Exam 3: Vascular Flashcards
3 layers (tunics) in wall of blood vessels
Tunica intima, Tunica media, Tunica adventitia
Tunica intima
innermost layer of blood vessel
Innermost endothelial cells are simple squamous connected to a basal lamina
External to basal lamina is thin layer of subendothelial connective tissue.
Most external component is internal elastic lamina
Subendothelial layer
middle layer of tunica intima
loose connective tissue, scattered fibroblasts and in arteries some smooth muscles
Internal elastic lamina
membrane around subendothelial layer of tunica intima
made of elastin
Contains fenestrae for diffusion of substances
Tunica media
concentric layers of smooth muscle cells
Has elastin, elastic fibers, reticular fibers, and proteoglycans
Outer layer is External elastic lamina (membrane) - made of elastin
Tunica adventitia (externa)
outermost layer of blood vessel
Connective tissue layer, type I collagen fibers, elastic fibers, and fibroblasts
Has blood vessels and nerve fibers - send branches to outermost layer of tunica media
Vasa vasorum
required for vessels greater than 1 mm in diameter
penetrate deeper in veins than arteries
contribute to angiogenesis and inflammation in atherosclerosis
Vasa vasorum of ascending aorta becomes inflammed in
syphilis
Endarteritis and periarteritis of vasa vasorum - become obliterated
Causes death and scarring of tunica media and elastic lamellae
Scarring causes depressions seen on surface of intima
Nervi vasorum
innervation - autonomic nerve fibers supply blood vessel walls
Mostly sympathetic nerve fibers
Travel with tunica adventita - innervate outer media, but don’t go inside in arteries
In veins, nerve endings found in adventitia and media
Release noroepinephrine
Endothelial cells
flattened, polygonal cells
long axis in direction of blood flow
Tight intercellular junctions between cells and to basal lamina
Contain pinocytotic vesicles to transport materials between lumen and deeper layers
Myoendothelial junction
Stress exerted by blood flow produces endothelial cell hyperpolarization
Conducted to vascular smooth muscle via gap junctions - they hyperpolarize and cause vasodilation
Weibel-Palade bodies
located in endothelial cells
Contain Von Willebrand factor (coagulating factor VIII) - promotes blood clotting; Tissue plasminogen activator; Interleukin 8; P-selectin - allows leukocyte to connect with wall of endothelium and migrate through wall of vasculature
Endothelial cells function to
Promote/inhibit blood coagulation (production of prostacyclin - vasodilator that inhibits blood clotting)
Modulate smooth muscle activity (vasodilation (NO) and vasocontriction factors (Endothelium 1)
Regulate inflammatory cell traffic
Transport material through pinocytotic vesicles
Regulate angiogenesis
Arteries have more __________, Veins have more __________.
Smooth muscle and elastin; connective tissue
Elastic (Large) artery
Aorta, brachiocephalic trunk
Have large tunica media with alternating layers of smooth m. and elastic lamellae (elastin, no elastic fibers)
Elastic lamellae increases with age (gets thicker tunica media)
Normal aging
causes increase in elastic lamellae and mild to moderate intimal fibrosis and fagmentation of elastic lamealle in media
Marfan’s syndrome
severe elastic medial fragmentation with GAG area
Muscular (moderate) artery
Tunica media has a lot of smooth muscle, diminishing elastic components
Prominent internal elastic and external elastic membranes
Aging results in progressive intimal fibrosis (thickening) and alterations of elastic elements
Arteriole
Ratio of wall thickness to diameter is about equal to 1
One prominent smooth muscle layer exterior to basal lamina
Metarterioles
vessels between arterioles and capillaries
Media is composed of a discontinuous layer of smooth muscle
Helps regulate blood flow into the capillary bed
Capillaries
Have tunica intima (with endothelium and basal lamina) & tunica media (true media is absent) - Pericytes in this layer
Tunica adventitia is absent
Pericytes
Mesenchymal cells
located in capillary tunica media
Contractile, around capillary - help control diameter
Can transform into smooth muscle cells and fibroblasts
Contribute to formation of scar tissue in CNS
Three types of Capillaries
Continuous, Fenestrated, Sinusoidal
Continuous capillaries
located in CNS, muscle, connective tissue, exocrine glands and lungs
Have tight junctions between endothelial cells, prominent marginal folds
Lack pores
Contain many pinocytotic vesicles
Well-developed basal lamina
Fenestrated capillaries
located in kidney, intestines, endocrine glands (where rapid exchange of substances between blood and tissues)
Contain pores, usually closed by thin diaphragm
Continuous basal lamina
Can contain or lack diaphragms
Sinusoid capillaries
have large fenestrations
Discontinuous or absent basal lamina
Associated macrophages
Located in spleen, liver, adrenal cortex and bone marrow (areas of rapid exchange and where cells can be exchanged)
Venules
thin walls, dilated, large lumen
Small Veins
Slightly larger and more muscular
Not too much layering of smooth muscle
Have valves - extensions of endothelium
Medium veins
Thicker walled Connective tissue predominates Tunica media - thin walled layer, only 2 cell layers of smooth muscle Tunica adventitia thickest layer No elastic
Large veins (portal veins)
Longitudinally arranged smooth muscle bundles in adventitia
Circular profiles in adventitia of smooth muscle - contracts and pushes blood back to heart
Vasculogenesis
de novo vessel formation
Angiogenesis
growth from existing EC-derived channels
Arteriogenesis
formation of arteries, arterioles, and collateral vessel remodeling
Neovascularization
overarching term to include vasculogenesis, angiogenesis, and arteriogenesis
Remodeling
vascular response to alterations in the environment
Blood vessel formation from endothelial precursor cells (EPCs)
angioblast-like cells in red bone marrow of adults
When needed, EPCs mobilize from etheir niches and migrate to site where blood vessel formation is to occur
From EPCs is used to
replace lost endothelial cells, re-endothelization of vascular implants, and neovascularization if ischemic organs, wounds, and tumors
Blood vessel formation from pre-existing blood vessels
Vasodilation - NO and increased vascular permeability induced by VEGF of parent vessel
Degradation of basal lamina - MMPs & lose of intercellular junction (plasminogen activator)
ANG 2 destabilizes vessel
Migration and proliferation of endothelial cells (VEGF and FGF)
Formation of endothelial capillary tube
Elaboration of basal lamina (TGF-beta) and recuritment of periendothelial cells (ANG1-Tie2 and PDGR)
Ang 1
Stabilizes endothelial cells by interacting with Tie2 receptor
Recruits periendothelial cells
Ang 2
Destabilizes vessels
MMPs
degrade basal lamina
VEGF & FGF2
endothelial cell migration and proliferation
TGF-beta
elaborates basal lamina
PDGR
recruitment of smooth muscle cells
Proangiogenesis for clinical benefit
Myocardial ischemia, peripheral ischemia, cerebral ischemia, wound healing, fracture repair, reconstructive surgery, transplantation of islets of Langerhans
Antiangiogenesis for clinical benefit
Tumor growth and metastases, ocular neovascularization, hemangiomas, Rhumatoid arthritis, Atherosclerotic plaque neovascularization, birth control
Tumor endothelial marker 8 (TEM8)
endothelial cells of tumor vessels express this protein
Marker can be used to specifically deliver drug molecules to tumor vessels
Adaptive vascular remodeling
Changes in stress drive transformational changes in wall of blood vessel to normalize wall stress
Elevation/drop in blood pressure or increased/decreased flow leads to an increase/decrease in vascular wall stress
Vascular remodeling in response to altered flow
high flow leads to increase in outside diameter and increase in luminal diameter
Low flow leads to decrease in outside diameter and decrease in luminal diameter
Vascular remodeling in response to increased pressure
Large artery response - outward hypertrophy (diameter of lumen unchanges, vessel becomes larger)
Small artery - inward hypertrophy (vessel diameter unchanged, diameter of lumen decreases)
Arteriole remodeling response to increased pressure
Inward hypertrophy
Inward (eutrophic) remodeling - wall thickness and wall diameter decrease
Rarefaction (vessels disappear)
Layers of heart
Endocardium (inner layer)
Myocardium
Epicardium (outer layer)
Endocardium consists of 4 layers
Endothelium (simple squamous) and basal lamina Subendothelial layer Myoelastic layer (smooth muscle and elastic and collagen fibers) Subendocardium
Subendocardium layer of endocardium consists of
Loose connective tissue
Small blood vessels
Nerve fibers
Purkinje cells or fibers (only in ventricles)
Myocardium contains three types of cardiocytes
Contractile
Myoendocrine
Specialized conductive
Epicardium consists of
Mesothelium (simple squamous) and basal lamina
Subepicardium
Myoendocrine
have euchromatic nucleus - very active
Electron dense vesicles contain atrial or B-type natriuretic factors
promote diuresis and vasodilation
B-type is elevated in congestive heart failure
Cardiac skeleton
Dense connective tissue (fibrous) where cardiac muscle and valves are anchored
Separates conduction system of atrium and ventricles
AV valve layers
Atrialis, Spongiosa, Fibrosa - between two layers of endothelium
Semilunar valve layers
Fibrosa, Spongiosa, Ventricularis - between two layers of endothelium
Atrialis
layer of elastic and collagen tissue subjacent to endothelium of atrial surface in AV valves
Spongiosa
middle layer of loose connective tissue that serves as a shock absorber in AV and Semilunar valves
Fibrosa
core of denser irregular collagenous tissue for mechanical integrity in valves
Subjacent to endothelium of ventricular surface (in AV valves) or aortic or pulmonic surface (in Semilunar vlaves)
Ventricularis
layer of elastic and collagen tissue subjacent to endothelium of ventricular surface in semilunar valves
Myxomatous
degeneration of AV valve - floppy valve
Sinoatrial (SA) node
cells smaller than atrial muscle cells
Contain fewer myofibrils
Doesn’t stain as acidophilic
Atrioventricular (AV) node
looks similar to SA node
Atrioventricular bundle (bundle of His)
Made up of Purkinje fibers cells
Travel in subendocardium
Connected to muscle cells by gap junctions
Twice the diameter of cardiac muscle cells
Few myofibrils (acidophilic), abundant glycogen (clear cytoplasm)
1 or 2 nuclei per cell
Cardiac stem cells and early committed cells
Can be activated to reconstitute necrotic myocardium
Identified in AV sulcus, migrate from AV sulcus to site of injury
Differentiate into cardiomyocytes, SMCs, and endothelial cells
Lymphatic capillaries
Thin blind-ended vessels lined by single layer of endothelial cells
Incomplete or absent basal lamina (would prevent flow into capillaries)
Anchoring filaments in extracellular environment (microfibrils) keep it from collapsing
No pericytes and smooth muscle cells
Lymphatic vessels
Similar to veins, thinner walls (and no RBC)
Has Valves
Larger LV become more muscular
Leukocytes transported in lymph - no RBC
Lymphatic ducts (thoracic and right lymphatic)
Similar to veins in structure
Smooth muscle found
Vasa vasorum
Lymphatic vessel density
Prognostic indicator for spread of malignant tumors
LYVE-1 is a lymphatic endothelial marker
Calcified degeneration of aortic valve most often occurs in
patients with atherosclerotic risk factors
Rheumatic fever
Caused by streptococcal pharyngitis
Immune response causes mitral valve vegetations and Aschoff body formation
Changes due to antibodies cross-reacting with self-antigens in heart and T-cell mediated reactions
