1b// Vascular Endothelium Flashcards
basic structure of blood vessels
Tunica adventitia
Tunica media
Tunica intimia
vasa vasorum
Tiny vessels that feed larger vessels
structure of capillaries and venules
endothelium mural cells (pericytes) basement membrane
function of the microvascuar endothelium
promotes tissue homeostasis
what is microvascular endothelium a source of
angiocrine factors - tissue homeostasis and organ regeneration
examples of tissue specific (organotypic) variations of microvasculature
fenestrated - kidney
non-fenestrated - lung, skin, muscle, BBB
dicontinuous - liver
properties of endothelial cells
flat
large surface area
one cell deep monolayer
what is contact inhibition
cell junctions allow communication and information to tell adjacent cells to stop growing and form a monolayer
functions of blood vessels
vascular tone angiogenesis tissue homeostasis haemostasis permeability inflammation
what is produced by endothelial cells for angiogenesis
matrix products e.g collagen
growth factors
what is produced by endothelial cells for haemostasis
antithrombotic factors
procoagulant factors
what is produced by endothelial cells for inflammation
adhesion molecules
inflammatory mediators
what is produced by endothelial cells for vascular tone
vasodilator factors - NO, prostacyclin
vasoconstrictor factors - thromboxane A2, ACE
what factors can activate the endothelium
smoking viruses mechanical stress inflammation high BP oxidated LDL highglucose
stimuli for athersclerosis
hypercholesterolaemia DM hypertension sex hormone imbalance - menopause ageing oxidative stress proinflammatory cytokines infectious agents environmental toxins - smoking disturbed blood flow
steps of leukocyte adhesion cascade
rolling activation arrest adhesion transmigration
Where does recruitment of leukocytes occur in atherosclerosis
leukocytes adhere to activated endothelium of large arteries (not post-capillary venules) and get stuck in subendothelial space
monocytes migrate into the subendothelial space, differentiate into macrophages and become foam cells
4 mechanisms that contribute to the formation of atherosclerotic plaques
Leukocyte recruitment
Permeability
Shear stress
Angiogenesis
how does vascular permeability end up in athersclerosis
Increased permeability results in leakage of plasma proteins through the junctions into the subendothelial space
role of vascular permeability in athersclerosis
lipoproteins pass through leaky junctions into subendothelial space
oxidated by proteoglycans
macrophages inglobinate these and become foam cells
increased permeability allows this to occur
what is fatty streak formation
follows after endothelial dysfunction
macrophage foam cells filled with oxidated lipoproteins
where does athersclerosis happen and why
branch points
shear stress- flow patterns arent uniform so promotes inflammation
how is non-laminar flow harmful
thrombosis and inflammation - leukocyte recruitment
endothelial apoptosis
smooth muscle cell proliferation
loss of NO production
how is nitric oxide protective (6)
reduces lipoprotein oxidation dilates vessels reduces platelet activation reduces free radicals inhibits leukocyte recruitment reduces proliferation of SMCs
how is angiogenesis both harmful and protective
promotes plaque growth
but prevents damage post ischaemia
