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(cardioresp) vascular endothelium Flashcards

1
Q

where are the majority of endothelial cells found?

A

approx 98% of the endothelial cells reside within the microvasculature

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2
Q

what is the endothelium?

A

thin membrane that lines the inside of the heart and blood vessels

endothelial cells are responsible for releasing substances that control vasoconstriction, vasodilation and enzymes that control blood clotting and platelet adhesion

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3
Q

describe the basic structure of a blood vessel

A

tunica intima = endothelium, subendothelium, internal elastic lamina (smooth muscle + connective tissue)

tunic media = smooth muscle, external elastic membrane

tunica adventitia = vasa vasorum and nerves

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4
Q

what are the three layers of blood vessels?

(except capillaries and venules)

A

tunica adventitia (vasa vasorum, nerves)

tunica media (smooth muscle cells)

tunica intima (endothelium)

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5
Q

what does the tunic adventitia consist of?

A

vasa vasorum and nerves

(connective tissue layer)

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6
Q

what does the tunic media consist of?

A

smooth muscle cells

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7
Q

what does the tunic intima consist of?

A

endothelium

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8
Q

what is the vasa vasorum?

A

small blood vessels that comprise a vascular network supplying the walls of large blood vessels

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9
Q

what is the lamina propia?

A

part of the tunica intima

consists of connective tissue and smooth muscle

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10
Q

what are capillaries?

A

tiny, narrow blood vessels made entirely out of endothelium

where exchange of nutrients and oxygen between the blood and tissues takes place

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11
Q

what are venules?

A

very small branches that collect the blood from the various organs and parts

unite to form veins, which return the blood to the heart

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12
Q

describe the structure of capillaries

A

made up entirely of endothelium, supported by some mural cells (pericytes) and a basement membrane

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13
Q

how do capillaries compare structurally to veins and arteries?

A

capillaries are made up of endothelium and basement membrane with a few, supporting pericytes

whereas larger blood vessels are made up of three different layers: tunica intima, tunica media, and tunica adventitia

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14
Q

what are pericytes and where are they found?

A

contractile cells that wrap around endothelial cells in capillaries and post-capillary venules

control blood flow and homeostasis (i.e. blood-brain barrier)

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15
Q

how small are capillaries?

A

approx 1/10th of the width of a hair (5-10 micrometres)

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16
Q

why is the microvascular endothelium important?

A

promotes tissue homeostasis

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17
Q

what can damage to the endothelium result in?

A

organ dysfunction

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18
Q

how does the microvascular endothelium promote tissue homeostasis?

A

the endothelium is a source of angiocrine factors that are required for the maintenance of tissue homeostasis and organ regeneration

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19
Q

what are angiocrine factors?

A

molecules found in blood vessels’ endothelial cells that can stimulate organ-specific repair activities in damaged or diseased organs + promote tissue homeostasis

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20
Q

which diseases are affected by a dysfunctional endothelium?

A

ischaemia

chronic inflammatory diseases

cancer

diabetes

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21
Q

what is vascular and endothelial heterogeneity?

A

the variety in endothelial cell structure and function depending on time and location and health/disease

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22
Q

what is the significance of tissue-specific microvasculature?

A

the function of the microvasculature is very different in different organs and regions (i.e. is tissue-specific)

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23
Q

how does the microvasculature of the kidney and liver vary compared to that of the brain?

A

liver & kidney = very permeable vasculature for filtration function

(so microvasculature of endothelium looks very different from that in the brain|)

brain = tight vascular endothelium to prevent leakage

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24
Q

define organotypic

A

tissue-specific

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25
what is the significance of endothelial cells and the microvasculature being organotypic?
endothelial cells and microvasculature have organotypic (tissue-specific) properties and expression profiles (depending on time and location)
26
what are the types of endothelial cell connections?
continuous (fenestrated, non-fenestrated) discontinuous
27
where are continuous non-fenestrated endothelial cells found?
muscle, lung, skin, blood-brain barrier
28
where are continuous fenestrated endothelial cells found?
kidney glomerulus, gastrointestinal tract
29
where are discontinuous endothelial cells found?
liver, marrow sinus
30
how does the endothelium act as a barrier?
vital barrier that separates blood from the tissues
31
describe the surface area of the endothelium
very extensive = surface area \> 1000 m2 = weight \> 100 g
32
describe the size of endothelial cells
very flat, about 1-2 µm thick and 10-20 µm in diameter
33
describe the thickness of the endothelium
formed by a monolayer of endothelial cells (one cell thick)
34
what is the proliferation rate of endothelial cells like?
low proliferation rate unless new vessels are required via angiogenesis + long life span (cells undergo contact inhibition and stop proliferating)
35
when do endothelial cells proliferate?
angiogenesis (i.e when new blood vessels are required)
36
what is the life span of endothelial cells like?
long life span
37
what is endothelial cell contact inhibition?
abrupt arrest of the cell cycle that occurs between rapidly proliferating cells at the point when a confluent monolayer forms = control growth and proliferation of endothelium
38
why is contact inhibition important for the endothelium?
to control the growth and proliferation of the endothelium = preventing uncontrolled growth
39
what are the key functions of the endothelium?
tissue homeostasis and regeneration permeability inflammation vascular tone angiogenesis haemostasis & thrombosis
40
which disease is endothelial dysfunction most commonly related to?
atherosclerosis
41
why are angiocrine factors essential?
for tissue homeostasis
42
endothelial cells are heterogeneous: what does this mean?
their function and phenotype depends on their location
43
give examples of substances that are released by endothelial cells to facilitate their function
44
what does the resting endothelium stimulate?
anti-inflammatory, anti-thrombotic and anti-proliferative pathways
45
what does the activated endothelium stimulate?
pro-inflammatory, pro-thrombotic, pro-angiogenic pathways = triggering coagulation and angiogenesis
46
what can stimulate the activation of the endothelium from its resting state?
inflammation, hypertension, hyperglycaemia, viruses, smoking, mechanical stress
47
how do foam cells form as a result of endothelial injury?
initial injury = endothelium activated = increased endothelial permeability = increased leukocyte migration and adhesion so leukocytes (and also macrophages) accumulate in the subendothelial space = subsequent phagocytosis of lipids also in the subendothelial space (by macrophages) = foam cell formation + plaque growth as the form cell number increases
48
how do foam cells progress to become part of an atherosclerotic plaque? (steps of advanced atherosclerosis)
more macrophages accumulate in the subendothelial space together w the leukocytes, lipids and debris = a necrotic core is formed (i.e. chronic inflammatory lesion) as part of the response to the initial injury, a fibrous cap forms and walls of the lesion from the lumen (angiogenesis can also be stimulated as a result from the vasa vasorum in the tunica adventitia)
49
what is the trigger for atherosclerosis?
initial injury to the endothelium (or one of the factors that activate the endothelium = oxidised LDL, hypertension, hyperglycaemia etc)
50
in which area do macrophages accumulate to contribute to an atherosclerotic plaque?
subendothelial space
51
how are macrophages converted into foam cells?
macrophages in atherosclerotic lesions actively participate in lipoprotein (lipid) ingestion and accumulation giving rise to foam cells filled with lipid droplets = accumulation of lipid-filled foam cells leads to atherosclerotic plaque growth
52
what is a necrotic core?
a core of leukocytes, foam cells, macrophages, debris lipid and dead/dying cells forms due to oxidative stress and depleted ATP levels at the atherosclerotic lesion site
53
explain the significance of the formation of the fibrous cap in atherosclerosis
serves as a subendothelial barrier between the vessel lumen and the atherosclerotic necrotic core
54
why is the stimulation of angiogenesis during atherosclerotic plaque formation important?
in atherosclerotic plaques, due to the thickening of the arterial wall and inflammation = impaired oxygen delivery resultant hypoxia causes release of angiogenic factors angiogenic factors stimulate angiogenesis in the vasa casorum
55
why is angiogenesis of the vasa vasorum specifically, stimulated in atherosclerosis?
vasa vasorum supplies the endothelium and muscle of the arteries and veins so to increase oxygen supply to the atherosclerotic plaque, a lesion of the blood vessel (arterial) wall, the vasa vasorum must be increased via angiogenesis
56
can atherosclerosis happen in veins?
it can do rarely = only if they are connected to high-pressure circulatory part of the system but most often, if not always, happens in arteries as high pressure is though to be a factor required for atherosclerosis
57
define atherogenesis
the process of atherosclerotic plaque formation
58
what are the risk factors/stimuli for endothelial cell dysfunction in atherogenesis?
hypercholesterolaemia (oxidatively-modified lipoproteins) hypertension oxidative stress proinflammatory cytokines. (IL-1, TNF) infectious agents environmental toxins (cigarette smoke, air pollutants) hameodynamic forces (disturbed blood flow) diabetes mellitus/sex hormon imbalance/ageing
59
how can hypercholesterolaemia stimulate atherogenesis?
increased deposition of oxidatively-modified lipoproteins into the subendothelial space
60
how can sex hormone imbalance stimulate atherogenesis?
oestrogen deficiency, menopause
61
which proinflammatory cytokines stimulate atherogenesis?
IL-1, TNF
62
which infectious agents stimulate atherogenesis?
bacterial endotoxins, viruses
63
which environmental toxins stimulate atherogenesis?
cigarette smoke, air pollutants
64
how do haemodynamic forces stimulate atherogenesis?
due to disturbed blood flow
65
what are the four mechanisms of atherosclerosis pathogenesis?
leukocyte recruitment vascular permeability shear stress angiogenesis
66
explain the leukocyte adhesion cascade
inflammatory mediators will activate the endothelium and stimulate them to express surface molecules that facilitate leukocyte adhesion and migration
67
when does leukocyte recruitment into tissues take place?
normally, during inflammation
68
how does leukocyte recruitment take place in post-capillary venules?
leukocytes adhere to the endothelium of post-capillary venules and transmigrate into tissues
69
compare the structure of a capillary to that of a post-capillary venule
capillary = single endothelial cell layer surrounded by basement membrane and pericapillary cells (pericytes) post-capillary venule = structure similar to capillaries but more pericytes
70
how does leukocyte recruitment differ in atherosclerosis?
leukocytes adhere to activated endothelium of large arteries and get stuck in the subendothelial space
71
how do monocytes act in atherosclerosis?
migrate into the subendothelial space, differentiate into macrophages and become foam cells that contribute to the atherosclerotic plaque
72
how does vascular permeability vary in atherosclerosis?
normally, endothelium regulates the flux of fluids and molecules from the blood to tissues and vice versa so increased permeability results in leakage of plasma proteins from the blood through the junctions into the subendothelial space (already filled w sticky molecules like proteoglycans and ECM) = contribute to the atherosclerotic plaque
73
how do plasma proteins contribute to the atherosclerotic plaque?
increased vascular permeability results in increased plasma protein leakage into the subendothelial space
74
where does lipoprotein modification take place?
subendothelial space
75
explain how increased permeability to lipids increases the risk of atherosclerosis
during inflammation, endothelial gaps become wider so = more leaky junctions lipoproteins that normally would not, are now able to squeeze through the wider junctions and enter the subendothelial space (= increased permeability to lipids) where they undergo oxidative modification
76
how do foam cells form?
the macrophages that migrate to the subendothelial space will combine w the oxidised lipoprotein = foam cell
77
where do atherosclerotic plaques preferentially occur?
at bifurcations and curvatures of the vascular tree
78
why do atherosclerotic plaques preferentially occur where they do?
at bifurcations and curvatures of the vascular tree = flow patterns and hemodynamic forces are not uniform in the vascular system
79
what are the two types of blood flow?
``` laminar flow (continuous) disturbed flow (discontinuous) ```
80
how is blood flow and wall stress in the straight parts of the arterial tree?
blood flow is laminar and wall shear stress is high and directional
81
how is blood flow and wall stress in the branches and curvatures of the arterial tree?
blood flow is disturbed with non-uniform and irregular distribution of low wall shear stress
82
what is the protective effect of laminar blood flow on the vascular endothelium?
anti-thrombotic, anti-inflammatory factors endothelial survival inhibition of SMC proliferation nitric oxide (NO) proliferation
83
what is the disruptive effect of disturbed blood flow on the vascular endothelium?
stimulates thrombosis, inflammation (leukocyte adhesion) endothelial apoptosis SMC proliferation loss of nitric oxide (NO) proliferation
84
what kind of blood flow is associated with high shear stress?
laminar blood flow
85
what kind of blood flow is associated with low shear stress?
disturbed blood flow
86
why is nitric oxide important for the endothelium?
has protective effects on the vascular endothelium
87
why is smooth muscle cell proliferation harmful?
contributes to vascular lesion formation
88
list the functions of nitric oxide in the endothelium
dilates blood vessels reduces platelet activation inhibits monocyte adhesion reduces proliferation of SMC in the vessel wall reduces release of superoxide radicals reduces oxidation of LDL cholesterol (major component of plaques)
89
define angiogenesis
the formation of new vessels from existing vessels (via endothelial cell activation and proliferation)
90
what triggers angiogenesis?
hypoxia
91
foe which processes is angiogenesis essential?
embryonic development menstrual cycle wound healing
92
in which scenario can angiogenesis be particularly harmful?
when an atherosclerotic plaque becomes a chronic inflammatory condition = stimulates angiogenesis to contribute to plaque growth (i.e. advanced atherosclerotic plaques)
93
in which scenario can angiogenesis be particularly useful?
when angiogenesis can be induced to revascularise and prevent the loss of ischaemic tissue
94
where does leukocyte trasnmigration occur?
post-capillary venules
95
what is thromboinflammation and why does it occur?
loss of the normal anti-thrombotic and anti-inflammatory functions of endothelial cells causes thrombosis with associated inflammation = thromboinflammation (occurs in sepsis, ischaemia etc)

brs (phase 1b) (71 decks)

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