:167, 1951.
37. Horvath, S. M., and Hollander, J. L.: The influence
of physical therapy procedures on the intra-articularly
temperature of normal and arthritic subjects, Amer. J.
Med. Sci., 218:543, 1949.
38. Harris, R., and Millard, J. G.: Clearance of radioactive
sodium from the knee, Clin. Sci., 15:9, 1956.
39. Fischer, F., and Solomon, S.: Therapeutic Heat. New
Haven, Connecticut: Elizabeth Licht, 1958, p. 146.
40. Wells, H. S.: Temperature equalization for the relief
of pain, Arch. Phys. Med., 28:135, 1947.
716 10URNAL OF THE AMERICAN PHYSICAL THERAPY ASSOCIATION
Downloadedfromhttps://academic.oup.com/ptj/article-abstract/44/8/713/4629164bygueston13December2019

5. 41. Parsons, C. M., and Goetzl, F. R.: Effect of induced
pain on pain threshold, Proc. Soc. Exp. Biol. Med.,
60:327, 1945.
42. Sand, A.: The function of the ampullae of Lorenzini,
with some observations of the effect of temperature on
sensory rhythms, Proc. Roy. Soc. Med., 125:524, 1938.
43. Euler, C. von, and Soderberg, U.: Co-ordinated
changes in temperature thresholds for thermoregulatory
reflexes, Acta Physiol. Scand., 42:112-129, 1958.
44. Eldred, E., Schnitzlein, H. N., and Buckwald, S. J.:
Response of muscle spindles to stimulation of sympa­
thetic trunk, Exp. Neurol., 2:13, 1960.
45. Hunt, C. C.: Effect of sympathetic stimulation on
mammalian muscle spindles, J. Physiol. (London), 151:
332, 1960.
SELECTED BIBLIOGRAPHY
1. Boes, M. C.: Reduce spasticity with cold, J. Amer.
Phys. Ther. Ass., 42:29-32, 1962.
2. Brendel, W.: Die Bedeutung der Hirntemperatur fur
die Kaltegegenregulation I. Der Einfluss der Hirntem­
peratur auf den respiratorischen Stoffwechel des Hun-
des in thermoindifferenter Umgebung, Pflueger. Arch.
Ges. Physiol., 270:607-627, 1960.
3. Brendel, W.: Die Bedeutung der Hirntemperatur fur
die Kaltegegenregulation II. Der Einfluss der Hirn­
temperatur auf den respiratorischen Stoffwechel des
Hundes unter Kaltebelastung, Pflueger. Arch. Ges.
Physiol., 270:628-647, 1960.
4. Cooper, K. E.: The peripheral circulation, Ann. Rev.
Physiol., 24:139-168, 1962.
5. Hardy, J. D., Fusco, M., and Hamel, H. T.: Responses
of conscious dog to local heating of anterior hypothal­
amus, Physiologist, 1:34, 1958.
6. Horvath, S. M., and Hollander, J. L.: Effect of vaso­
dilating and vasoconstricting drugs on the temperature
of normal and arthritic joints, Arch. Phys. Med., 34:
162-168, 1953.
7. Miglietta, O. F.: Evaluation of cold in spasticity,
Amer. J. Phys. Med., 41:148-151, 1962.
8. Strom, G.: Influence of local thermal stimulation of
the hypothalamus of the cat on cutaneous blood flow
and respiratory rate, Acta Physiol. Scand., Supp., 70:
46-76, 1950a.
9. Strom, G.: Effect of hypothalamic cooling on cuta­
neous blood flow in the unanesthetized dog, Acta
Physiol. Scand., 21:271-277, 1950b.
10. Strom, G.: Vasomotor responses to thermal and elec­
trical stimulation of frontal lobe and hypothalamus,
Acta Physiol. Scand., Supp., 70:33-112, 1950c.
Hardening of Cerebral Arteries Not Caused by Aging
Aging accompanies hardening of the cerebral
arteries but is not a causal factor in this degenera­
tive process, according to Drs. J. A. Resch and A.
B. Baker, of Minneapolis.
Their conclusion was drawn from a study of
atherosclerosis within the circle of Willis based on
3,839 autopsies. A preliminary report on the study
appears in the June 1964 Archives of Neurology.
Within the brain, true atherosclerotic changes
are found chiefly along the vessels of the circle of
Willis and the changes, even in the earliest stages,
are visible to the naked eye, the authors explained.
The study revealed a correlation between age
of the patient and atherosclerotic changes, where
parts of the artery lining have thickened because
of deposits of fat or other material.
"There can be no question that atherosclerosis
gradually increases in the cerebral arteries with
age," the physicians said. "This is particularly
true of the more severe degenerative lesions.
"However, it is readily apparent that age alone
is not specifically related to this process.
"In our series, the atherosclerotic process was
first apparent in the second decade of life where 5
per cent of the cases showed some vascular
changes. Our youngest patient was fourteen years
of age. Moreover, 4 per cent of our patients in
the ninth and tenth decades of life showed no
grossly visible atherosclerotic changes.
"These observations would suggest that age
alone is not specifically related to this process but
rather that atherosclerosis is a chronic degenerative
disease of blood vessels requiring years for its de­
velopment and in which many factors no doubt
play an etiologic role. It appears more commonly
in older individuals where the causative factors
have ample time to produce the changes.
"Age, therefore, would be an accompanying fac­
tor rather than an etiologic agent in this degenera­
tive process."
The study also revealed sex differences in the
occurrence of atherosclerosis.
Cerebral atherosclerosis is less common in
younger women than in men of the same age
groups, the researchers reported.
This was particularly true in women between
forty and sixty who had from 11 to 19 per cent
less atherosclerosis than men of the same age. Be­
yond the age sixty, the two sexes showed very little
difference.
"From our present studies, it would appear that
there probably is a sex difference in cerebral
atherosclerosis and that this degenerative process is
represented in women in the younger age groups
in whom estrogenic activity is active," they said.
When a larger series of autopsies have been
completed, the question of sex differences and the
possible importance of estrogens, the female sex
hormone, in cerebral atherosclerosis may finally
be settled, they added.
The authors are affiliated with the University of
Minnesota Medical School.
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