This document discusses vessel wall biology, including the anatomy and structure of arteries, veins, and lymphatics. It describes the layers of the arterial wall - intima, media, and adventitia - and their components. It also discusses the endothelium, internal elastic lamina, and mechanics of arterial walls. Hemodynamics and the effects of shear stress and circumferential stress on vascular cells are summarized.

1. VESSEL WALL BIOLOGY
DR. SHRIKANT PANDURANG GHANWAT
DNB RESIDENT
MEDANTA HOSPITAL

2. ARTERIAL/VEIN/LYMPHATIC
• ANATOMY
• SYSTEM
• HEMODYNAMICS AND VASCULAR WALL
BIOLOGY

3. ARTERIAL WALL ANATOMY

4. ARTERIAL WALL ANATOMY

5. INTIMA
• Innermost luminal layer
Lumen IEL
• Lined by endothelium
• The actual intimal layer
- Few scattered leucocyte
- SMC
- Connective tissue

6. ENDOTHELIUM
 Simple squamous epithelium
 Continuous layer of flat polygonal /
elongated endothelial cells.
 Cell thickness <0.1 um – 1 um
 Participate – Physiological
Pathological process
 Reacts to – Physical forces, chemical signaling
and immunologic mediators
 Interacts - cellular and acellular environment
 Regulator of - Vasomotor tone
Hemostatic balance
Permeability
Cell proliferation, survival
Immunity

7. Junctions -
A) Tight junctions ( zona occludence)
- Well developed looser
( large artery) (arteriols,cappilary)
- Barrier to the transport between ECs.
- Blood brain barrier – rigid tight junction
- Help to maintain polarity
B) Adherens junctions ( zona adherans)
- Less common
- Large arteries
- Permits inter ECs communications – movt of ions,
metabolites, RF

8. GLYCOCALYX
ANTITHROMBOGENIC PROPERTY
INFLAMMATION - SHEARED OFF
- PERMITTING ATTACHMENT OF LEUCOCYTE
- TRANSPORT OF WATER FROM MICROVESSELS
- INITIATING DEVELOPMENT OF ATHEROSCLEROTIC
LESIONS.
IMP

9. TYPES

11. BASAL LAMINA
• Borders the ECs on their abluminal surface.
• It involves in - Regeneration and attachment of endothelial layer.
- Barrier to cellular migration.
- Hemostatic balance ( initiation of blood clot)
- Permeability
- Immunity
• Two zones –
A) Lamina rara ( clear inner zone) – contain gylcoprotein- laminin
B) Lamina densa ( dense fibrilar zone) – type IV collagen
• Formed by –
- Glycoprotein,adhesion molecules like laminin, enactin, fibronectin,thrombospondin
proteoglycans like heparin sulfate, microfibril of collagen type IV and V
• Mechanically strengthen wall
• Provide pliable extensive bond which permits ECs to comply with change in
configuration related to cardiac pulsation and to vessel torsion and flexion.

12. INTERNAL ELASTIC LAMINA
• Is layer of elastic fibers 70-100 nm in thickness.
• Separate subendothelial layers from medial layer.
• In large arteries IEL and elastic lamellae may function as barrier to
macromolecular accumulation.
• Defective IEL result in abnormal attachment with ECs causing gap – entry
of macromolecules, lipids, leukocyte into intima.
• Advanced plaque – fragmentation of the IEL and disruption of medial
layers.
• Structural defects within IEL are directly implicated in the onset of intimal
thickening
IMP

13. MEDIA
 Extend from IEL to adventitia.
 Is porous heterogenous medium consisting of ECM phase with
embedded SMCs.

14.  Consist of SMCs, elastin and collagen fibres arranged in highly oraganised
fashion.
 At low and physiologic pressure, media is chief determinant of arterial
properties.
 So arteries classified according to cellular and fibrous components of
media
A) Elastic arteries
- Well defined elastic lamellae and collagen fibres are prominent in media
- Connective tissue fibres - less frequent .
- E.g arteries close to heart - aorta, brachiocephalic trunk, iliac arteries.
- Lamellar units 40-60 in aorta , decreases from heart to periphery.
B) Muscular arteries
- Primarily SMCs with fewer connective tissue.
- Nonparallel branching elastin strands increases capacity to change in
diameter under neuro humoral stimulation.
- e.g - femoral, popliteal, radial, ext carotid artery, etc

15. ADVENTITIA
• From EIL to ill defined boundary
continuous with the perivascular
connective tissue.
• Cells are more sparse and consist
mainly of fibroblast.
• Aorta – minimal fibrous connective
tissue.
• Muscular arteries- prominent elastic
and collagen fibers
• Contains vasa vasorum and nerves.

17. Emotion stress dilate arteriole while increases blood pressure and
velocity in large arteries.

20. VEIN WALL ANATOMY
• Venous system is adaptable with unique mechanism for accomodating
hemodynamic stress.
• A) INTIMA
- One layer ECs sitting on incomplete elastic basement membrane
• B) MEDIA
- Less developed than that of arterial system varicosities
- SMCs of this layer held in quiescent state by various factors
- TGF-B downregulate mitogenesis and stabilize the ECM
- Heparin like molecule neutralize FGF to downregulate cell
proliferation.
- When vein exposed to arterial flow - increase cell proliferation
• C) ADVENTITIA
- Thickest layer
- Large vein – abundant collagen fibre
- Vasa vasorum is much more extensive compared with arteries
low oxygen tension

21. VEIN WALL SYSTEM
• VENULES
 Smallest of venous vessel, formed from confluence of several cappilaries
 10-50 um in diameter and 50 -650 um in length
 Structure llar like cappillary
 During inflammation - Main site for blood cell diapedesis and tissue
exudate from circulation to interstitial tissue
• VENOUS VALVES
 Characteristic of small and medium sized vein- > 2mm dia.
 Local intimal semilunar infolding
 Reverse velocity of 30 cm/s – for valve closure
 Exceptional note – IN FEET - Flow from deep muscle in sole to superficial
vein in dorsum of foot
 In arterial bypass turbulace caused by valves – endothelial injury- intimal
hyperplasia
 Chronic venous insufficiency – reduction in number
abnormal high pressure – remodeling

22. LYMPHATIC WALL ANATOMY/SYSTEM
• ANATOMY
 Initial lymphatics - single layer of ECs with large gap between
cells and incomplete basal lamina.
 Large lymph vessels – 3 concentric tunicae
 Valves + in greater numbers
• SYSTEM
 Is unidirectional flow network originating in the interstitial space
Draining fluid
from ECM
INITIAL
LYMPHATICS
LARGE
PRECOLLECTING
LYPHATICS
COLLECTING
LYPMHATICS
TRUNKS
DUCTS

23. HEMODYNAMICS
VASCULAR WALL BIOLOGY
• Blood vessels constantly experience the mechanical forces of
Cyclic/Circumferntial strain Shear stress
• All cells Endothelium
• Blood pressure Blood flow velocity
• σ = Pr/h ꚍ = 4µQ/πr3

24. SHEAR STRESS
• ENDOTHELIUM
• ECs align in the direction of stress –
Greater is stress – more elongated cells.
Correlated with
Redistribution of intracellular Fiber quantity
stress fibers.
• Higher stress – ECs express higher amount of stress fibers
including actin, myocin and other contractile proteins.

25. MECHANOTRASDUCTION
 Begins on luminal side of ECs
 Deformation at level of individual cells
 Transduced through cytoskeleton to
other points – Basal adhesion pts, cell
junctions, nuclear membrane
 The redistribution forces stimulates
immediate and delayed process.

26. MECHANOTRASDUCTION

27. MECHANOTRANSDUCTION
• Glycocalyx, Potassium channels, calcium
channels are the mechanoreceptors by which
ECs respond to shear stress and pressure.
• Cell membrane respond by activation of strech
induced ions, phspholipids, integrins.
• The nuclei upregulate the production of
- Platlet derived growth factors
- Endothelin -1
- NO synthase III
- TPA
- ICAM -1
- TGF-B
• Stress – ICAM
• Steady stress – VCAM
• Oscillatory stress - BOTH

28. • Acute changes in strech and shear stress
- Transient changes
- Release of vasoactive agents and alternation
in vessel diameter
• Chronic changes –
- Enhance L- anginine / NO pathway
- Marked increase in NO synthase mRNA and cGMP.
- NO and SOD anions help to activate MMP
- MMP induces remodeling
IMP

29. CIRCUMFERENTIAL STRESS
• In Endothelial cells –
 Induce cell proliferation
 Endothelin release
Total protein content
Gene expresion
SMCs hypertrophy
- Fail to align
ECM FIBROBLAST ELASTIN
In sctreched
SMC
Collagen I ,III
Collagen II/ I
• It represent the constant, rhythmic deformation of the vascular wall caused by
pulsatile, hydrostatic pressure linked to oscillation of systole and diastole.

30. THANK YOU

31. DIFFERENCE IN LARGE AND SMALL ARTERIES
LARGE/ELASTIC SMALL/MUSCULAR
THICKNESS – 1/10 TH OF DIA. 1/4 TH
INTIMA
- THICKER 20% OF WALL THICKNESS THINNER
- MORE ELASTIC FIBRES IN SUBENDO LESS
CT LAYER
- IEL – NOT INDISTINCT WELL DEMARCATED
MEDIA
- MORE ELASTIC FIBERS MORE SMC
- EEL- NOT WELL DEMARCATED WELL DEMARCATED
ADVENTITIA
- THIN THICKER