Pathophysiology of

Hypertensive Retinopathy
MARK O. M. TSO, MD, * LEE M. JAMPOL, MDt

Abstract: The effects of systemic hypertension on the posterior segment of the eye are discussed under the headings of hypertensive
choroidopathy, hypertensive retinopathy, and hypertensive optic disc
edema. The sympathetic nervous control and autoregulatory mechanisms of the retinal and chorodial vasculatures are briefly reviewed. In
hypertensive choroidopathy focal occlusion of choriocapillaris leads to
necrosis of retinal pigment epithelium (Elschnig spots). Hypertensive
retinopathy is described in vasoconstrictive, exudative, and sclerotic
phases, followed by complications of the sclerotic phase. Hypertensive
optic disc edema is influenced by the blood supply and extracellular
tissue fluid pressure of the optic nervehead. In baboons with hypertensive disc edema, accumulation ofaxoplasmic components is observed
in the optic nervehead. [Key words: axoplasmic transport, blood-retinal
barrier, choriocapillaris, hypertensive choroidopathy, hypertensive optic
disc edema, hypertensive retinopathy, retinal blood vessels.] Ophthalmology 89:1132-1145, 1982

The histopathologic changes of the retina and

choroid in hypertensive retinopathy have been previously described meticulously, but in recent decades,
new observations of the physiologic response of the
ocular vasculatures to systemic hypertension have
been made. Furthermore, newer research tools, such
as the use of vitreous fluorophotometry and horseradish peroxidase to examine the blood-retinal barrier
and autoradiography to study axoplasmic transport,
have been applied to investigate further the pathophysiologic mechanisms of hypertensive retinopathy.
From the Georgiana Theobald Ophthalmic Pathology Laboratory,
Department of Ophthalmology, University of Illinois Hospital Eye
and Ear Infirmary.
Supported in part by Public Health Service Grants EY01903,
EY01904, EY2183 and core grant IP30 EY01792* and PHS EY
02214t
Dr. Tso is a Research to Prevent Blindness-William Friedkin
Scholar.
Presented at the Eighty-sixth Annual Meeting of the American
Academy of Ophthalmology, Atlanta, Georgia, November 1-6,
1981.
Reprint requests to Mark O.M. Tso, MD, Department of Ophthalmology, University of Illinois Hospital Eye and Ear Infirmary, 1855 West
Taylor Street, Chicago, IL 60612.

1132

In order to review the pathophysiology of hypertensive retinopathy, we have examined clinical data from
42 patients with hypertension. These clinical observations were compared with the histopathologic alterations in the retina and choroid noted in nine enucleated eyes from patients with a history of hypertensive
retinopathy. The pathophysiologic mechanisms of
hypertensive retinopathy were examined further in
three baboons with experimental hypertension.

MATERIALS AND METHODS

The clinical records of 42 adult patients with moderate to severe essential or renal hypertension have been
reviewed. 1 All patients had systolic blood pressures
above 170 mm Hg or diastolic pressures above toO mm
Hg at some time during their clinical course. Most of
the patients have been seen at three- to six-month
intervals by one of us (LMJ) for up to seven years.
Fundus photography, fluorescein angiography, and
vitreous fluorophotometry have been performed repeatedly on many of these patients. Eight of the patients had vitreous fluorophotometry performed when
their blood pressure was uncontrolled and sub0161-6420/82/1000/1132/$1.50

American Academy of Ophthalmology

TSO AND JAMPOL HYPERTENSIVE RETINOPATHY

sequently repeated at least once following control of

the blood pressure.
The histopathologic alterations of hypertensive retinopathy in patients were reviewed in nine eyes from
eight patients, all with a definitive history of hypertensive retinopathy. Seven of these eyes were enucleated
surgically for trauma or complications of chronic
glaucoma. Two eyes from a 38-year-old man who died
of acute renal failure were obtained at autopsy. Systolic pressures of these patients ranged from 160 to 220
mm Hg, and the diastolic pressures ranged from 100 to
160 mm Hg.
In order to study the ultrastructural changes of
hypertensive retinopathy and the disruption of the
blood-retinal barrier with horseradish peroxidase
tracer technique, systemic hypertension was produced
in three baboons with a modified two-stage Goldblatt
procedure. 2 A Goldblatt clamp was placed on the left
renal artery. Two to three weeks later the right renal
artery was narrowed by a suture ligature. The animals
were also fed a high cholesterol diet. The blood pressures ranged from 120/100 to 200/135 mm Hg. Six
hours before they were killed, 250 uCi of H3-leucine
were injected into the vitreous cavity. Thirty ininutes
before enucleation, horseradish peroxidase was injected intravenously. The retina and optic nerve were
processed for electron microscopy and horseradish
peroxidase tracer technique. Axoplasmic transport
was examined by autoradiography.

RESULTS AND COMMENTS

FIg 1 FluorescelO angIOgram of a 24-year-old patIent WIth Goodpasture's syndrome, renal fadure, and a blood pressure of 200/120
mm Hg HypertensIve chorOIdopathy WIth areas of hypoperfuslOn
(arrows) IS seen

patIents show fibrinoId necrosIs of the choroidal artenes and artenoles WIth occlUSIOn of the chonocapdlans (FIg 3) FIbrin and platelets are noted m the lumen
of the occluded caplllanes. A protem-nch exudate may
be seen III the subretmal space and in the external
pleXIform layer of the retma (FIg 4). The retinal pIg-

The retinal, choroidal, and optic nerve vasculatures

are supplied by different systems of blood vessels,
each having distinct anatomic and physiologic properties. In response to systemic hypertension, the tissues supplied by each of these vascular systems of the
eye are affected differently and show different manifestations. 3- 1o It is thus appropriate to approach the
pathology and pathophysiology of hypertensive retinopathy under the headings of (1) hypertensive
choroidopathy, (2) hypertensive retinopathy, and (3);
hypertensive optic disc edema.
HYPERTENSIVE CHOROIDOPATHY

Hypertensive choroidopathy ll-14 is seen in association with acute hypertension; it occurs in relatively
young individuals whose blood vessels are pliable and
not sclerotic. Patients may show signs of malignant
hypertension including encephalopathy. Hypertensive
choroidal changes may occur in patients with toxemia
of pregnancy, essential hypertension, renal disease,
pheochromocytoma, and acquired diseases of connective tissue.
Clinically, patchy areas of hypoperfusion of the
choriocapillaris may be detected by fluorescein angiography (Fig 1), and focal bullous detachment of the
retina may result (Fig 2). Histopathologically, these

FIg 2 HypertensIve chorOIdopathy 10 a 37-year-old woman WIth

blood pressure of 236/140 mm Hg Focal serous detachment of ret lOa
IS present'(arrow) Macular star WIth leakage of hard exudate IS seen
(arrowhead)

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OPHTHALMOLOGY OCTOBER 1982 VOLUME 89 NUMBER 10

-FIg 3 Hypertensive chorOIdopathy showIng flbnnOId necrosIs of artenal wall

(arrow), and focal occlUSion of chonocapIllans (arrowheads) (hematoxylmeosm, X320)

Fig 4 Hypertensive chorOIdopathy WIth

focal serous detachment of the macula (arrow) CystOId spaces (C) 10 the outer plexIform layer are filled wIth protemaceous flUId
The rest of the retma IS artefactltlOusly detached (hematoxylIn-eosIn , x 15)

...'.

.
" ..
'

-'

1134

~,

TSO AND JAMPOL HYPERTENSIVE RETINOPATHY

FIg 6 A, Elschmg spots (hypertensIve choroldopathy) m the

"healed" stage LesIOns (arrow) have a pIgmented center and a
hypoplgmented halo ThIS 48-year-old black man was hospItalIzed
SIX months earlIer for hypertensIve encephalopathy B, fluorescem
angIogram shows no leakage at the level of the retmal pIgment
epltheltum

FIg 5 A, Elschmg spots (arrows) m same patIent seen m FIg 2,

patchy yellow areas of retmal pIgment epIthelIum are seen B, leSIOns leak fluorescem dIffusely (arrows)

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OPHTHALMOLOGY. OCTOBER 1982 VOLUME 89 NUMBER 10

Fig 7 RetInal capillary

In a baboon with severe
systemic hypertensIOn
Severe narrOWIng of the
vascular lumen (L) and
early disruption of the
blood-retInal bamer with
leakage of horseradish
peroxidase tracer are
seen Leakage causes an
eosInophilIc granular
staInIng of the basement
membrane (arrows) and
extracellular space of
the retIna E, endothelium (x 11 ,200)

Fig 8 RetInal capillary

In a baboon with hypertensive retInopathy Vascular lumen IS extremely narrowed (arrowheads) and horseradish
peroxidase tracer leaks
Into the basement membrane (arrow) of the
endothelIal cells and
pencytes Focal degeneratIOn of the pencytes
IS seen E, endothelIum
(x8,OOO)

1136

FIg 9 Retmal capillary m

a hypertensive baboon
showmg degeneratIOn of
pencytes (P) E, endothelium. L. lumen (X5,667l

FIg 10 Retma m a hypertensIve baboon showmg leakage of horseradish peroxidase tracer (brownIsh deposit m the basement membrane of the retmal vessels, arrowhead), and through the retmal
pigment epithelium mto the subretmal space (arrows) (x200)

ment epIthelium (RPE) overlying regIOns of extensIve

occlusion of the chonocapIllaris appears yellow and
leaks fluoresceIn dIffusely (acute Elschnig spots) (Fig
5) Later, healing of the RPE takes place and results in
pigmented leSIOns with depigmented halos Leakage of
fluoresceIn is no longer seen (FIg 6), although WIndow
defects are present. In most cases, the retinal artenoles only show mIld narrowing but are otherwise
Intact (FIgs 2, 5), fibnnOId necrOSIS of the retInal vessels occurs In the most severe cases
PathophYSIOlogIcally, there are several explanatIOns
why the chorOIdal vasculature is affected more severely by acute hypertension than the retinal vasculature. 15- 19 AnatomIcally, the chorOIdal artenes run a
short course, without much branching, and supply the
choriocapillaris at right angles. The systemic blood
pressure IS therefore transmitted more directly to the
chonocapIllaris The lobular arrangement of the
chonocapillaris 13.20.21 in the postenor pole of the eye
explaInS the scattered array of Elschnig spots seen
WIth hypertenSIve choroidopathy.
Even though the choroidal vasculature has some
autoregulatory properties, vascular tone IS controlled
primarily by the sympathetic nervous system. In response to systemic hypertenSIOn, the choroIdal artenoles will InitIally undergo constnctIOn. A further
Increase In blood pressure overcomes the compensatory tone of the sympathetic response, resultIng in
damage to the muscle layer and endothelium. 17 In
contrast, the retInal circulatIOn has no sympathetic innervatIon and IS largely under the mfluence of autoregulatory mechanisms. It appears that, even with
severe elevatIOns of blood pressure (for short penods
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OPHTHALMOLOGY OCTOBER 1982 VOLUME 89 NUMBER 10

FIg 11 Focal degeneratIOn of retmal pIgment

epltheltum (R,) wIth
marked mflltratlOn of
horseradIsh peroxIdase
tracer The adjacent cell
(R , ) shows no mfiltratlon of the tracer mto the
c ytoplas m However ,
the tracer (arrow) passes
between the retmal pIgment epltheltal cells
( X 4,800)

1138

TSO AND JAMPOL HYPERTENSIVE RETINOPATHY

FIg 12 ExudatIve hypertensIve retmopathy wIth vascular occlUSIOn and remodeling m a 28-year-old black man wIth blood pressure of
240/180 mm Hg A, acute exudatIve retmopdthy wIth narrowmg (drrow) of the supenor temporal artery and dIlatatIOn of the dIstal segment of
the artery B, fluore.,cem dnglOgram show, focdl narrowmg of superotemporal retmal artery (arrow) and dIffuse dIlatatIOn and leakage of

fluorescem dI,tal to the sIte of narrow 109 Lo~s of retmal capIllanes and dIlatatIOn dnd leakage of the adjacent retmal vems are seen C, fundus
photograph three years later WIth better control of blood pressure Vascular remodelmg IS apparent The artery that was once narrowed IS now
a fine thread (arrow) Irregular pIgmentatIOn of the macula IS seen D, the narrowed vessel does not perfuse WIth fluorescem. and the vascular
bed has reperfu,ed The centrdl VISIOn I, permanently dIsrupted

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OPHTHALMOLOGY. OCTOBER 1982 VOLUME 89 NUMBER 10

Fig 13. A, a 26-year-old hypertensive patient with a blood pressure

of 160/100 mm Hg, showing focal areas of inner retinal thinning. B,
the same patient omitted medication and the blood pressure rose to
250/ 190 mm Hg. Hemorrhages (arrows) and cotton-wool spots (arrowhead) are seen.

of time) , the autoregulatory mechanisms of the retinal

vessels are able to maintain vascular tone and preserve
an appropriate physiologic milieu for the inner retina.
HYPERTENSIVE RETINOPATHY

Hypertensive retinopath y 4 ,5,9, lo,22- 28 may be conveniently divided into (1) a vasoconstrictive phase, (2) an
exudative phase, (3) a sclerotic phase, and (4) complications of the sclerotic phase. In the vasoconstrictive
phase (Figs 1, 5), an abrupt rise in systemic blood
pressure excites pliable and nonsclerotic retinal vessels to increase their vascular tone by autoregulation.
It is believed that there are basically two mechanisms:
(1) a metabolic mechanism , whereby the blood vessels
alter vascular tone and resistance so that the concentration of some important metabolite(s) in the retinal
tissues is maintained at a reasonable level, and (2) a
myogenic mechanism, whereby the adjustment of the
1140

vascular tone is regulated by pacemaker cells in the

vessel wall, which determine the transmural.pressure .
It must be remembered, however, that even though the
retinal vasculature within the eye has no sympathetic
innervation and is controlled by autoregulatory mechanisms , the central retinal artery outside the eye and
the ophthalmic artery are innervated by the sympathetics.
If elevated blood pressure is controlled promptly
with medications or surgery , the retinal blood vessels
may return to a normal state with no permanent
pathologic changes. On the other hand, if the blood
pressure remains highly elevated, the vascular tone
further increases with a great reduction in the lumen of
the retinal vessels. Disruption of the blood-retinal barrier occurs. By electron microscopy Ashton 23 suggested that endothelial necrosis was essential for leakage to occur. However, by horseradish peroxidase
tracer technique and electron microscopy, we have
demonstrated that leakage of horseradish peroxidase is
noted from blood vessels , which do not show necrosis
of the endothelium (Figs 7,8) . As plasma and blood
products leak into the vessel wall and infiltrate the
degenerated pericytes and muscle cells (Fig 9), "plasmatic vasculosis" is said to be present. The vascular
tone may be lost and the blood vessel dilates. The
capillary bed is exposed to higher pressures as autoregulation fails. At this stage in our baboon model,
we observed disruption of both the outer blood-retinal
barrier at the RPE and the inner blood-retinal barrier at
the retinal vasculature using ultrastructural tracers
such as horseradish peroxidase (Figs to , 10. This
series of events heralds the exudative phase of hypertensive retinopathy.
In the exudative phase , the blood-retinal barrier is
disrupted (Figs 12, 13). Plasma and formed blood elements leak into the retina, particularly in the region of
the macula. A macular star ma y be seen. Blood is extravasated, particularly in the nerve fiber layer of the
retina, to form flame-shaped and splinter hemorrhages . Retinal capillary dropout with areas of nonperfu sion may be observed by fluorescein angiography.
Cotton-wool spots are seen scattered in the posterior
pole . It has been demonstrated that the cotton~
wool spots are an accumulation ofaxoplasmic components 29 ,30 consisting of mitochondria, lamellated dense
bodies, and axoplasmic ground substance in the
proximal or distal ends of disrupted axons. Disturbance of both retrograde and orthograde axoplasmic
transport occurs in the area of a cotton-wool spot and
is believed to be due to focal retinal ischemia.
Disruption of the blood-retinal barrier during the
exudative phase of hypertension can be quantitated by
vitreous fluorophotometry. lOne hour following an intravenous injection of sodium fluorescein , the accumulation of fluorescein in the vitreous is measured.
Patients who have hypertensive retinopathy in the
exudative phase will have increased fluorescein concentration in the vitreous (Fig 14) . It is our experience,
in general, that patients with mild vasoconstrictive or

TSO AND JAMPOL HYPERTENSIVE RETINOPATHY

Fig 14 VItreous fluorophotometric tractng of a

patient In the exudative
phase of hypertensIOn
showing Increa~ed accumulatIon of fluorescein
In postenor vitreous one
hour after injectIOn of
sodIUm fluorescein (compare with Fig 15) R-retlna,
L-lens, Pv-postenor vitreous, my-mid-vitreous, a,antenor vitreous

Fig 15 Vitreous fluorophotometnc tracing of another patIent In the sclerotiC pha~e of hypertensIOn
showing normal level of
fluorescein accumulation
In vitreous one hour after
Intravenous fluorescein inJection (See legend, Fig 14)

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OPHTHALMOLOGY. OCTOBER 1982 VOLUME 89 NUMBER 10

Fig 16 Retmal vessels m sclerotic phase

of hypertensIve retmopathy showmg
moderate hyperplasIa of the tUnIca medIa (arrow) (hematoxylIn-eosm, x320)

Fig 17 HyalIne degeneratIOn of a retmal

vessel m a patIent wIth hypertensIve retmopathy, showmg loss of muscle cells m
the vessel wall (arrow) (hematoxyhneosm, x320)

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TSO AND JAMPOL HYPERTENSIVE RETINOPATHY

Fig 18 Retinal arterial macroaneurysm (arrow) In a patient With

advanced sclerotic phase of hypertensive retinopathy

sclerotic changes have normal vitreous fluorescein

concentrations (Fig 15). Patients with acute cotton
wool spots, flame-shaped hemorrhages, and exudates
have breakdown of the blood-retinal barrier with elevated vitreous fluorophotometric measurements.
Control of the blood pressure results in a return of the
vitreous fluorophotometric reading to normal. It is impossible to tell by this technique whether the fluorescein leakage occurs at the level of the RPE or the
retinal vasculature.
If the elevation of systemic blood pressure is not
severe, an exudative phase may not take place but
sclerotic changes gradually develop. Clinically, the
retinal vessels show copper wiring or, eventually,
silver wiring. Pathologically, the vessels disclose
hyperplastic sclerosis with thickening of the tunica
media and hyperplasia of muscle cells (Fig 16). Endarteritis fibrosa, consisting of thickening of the intima
by concentric lamination of myofibroblasts in a hyaline
ground substance, may be seen in the more severe
cases. As this degenerative state progresses, the retinal vessels develop hyalinized walls with loss of muscle cells (Fig 17).
Many complications may occur as the sclerosis advances; these include macroaneurysm formation 31 (Fig
18), microaneurysm formation, central retinal artery or
vein occlusion, branch vein occlusion, and epiretinal
membrane formation. In patients with vascular
obstructions, cystoid macular edema may also be
present. Vascular remodeling is seen commonly in the
late sclerotic phase, especially if the blood pressure
has been controlled (Fig 12). The nonperfused vessels
may recanalize, capillaries may open, and a smooth
muscle will deVelop around the dilated capillaries. Unfortunately, in spite of this vascular remodeling, visual
function may not return to these areas of the retina
because of previous infarction.
HYPERTENSIVE OPTIC DISC EDEMA

Patients with malignant hypertension show swelling

of the optic nervehead, with blurring of the margins of

Fig 19 A 26-year-old black female patient With hypertensive optic

diSC edema Note the absence of extenSIve hypertensIve retinopathy.

the optic disc (Fig 19). The pathogenesis of papilledema in hypertension has been a subject of dispute. 32
Some claim this to be secondary to hypertensive encephalopathy with elevated intracranial pressure. Venous stasis has been implicated. Others have observed
papilledema without increased intracranial pressure,
and an ischemic component has been suggested.
The optic nervehead has a complicated blood supply that reacts differently from that of the retina. The
optic nervehead is supplied anteriorly by branches of
the central retinal artery and posteriorly by pial vessels
and short posterior ciliary arteries passing through the
choroid and border tissue of Elschnig. Furthermore,
the optic nervehead is under the influence of intraocular pressure anteriorly and intracranial pressure
in the subarachnoid space posteriorly. With alteration
of the cerebrospinal fluid or intraocular pressure, there
may be changes in the tissue fluid pressure, which affects the blood flow of the optic nervehead. Thus, in
hypertensive retinopathy, there may be alterations in
the vascular supply to the optic nerve and changes in
tissue pressure. Ischemia may playa role in development of disc edema. A recent study in our laboratory
shows that in animals with papilledema secondary to
systemic hypertension, there is a delay in the axoplasmic transport at the optic nervehead. Axoplasmic
components accumulate in the region of the lamina
retinalis and lamina choroidalis anterior to the lamina
scleralis, resulting in swelling of the axons of the optic
nervehead (Figs 20, 21) and leading to optic disc
edema. It is uncertain if this axoplasmic stasis is a
result of ischemic or mechanical factors.

CONCLUSION
Professor Norman Ashton discussed the pathology
of hypertensive retinopathy at the Academy meeting
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OPHTHALMOLOGY. OCTOBER 1982 VOLUME 89 NUMBER 10

ten years ago, Dunng the past decade, advances have

been made In our understanding of the architecture of
the retInal and choroIdal vessels, the blood-retinal barners, and regulatory mechanisms of the ocular blood
vessels AxoplasmIc transport has been studied in the
optic nervehead and nerve fiber layer of the retina,
and the blood-retInal barner has been studied with VItreous fluorophotometry and horseradIsh peroxidase
tracer techmques, As a result of these advances, our
understanding of hypertenSIve retinopathy, choroidopathy, and dISC edema has Improved.

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Fig 20 An autoradtograph of the optiC nervehead of a hypertensive

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anterIor to lamma sclerahs (tolUIdme blue, x320)

7
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10

11

12

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15
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Fig 21 OptIc nervehead of a baboon with systemic hypertension,

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region of lamma chorOidahs (x8,OOO)

1144

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