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The vasculature of the human penisA reexamination of the morphological basis for the polster theory of erection.

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THE ANATOMICAL RECORD 203:475-484 (1982)
The Vasculature of the Human Penis: A Reexamination of the
Morphological Basis for the Polster Theory of Erection
Department of Neurobiology and Anatomy (J.M.1,Department of Surgery
(Division of Urology1 (G.S.E.1, and Department of Pathology and Laboratory
Medicine (Division of Surgical Pathology1 (W.A.S.),The University of Texas
Medical School, Houston, Texas 77025
The morphology of human penile blood vessels has been studied
to characterize columns of smooth muscle found in the intima. Although previous
workers (Kiss, 1921; Conti, 1952)termed these intimal pads or polsters and concluded that they were actively responsible for the production of erection, more recent work has questioned these conclusions (Benson et al., 1980; Newman and
Tchertkoff, 1980).
Serial sections were taken throughout the length of the penis from 11 cadavers
and stained with various histopathological stains. Numerous polster-like structures were found, but all could be identified as either branch points in vessels, intimal cushions located at branch points, or arteriosclerotic lesions at various
stages of development. None of these structures seem capable of functioning in
the manner attributed to them by Conti (1952)and others. Furthermore, comparison of the structures found in the present study to illustrations of polsters in Conti’s paper suggest that these are identical.
The present study refutes the polster theory of erection and leaves open to further question the mechanisms involved in the control of blood flow into and within
the penis.
Myoendothelial cells, clusters of smooth
muscle cells within the intima of human blood
vessels, were first noted over a century ago,
but controversy over the function of these
structures continues today. Some have concluded that they control the flow of blood
through various organs (Bjorkman, 1947;Conti, 1952; Hibbs et al., 1958; Puchtler et al.,
1969; Meloan et al., 1972; Elias, 1977), while
others see them as evidence of pathological
processes in the arterial wall (Haust and More,
1958; Haust et al., 1960; Balis et al., 1964;
Rodgers et al., 1968; Ross and Glomset, 1977;
Irey et al., 1978). The most elaborate functional role proposed for these structures is
related to penile erection.
Early in this century, Von Ebner (1900)described muscular cushions and ridges in human penile vasculature (“polsterartige”) and
Kiss (1921)finding the same structures, agreed
that they might play a role in the process of
erection. Conti (1952).in a histological study of
penile tissue from 20 normal individuals varying in age from newborn to 77 years, found
many columns of primarily longitudinally oriented, intimal smooth muscle in both arteries
and veins; he termed these “polsters,” or intimal cushions, pads or bands, using these
terms interchangeably. He provided a detailed
explanation for the production of tumescence
and maintenance of detumescence based on
the function of these structures, which increased and decreased in size to control the
flow of blood through the penile vessels. Although Conti’s study was strictly anatomical,
and the physiological conclusions were purely
theoretical, the polster theory of erection has
been well accepted for many years.
In earlier studies of human and other mammalian penes (McConnellet al., 1979; Benson
et al., 1980),we were unable to find polsters in
any of the specimens. However, since the human penile tissue in these studies came from
young males who had received estrogen on a
daily basis for at least a year prior to undergoReceived July 8. 1981: accepted April 1. 1982
ing transsexual operations, it seemed advisable to examine a more heterogeneous, nonestrogen-treated population. In a subsequent
study of biopsy tissue from six (nontranssexual) males of varying ages (2-62 years; Benson
et al., 1981). we still found no evidence of
polsters as described by Conti (1952). Structures resembling polsters were found, but were
identified as branch points of vessels, intimal
smooth muscle cushions, or arteriosclerotic
lesions in various stages of development, none
of which seem capable of the function attributed to polsters by Conti (1952);arteriosclerotic
lesions are clearly pathologic, and subendothelial cushions have been implicated as prearteriosclerotic (Wilens, 1951; Lauper et al.,
1975; Kottke and Subbiah, 1978). Nevertheless, as these were negative data, and since
the study involved a limited population (only
six patients, the oldest of which was 62), and
biopsies which were generally small, superficial, and primarily from or near the glans, it was
considered necessary to make a more extensive
survey. The present study localizes and characterizes the smooth muscle columns found in
blood vessels throughout the entire penis, includes tissue from males over a wide range of
ages for comparison with the work of Conti
(1952),and critically evaluates Conti’s findings
and theory.
Serial sections were cut at 10-12 pm through
half of each block (ca. 50 sections). Every 10th
section was stained with hematoxylin and
eosin (H and E) for preliminary scanning; this
examination of the H and E sections was done
without the scanner’s knowledge of the age of
the individual. Whenever a polster-like structure was seen in an H and E section, the neighboring sections were treated with more specific
staining methods. These included phosphotungstic acid hematoxylin (PTAH), periodic
acid-schiff (PAS)with and without diastase digestion, Snook’sreticulin, Masson’s trichrome,
Verhoff-van Gieson’s elastica, Alizarin Red S.
and von Kossa’s calcium method.
Polster-like structures containing longitudinal smooth muscle cells were observed in
both intra- and extracorporal blood vessels of
the penis, but upon careful examination of
serial sections, most of these were identified as
either branch points of vessels (Fig. l),intimal
cushions (Fig. 2), or arteriosclerotic lesions in
various stages of development (Fig. 3); the
greatest number of cushions was seen in large
extracorporal veins and arterioles. Large
clusters of smooth muscle seen in the walls of
veins of the corpus spongiosum may be similar
to cushions or may be individual variations in
venous structure; nevertheless, they can be of
little significance in the erectile process as the
The entire penis, from the pubic arch to and corpus spongiosum does not contribute to
including the glans penis, was obtained from erection.
11cadavers varying in age from 38 to 83 years
Several specimens demonstrated no arterial
(Table 1). The penes were hemisected, cut cushions or arteriosclerosis, a finding unretransversely into blocks 5-7 mm in thickness, lated to the age of the individual. The
and processed for routine paraffin embedding. respective ages and the incidence of polster-
T A B L E 1. Extent and character of intimal thickenings in penile tissue from 11 cadavers.
Age of
‘Calcification of the wall of small vessels similar t o t h a t seen
Fig. 1. A tributary of the dorsal vein of the penis containing a polster-like structure (arrow)which is actually the
point a t which a smaller tributary enters. A large blood clot
(C)nearly fills the lumen of the larger vein. 61-year-old male.
FTAH. x 50.
Fig. 2. Branch of the dorsal artery of the penis containing intimal cushions (arrowheads) a t the point where two
small arterioles (arrow) exit. 49-year-old male. Verhoff-van
Gieson. x 132.
like structures found in each is shown in Table increased length of the penis during erection,
1; note that the greatest number of arterio- the intima may appear unusually thick in some
sclerotic lesions appear in some of the younger sections. These intimal thickenings (Fig. 5) are
men. Many of these structures are similar in easily differentiated from arteriosclerotic
appearance to Conti's illustrations of polsters changes by studying serial sections using sev(Fig. 4).
eral criteria, and special stains for elastic fiNonpathologic or typical arteries were en- bers, reticular fibers, mucopolysaccharides,
countered most frequently. These arteries are and smooth muscle cells. Arteriosclerotic
composed of three morphologically distinct lesions in their early stages and intimal
layers, the tunica adventitia, media, and cushions are characterized by intimal
intima. The tunica adventitia normally con- thickening from edema and smooth muscle intains loose connective tissue, blood vessels, filtration (Fig. 6A). In advanced stages of the
and small nerves. The tunica media is com- disease, the intima is significantly thickened,
posed of smooth muscle cells embedded in con- containing more smooth muscle, extensive colnective tissue and bordered by a layer of elastic lagen, and fibrotic tissue (Fig. 6B),and there is
fibers, the external elastic lamina. The normal fragmentation and duplication of the internal
intima consists of a single layer of endothelial and occasionally, the external elastic lamina
cells bounded by a narrow band of connective (Figs. 6B, C). The most advanced lesions
tissue, often containing a few smooth muscle demonstrate foamy histiocytes and fibrin decells, and a single layer of elastic fibers, the posits (Fig. 6D).
Most of the polster-like structures seen in
internal elastic lamina.
However, since penile blood vessels are ex- our study represent lesions at various stages in
tremely tortuous, in order to accommodate the the currently accepted sequence of the patho-
genesis of atherosclerosis as described by
Haust (1971), Ross and Glomset (1977), and
Kottke and Subbiah (1978).Structures identified as atherosclerotic lesions in our tissue
were compared with Conti’sillustrations (1952)
demonstrating polsters. As reported earlier
(Benson et al., 1981),the structures were virtually identical (Figs. 3,4,6).
During the mid 1880s, several histological
investigators, including Henle (1841), Remak
(1850), and Koelliker (1854),reported finding
cells that resembled smooth muscle within the
intima of blood vessels. In addition, Koelliker
stressed the resemblance of these cells to the
endothelium, and Henle concluded that the
morphological similarities suggested a developmental relationship between the two. Langhans (1886)reasoned that the intima was connective tissue, and thus the cells in the subendothelial layers must be considered fibroblasts
or fibrocytes. For over a century, there was
disagreement over the identity as well as the
origin of these cells. Finally, using the electron
microscope, Balis et al. (1964) and Reale and
Ruska (1965) demonstrated conclusively that
the subendothelial cells are smooth muscle.
The origin of these cells, however, remains
Curiously, the subendothelial cells closest to
the internal elastic lamina have always been
considered to be smooth muscle, and were
noted to occur frequently near areas when the
lamina was split or frayed. These clusters of
cells were thought to originate from the tunica
Fig. 3. Penile arteries demonstrating polster-like arteriosclerotic lesions a t various stages of development. A)
Central artery of the corpus cavernosum (deep artery of the
penis) demonstrating several regions of intimal smooth
muscle proliferation and edema (arrows). 83-year-old male.
H and E. x 96. B) Branch of the dorsal artery of the penis
with a small area of arteriosclerotic intimal thickening
(arrow).This Verhoff-van Gieson stain shows the disruption
and duplication of the internal elastic lamina typical of arteriosclerosis. 83-year-old male. x 70. C) Branch of the dorsal
artery of the penis with two more advanced arteriosclerotic
lesions (arrows).These structures contain longitudinally oriented smooth muscle interspersed with some disorganized
smooth muscle cells a s well as collagen and fibrin, and show
some disruption of the internal elastic lamina (arrowhead).
81-year-old male. Masson trichrome. x 64. D) Advanced
atheroma in a branch of the dorsal artery of the penis. The
lumen has been significantly decreased by proliferation of
smooth muscle, collagen, and fibrin in the intima. Note the
duplication and thickening of the internal elastic lamina.
66-year-old male. Verhoff-van Gieson. x 88.
media. Thoma (1883) proposed that such
smooth muscle appeared within the intima
after disruption of normal hemodynamics.
Borst and Enderlen (1909), studying wound
healing in blood vessels, particularly vascular
transplants, found that many cells resembling
smooth muscle appeared in the intima within a
few days after suturing. After histological
studies, they concluded that these arose by
transformation of endothelial cells. Electronmicroscopic studies have likewise demonstrated that smooth muscle seen in arteriosclerotic
lesions may also arise from the endothelium
(Haust et al., 1960). How the subendothelial
smooth muscle relates to wound healing or to
the disease process of arteriosclerosis is still
not fully understood. I t has been suggested,
however, that these muscle clusters may represent a reaction to the stresses of normal blood
flow, thus being a response to injury (Neufeld
et al., 1962). and an attempt to counteract the
decreased contractility of the weakened vessel
wall (Haust et al., 1960). This same function
might be expected in a vessel which is in the
process of healing after transplantation.
During the past 20 years, careful study of autopsy specimens correlated with results of various experimental studies and the use of animal models have revealed the major elements
and details of the pathogenesis of atherosclerosis. The major current theories of atherogenesis share the belief that the lesions begin as
localized, excessive accumulations of intimal
smooth muscle (intimal thickenings, intimal
cushions, intimal hyperplasia). The theories
differ, however, in what initiates these accumulations and what makes them grow. It is not
yet clear whether the increased smooth muscle
is derived from endothelial cells, from a
relatively small preexistent population of intimal smooth muscle, or from smooth muscle
cells of the tunica media which migrate into the
intima and subsequently proliferate. Regardless, the intimal smooth muscle cells proliferate in response to endothelial injury, and such
smooth muscle clusters are generally considered to be a sign of vascular disease (Kottke
and Subbiah, 1978; Irey et al., 1978).
In experimental studies, injury to or removal
of the endothelium from an artery stimulates
the migration of smooth muscle cells from the
media. The endothelium starts to regenerate in
3-5 days, and the smooth muscle cells appear
shortly thereafter. A t the end of 2 weeks, the
endothelium is completely regenerated, but
the intima is thickened considerably by a p
proximately 5-10 layers of smooth muscle
Fig. 4. Illustrations of “polsters” from Conti’s paper
(1952).Left, A, B (from Figs. 9A. D). Intracavernous branches of the deep artery of the penis (central artery). Right, C, D
(from Figs. 8B. D). Branches of the dorsal artery of the pe-
nis. Hollborn elastic stain. (Reprinted from Conti G: Lerection du penis humain et ses bases morphologico-vasculaires.
Acta Anat.. 14.217, 1952. with permission from S. Karger
AG. Basel.).
cells which remain there permanently (Ross
and Glomset, 1973). The injury site is easily
distinguished from an area of normal intima
which contains only a few smooth muscle cells.
Endothelial damage also can be accomplished
by injecting fatty acids into the ear vein of rabbits (Sedar et al., 1978), and intimal thickenings composed of smooth muscle cells occur
when rabbits are fed cholesterol (Parker, 1960).
Further, in diseased segments of blood vessels
replaced by tubes of artificial fibers, the pseudointima which subsequently lines these fabric
grafts is composed of connective tissue and
smooth muscle cells covered by neo-endotheli-
um (Florey et al., 1961); indeed, a common
problem in these grafts is intimal proliferation
to such an extent that it causes lategraft occlusion (Kottke and Subbiah, 1978). Considering
the above, it is not difficult to comprehend that
the incidence of intimal smooth muscle increases with age, and that there is a greater
chance of finding atherosclerotic plaques in an
elderly individual.
Almost all of the above data on intimal hyperlasia and atherosclerosis was not available
at the time Conti (1952)put forth his theory of
erection. Conti’s work was part of an extensive
effort to demonstrate that blood vessels were
Fig. 5 . Small branch of the central artery demonstrating a thickened and uneven intima due to the tangential cut of this
very tortuous arteriole. 73-year-old male. H and E. x 280.
not passive carriers of blood, but were active in
regulating blood flow. Bucciante, one of the
leaders of this school, had previously shown
that elastic fibers and smooth muscle in blood
vessels increased with the age of the individual, and had concluded that these were adaptations to improve the local flow of blood (cf.Conti, 1952). Conti’s report of clusters of intimal
smooth muscle which he named “polsters” or
“polsterkissen”(German, cushions) in penile arteries and veins of newborn and infant males
added support to the belief that these were
functional structures. These early-appearing
clusters of smooth muscle were found most
often at branch points of vessels, and are still
generally considered to be “intimal cushions.”
The difference, however, is that they are no
longer accepted as functional elements since
they have been implicated in arterial disease.
(A distinct problem arises with respect to terminology in this field. Von Ebner, Kiss, Conti,
and others employed the terms “polsterkissen”
and “coussinet,” both of which translate as
“cushion,” and used these terms interchangeably with words meaning “pad,” “column,”
“fascicle,” and “cluster” when referring to intimal thickenings. “Polster” in the present terminology refers specifically to those structures of widely varying size in the penile
vasculature which have varying amounts of
smooth muscle, edema, and connective tissue,
and which are supposed to regulate blood flow
to effect erection and detumescence. “Intimal
cushions,” however, are generally considered
to be regions in the vascular intima with some
smooth muscle proliferation and minimal
edema and connective tissue. Some consider
the latter structures to be the first sign of arteriosclerosis, but others feel that these are
regions which may develop into arteriosclerotic lesions.)
Although penile tissue from very young individuals often contains a few of these structures, their number is variable (Newman and
Tchertkoff, 1980). The incidence of cushions
generally increases with age, and they appear
related to arteriosclerosis in both man and
laboratory animals (Wilens, 1951; Neufeld et
al., 1962; Kottke and Subbiah, 1978); most
cushions are found at branch points of vessels
which is also the site of early atherosclerotic lesions. Nevertheless, the precise relationship of
cushions to atherosclerotic plaques has not
been determined conclusively, and it would appear that all intimal cushions do not become
atherosclerotic plaques and that all plaques do
not develop in preexisting intimal cushions
(Kottke and Subbiah, 1978).
Fig. 6. High power photomicrographs of arteriosclerotic
lesions in penile arteries. A) Enlargement of small lesion on
left of artery in Figure 3C showing some longitudinally oriented and some disorganized smooth muscle (arrows),edema in the intima, and gaps in the internal elastic lamina (arrowheads). 81-year-old male. Masson trichrome. x 320. B)
Nearby section from the artery shown in Figure 3D demonstrating smooth muscle surrounded by extensive collagen
and some fibrin deposits. 66-year-old male. Masson
trichrome. x 190. C. Section adjacent to t h a t shown in
Figure 6B. The Verhoff-van Gieson stain demonstrates that
duplication, thickening, and occasional fragmentation of the
internal elastic lamina. x 190. D) Advanced atheromatous
lesions in a branch of the dorsal artery of the penis contain
ing foamy histiocytes (arrows). fibrin (arrowhead). and
general disruption of the intima. 49-year-old male. H. and E.
x 340.
Conti’s (1952)study of human penile vasculature and his explanation for penile erection
have been completely accepted by the medical
community even though his hernodynamic
conclusions were based solely on histologic
data. In his examination of penile tissue from
20 individuals varying in age from birth to 77
years, he found many instances of intimal
smooth muscle clusters and columns. From
their organization, he assumed that they were
functional elements subserving the control of
blood flow and postulated a detailed schema
for tumescence and detumescence. Although
Conti’s paper was published less than 30 years
ago, the photomicrographs showed little
detail, and many illustrations were drawings of
blood vessels taken from earlier papers. A
detailed description of the smooth muscle columns seen in various individuals with various
histological stains was provided, but no information was given about the innervation of
these structures. We consider these micrographs, drawings, and descriptions to depict
branch points, arterial cushions (which may or
may not be pre-atherosclerotic), and atherosclerotic plaques in various stages of development. Conti (1952), in fact, characterized a
well-developed polster as having duplication of
the internal elastic lamina as well as many intimal smooth muscle cells surrounded by collagen and other connective tissue elements.
These are now considered indicative of an intermediate stage of atherosclerotic plaque formation. That polsters are actually evidence of
atherosclerosis is further supported by the
findings of Ruzbarsky and Michal (1977)who
found that the most characteristic change in
the penile vasculature due to age and diabetes
is “fibrosis of the polsters and fibrotic proliferation of the intima in other areas.” They
described the gradual replacement of the
smooth muscle cells, the “functional element”
of polsters, by inelastic collagenous connective
tissue, and the thickening, fragmentation, and
eventual fibrosis of elastic membranes. Endothelial defects often occurred over these
fibrotic polsters and, in some cases, the intima
was obliterated by fibrotic proliferations
within the polster. Calcium deposits were
usually found within polsters which showed
advanced stages of fibrosis. Such changes
describe exactly the presently accepted sequence of the pathogenesis of atherosclerosis
(Ross and Glomset, 1977).
Furthermore, if polsters were to function as
hypothesized, they would have to receive innervation from their periphery or be otherwise
stimulated to change shape. As yet, no information showing the innervation of these structures has appeared in the literature or been obtained in this laboratory. Indeed, to stimulate
these muscle clusters, neurotransmitters
would have to diffuse through the entire thickness of the vessel wall or through the endothelium since nerve fibers are found only in the
vascular adventitia (Keatinge, 1979).
In conclusion, the present study presents
data refuting the polster threory of erection
and leaves open to further question the physiologic mechanisms responsible for control of the
regional blood flow of the penis.
The authors wish to express their appreciation for the excellent technical assistance of
Ms. Donna Harrison who made significant contributions to the analysis of the data as well as
the preparation of the histological material and
the photographic reproductions .
This investigation was supported in part by
a NIAMDD Clinical Investigatior Award ( # 5
KO8 AM00824-02)from the National Institute
of Arthritis, Metabolic and Digestive Diseases
awarded to George S. Benson, M.D.
Balis, J.U., M.D. Haust, and R.H. More (1964) Electronmicroscopic studies in human atherosclerosis. Exp. Mo.
Pathol., 3:511-525.
Benson, G.S., J.A. McConnell. L.I. Lipshultz. J.N. Corriere.
and J oe Wood (1980) Neurornorphology and neuropharmacology of the human penis. J. Clin. Invest..65:506-513.
Benson, G.S.. J.A. McConnell. and W.A. Schmidt (1981)
Penile “polsters”: Functional structures or atherosclerotic
changes? J. Urol., 125:800-803.
Bjorkman. S.E. (1947) The splenic circulation with special
reference to the function of the spleen sinus wall. Acta
Med. Scand. Suppl.. 191:l-89.
Borst, H.. and V. Enderlen (1909) Die Transplantation von
Gefassen and ganzen Organen. Dt. 2. Chir.. 99:54-163.
Conti. G. (1952)Lerection du penis humain et ses bases morphologico-vasculaires. Acta Anat., 14:217-262.
Elias, H. (1977)Smooth muscle cushions in arteries (letter).
N. Engl. J. Med., 2%:944.
Florey, H.W.. S.J. Green, J.C.F. Poole. andN.T. Werthessen
(1961)The pseudointima lining fabric grafts of the aorta.
Br. J. Exp. Pathol., 42:236-246.
Haust. M.D. (1971)The morphogenesis and fate of potential
and early atherosclerotic lesions in man. Hum. Pathol.,
Haust. M.D., and R.H. More(1958) New functional aspects
of smooth muscle cells. Fed. Proc., 17:440.
Haust, M.D., R.H. More, and H.Z. Movat (1960)The roleof
smooth muscle cells in the fibrinogenesis of arteriosclerosis. Am. J. Pathol., 37:377-389.
Henle J. (1841) Allgemeine Anatomie. Lehre von den Mischungs-und Formestandteilen des menschlichen Korpers.
L.Voss, Leipzig (cf. Puchtler e t al., 1969).
Hihbs. R.G., G.E. Burch, and J.H. Phillips (1958) The fine
structure of the small blood vessels of normal human dermis and subcutis. Am. Heart J.. 56:662-678.
hey. N.S., H.A. McAllister, and J.M. Henry (1978)Oral contraceptive and stroke in young women: A clinicopathologic correlation. Neurology, 28:1216-1219.
Keatinge. W.R. (1979) Blood vessels, Br. Med. Bull.,
Kiss, F. (1921) Anatomisch-histologishe untersuchungen
uher die Erektion. Z. Anat., 61:455-521.
Koelliker, A. (1854) Manual of Human Microscopic Anatomy (translated by G. Busk and T. Huxley; edited by J.
DaCosta). Lippincott, Grambo, and Co., Philadelphia.
Kottke. B.A., and M.T.R. Subhiah (1978) Pathogenesis of
atherosclerosis: Concepts based on animal models. Mayo
Clin. Proc., 53:35-48.
Langhans, T. (1866) Beitrage zur normalen und pathologischen anatomie der arterien. Virschows Arch. [Pathol.
Anat. Physiol.], 36:187-205.
Lauper, N.T., K.K.Umni, B.A. Kottke,andS.L.Titus(1975)
Anatomy and histology of aorta of White Carneau Pigeon.
Lab. Invest., 32:536-551.
McConnell, J.A.. G.S. Benson, and Joe Wood (1979) Autonomic innervation of the mammalian penis: A histochemical and physiological study. J. Neurol. Ransm.,
Meloan. S.N., F.S. Waldrop, H. Puchtler. and L.S. Valentine
(1972)Cross-striated myoendothelial cells in splenic venous sinuses. J. Reticuloendothel. Soc.. 11:566-578.
Neufeld, H.N., C.A. Wagenvoort, and J.E. Edwards (1962)
Coronary arteries in fetuses, infants, juveniles, and young
adults. Lab. Invest., 112337-844.
Newman, H.F., and V. Tchertkoff (1980) Penile vascular
cushions and erection. Invest. Urol., 18:43-45.
Parker, F. (1960) An electronmicroscopic study of experi-
mental atherosclerosis. Am. J. Pathol., 36:16-53.
Puchtler. H.. F. Sweat, M.S. Terry, andH.M. Conner(1969)
Investigation of staining polarization and fluorescencemicroscopic properties of myoendothelial cells. J.
Microsc., 89:95-104.
Reale, E., and H. Ruska (1965)Die Fienstruktur der Gefasswande. Angiologia, 2:314-366.
Remak. R. (1850)Histologische Bemerkingen uher die Blutgefasswande. Mullers Arch. Anat. (cf. Puchtler et al.,
Rodgers. J.C., H. Puchtler, and S. Gropp (1968)Histochemical polarization and fluorescence-microscopic studies of
hyaline arteriosclerosis in spleens. Lab. Inves.,
Ross, R., and J.A. Glomset (1973) Atherosclerosis and the
arterial smooth muscle cell. Science, 180:1332-1339.
Ross, R., and J.A. Glomset (1977)The pathogenesis of atherosclerosis. Parts I and 11. N. Engl. Med. J., 295:
Ruzharsky, V., and V. Michal(1977)Morphologic changes in
the arterial bed of the penis with aging. Invest. Urol..
Sedar, A.W., M.J. Silver, J.J. Kocsis, and J.B. Smith (1978)
Fatty acids and the initial events of endothelial damage
seen by scanning and transmission electronmicroscopy.
Atherosclerosis, 30.273-284.
Thoma, R. (1883) Ueber die abhangigkeit der Bindegewehsneubildung in der Arterieintima von der mechanischen
Bedingungen des Blutumlaufes. Arch. Pathol. Anat.
Physiol. Klin. Med., 93t433-505.
Von Ebner. V. (1900)Ueber klappenartige Vorrichtungen in
den Arterian der Schwellkoroer. Verh. Anat. Ges..
Wilens. S.L. (1951)The nature of diffuse intimal thickening
of arteries. Am. J. Pathol., 275325-833.
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