Eye (1991) 5, 438-439
Response of Vessels to Ischaemia
G. A. GRESHAM
Cambridge
Ischaemia literally means the reduction or
In addition a variety of metabolic products
arrest of the blood supply to a tissue. The
accumulate which are numerous and have
result is a state of hypoxia in the territory sup­
diverse effects on the vascular wall. Hypoxia
plied by the compromised blood vessel. The
may result from causes other than vascular
effects of hypoxia on blood vessels in the pul­
obstruction and in general the effects upon
monary circulation have received consider­
the organ are similar to those produced by
able attention in the past but the effects on
ischaemia.
blood vessels in other parts of the body have
shunts, anaemia and histotoxic agents can all
not been so intensively studied.! Arteries,
lead to hypoxia.
circulatory
Pulmonary disease,
veins and capillaries do not respond in the
In some animals and particularly in man
same way to hypoxia and arteries in some
arteries are naturally hypoxic. This is largely
organs, such as the lung, respond differently
determined by the thickness of the vessel wall
to arteries in other organs such as the heart. In
and the number of lamellar units composed of
the eye, arteries and veins respond differ­
elastin and smooth muscle that are present. In
ently. In the hypoxic retina produced by sim­
thick
ulated high altitude conditions small arteries
depends upon the adequacy of blood supply
dilate, larger ones constrict and veins are
to the vessel by the vasa vasorum. In the dog
unaffected.
Furthermore,
the
walled
vessels
the
hypoxic
effects
vascular
vasa permeate the vessel wall as they do in
response in the retina varies from one subject
veins in many species. In man vasa supply a
to another. 2
limited territory of the outer third of the
To some extent the effects of ischaemia on
artery. Spontaneously occurring atherosclero­
blood vessels depends upon their structure.
sis in the dog is not described and extreme die­
The central retinal artery has features similar
tary
to those of arteries in skeletal muscle. After
produce it experimentally.
and
other
measures
are
needed to
the first division of the retinal artery the inter­
The inner part of the media of human arter­
nal elastic lamina is lost. This affects the per­
ies is a vulnerable structure. It survives on dif­
meability of the vessel wall to substances such
fusion from the capillary bed of the vasa and
as lipid.3 The capillaries of the choroid have
upon diffusion of nutrients from the lumen of
highly
the artery. It is a precarious existence and any
fenestrated
endothelial cells
again
affecting vascular permeability.4
Ischaemia can be caused either by organic
limitation of diffusion of nutrients as for
example
by
intimal
thickening
leads
to
disease of blood vessels such as atherosclero­
smooth muscle damage of the inner media.
sis or thrombosis or by functional changes
This is followed by a repair process which con­
such as vascular spasm or impaired blood flow
sists of smooth muscle cell proliferation. This,
due to changes in blood pressure or blood vis­
in turn, further thickens the arterial wall and
cosity. The obvious effect of ischaemia is to
aggravates the hypoxic state. Medial smootb
produce defective oxygenation of the tissue.
muscle cells that have proliferated migrate to
Correspondence to:
G.
A.
Gresham, TD, MD,
SeD,
FRCPath, Professor of Morbid Anatomy and
Histopathology, Department of Morbid Anatomy and Histopathology, John Bonnett Clinical Laboratories
Addenbrooke's Hospital, Cambridge CB22QQ .
RESPONSE OF VESSELS TO ISCHAEMIA
439
the intima and an atherosclerotic plaque is
The effects of drugs and vasoactive agents on
formed.
the process are being studied. Using subcuta­
Intimal changes leading to atherosclerosis
neous implants of plastic sponges in the rate of
are the result of endothelial injury. The injury
growth of new vessels in the sponges is being
is hypoxic. Many agents damage endothelium
investigated.
but haemodynamic changes figure largely in
measured by the rate of radioactive xenon
the process. Increased intraluminal pressure
clearance instilled into the centre of the
Vascular
development
leads to increased oxygen demand by the
sponge and
vessel wall. Rapid changes of pressure, either
europeaus labelling of endothelial cells in his­
increase or decrease, reduce flow in the vasa
tological sections. This is a useful model for
vasorum
the study of promoters and inhibitors of vas­
producing
hypoxic
conditions.
Rapid flow can produce axial streamlining
by morphometry using
is
Ulex
cular proliferation. Y
effects of red blood cells with flow stagnation.
Ischaemic damage is a common pathologi­
The localisation of atherosclerotic lesions is
cal process which plays a part in many diseases
best explained by haemodynamic forces.6
of degenerative, inflammatory and neoplastic
Other
origins. The facts that come into play when
factors
contribute
to
the
process,
diabetes: cigarette smoking and hyperlipid­
ischaemia develops are numerous and as yet
aemia are examples. High low density lipo­
only partly elucidated. Changes in the walls of
proteins
(LDL)
lead to transcellular and
pinocytotic uptake by endothelial cells. Oxi­
disation of imbibed
toxic
substances
LDL
blood
aggravate
the
ischaemic
are
still
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