PHYSIOLOGY OF BLOOD VESSELS

Dr Ramya Jayakumar
Assistant Professor
 Introduction

 Systemic vascular tree

 Structure of blood vessel

 Function of various segments

 Control of blood flow

 Applied
 INTRODUCTION
 William Harvey –Blood is in continuous circulation.

 Function of circulation:
Maintain an appropriate environment in all tissue fluids of the
body for optimal survival & function of the cells
-Distribute O2 & nutrients
-Remove co2 & waste from tissue cells
-Thermo regulation
-Distribute hormones to target tissue
-Distribute Abs & cells concerned with defense
 Vascular
system is divided into 2 separate circulation:
-Systemic circulation
-Pulmonary circulation

 Function of the heart:

Systemic circulation:
-Blood from left ventricle(LV) is pumped into
systemic organs which returns back to Right
atrium(RA) & right ventricle(RV)
Pulmonary circulation:
Blood from RV is pumped
into the lungs for
oxygenation of blood
which returns back to Left
atrium(LA)
 SYSTEMIC VASCULAR TREE

 Large elastic arteries  Windkessel /

distensible vessels
 Large muscular arteries  Distribution/
conduit vessels
 Arterioles & precapillary
sphincters  Resistantvessels
 Capillaries  Exchange vessels

 Venules & Veins  Capacitance vessels

 Arteriovenous  Shunt/thoroughfare

anastomoses
STRUCTURE OF BLOOD VESSEL
 Tunica intima-innermost layer
endothelial lining
Basal lamina
Subendothelial connective tissue
Internal elastic lamina
 Tunica media- middle
run circular
Thickest coat
Smooth muscle & elastic tissue
External elastic lamina
 Tunica adventitia- outermost
Connective tissue-collagen
SPECIFIC STRUCTURAL CHARACTERISTICS
 Largearteries:
Prominent elastic tissue in Tunica media
Property of distensibility & elastic recoil

 Medium size arteries:

Elastic tissue is less, smooth muscle increases

 Arterioles: no elastic tissue

Thick layer of smooth muscles
Act as resistance vessels
 Meta-arterioles: high resistance conduits

 Capillary:

Pre capillary sphincter- cuff of smooth muscle

No tunica media, tunica adventitia
Formed by purely endothelial cells
Lined outside by basal lamina, pericytes

 Veins: very little elastic tissue & smooth muscle cells

VASCULAR SMOOTH MUSCLE
 Found in all vessels except capillaries
 In Windkessel vessel- its in spiral fashion

 Arterioles – circular, results in obliteration on

contraction.
 Innervated by sympathetic nerve fibers

 Contain β2 receptors & α receptors.

 FUNCTION OF VARIOUS SEGMENTS
1. Large elastic arteries(Windkessel / distensible
vessels )
- Windkessel means “elastic reservoir”
-Eg: aorta, pulmonary artery, larger branches

-Heart contracts intermittently

-Pressure & Flow is pulsatile
-Pulsatile flow is Converted to steady flow
Achieved by:
-Windkessel effect
Windkessel effect: The
stretch produced during
cardiac contraction on the
walls of the elastic tissue of
aorta and its branches
comes back to its original
position during the diastolic
phase converting a Pulsatile
flow to a steady blood flow.

-Helps in reducing energy

expenditure by the
heart.
2. Large muscular arteries(Distribution
vessels/conduit vessels)

-Serve as distributing channels

-Large lumen minimizes the pressure drop that

occurs as a result of resistance.

- Radial artery, facial artery

3. Arterioles , meta-arterioles & pre-capillary
sphincters (Resistant vessels)
- Major site of peripheral resistance
-Thick muscular wall
-Help in control of blood flow
-Decrease the hydrostatic pressure within the
capillaries –
-R α 1/r 4 (R- resistance, r- radius)
-Efficient local myogenic control
-Superimposed by extrinsic neural control
-Profuse sympathetic innervation
-meta-arterioles & pre-capillary sphincters
determine the size of capillary exchange area.
4. Capillaries(Exchange vessels)
-Contain single layer of endothelial cells lined
outside by basal lamina
-Overlying it is the pericytes
-Allow easy exchange of gases & nutritive
substances.
-10 billion capillaries
-Total surface area of 500-700square meters
-Cross sectional area is 2800 times aorta
 At rest only 25% is open & blood bypasses through
thoroughfare vessels
In active capillaries meta-arterioles & pre- capillary
sphincters dilate.
3 types of endothelial cells

Continuous/ non-fenestrated

Fenestrated

Discontinuous
Continuous capillaries:
-Single layered cells
-Small clefts
-Let pass water soluble ions & molecules
-Found in most body tissues, skeletal muscle, pulmonary
circulation

-Blood brain barrier

Blood retinal barrier- tight junction& intact basement
membrane.
Fenestrated capillaries:
-Large fenestration
-Thin basement membrane
-Permit large molecules to pass through
-Transport of fluid
-Seen in renal glomeruli, intestinal villi,

Discontinuous capillaries:
-Large gaps between endothelial cells
-For movement of formed elements
-Not closed by basement membrane
-Seen in sinusoids: bone marrow, spleen, liver.
5.Venules & Veins (Capacitance vessels)
 Thin walled, small amount of elastic tissue & smooth
muscle.
 More distensible & more collapsible

 lumen is larger with large cross sectional area

 Valves present in the veins of the dependent parts of

the body- prevent backflow of venous blood.

Function:
-Blood reservoir
-Carry blood from tissue to the right atrium
-Pulmonary veins carry blood from lungs to
left atrium
-Maintenance of cardiac output.
6. Shunt vessels
/thoroughfare vessels
 Bypass capillaries
 Directly connect meta-arterioles
with venules
 A-V anastamoses

 When patent permits rapid flow

 Occur notably in skin- maximum

cooling
 Strong muscle coat innervated
by sympathetic nerves
helpful during thermal stress
CONTROL OF BLOOD
Importance :
Continuous large amount of blood flow?
Heart would require many times more blood flow
than the heart can pump.

With control:
tissue will never suffer O2 & nutrition deficiency
Workload on heart is kept minimum.
MECHANISM
 Local acute
 long term
 Humoral vasodilators

vasoconstrictors
ions & chemical factors
 Neural
1. Local control:
 Acute- rapid changes

few seconds to minutes

 Long term- slow, controlled changes

few days, week, months
 Acute control of local blood flow:

Metabolic mechanisms
 Oxygen availability
 Role of nutrients

 Oxygen decreases
decreases blood flow through tissue
increases
2 theories:
 Vasodilator theory
 Oxygen lack theory
VASODILATOR THEORY
 Greater the rate of metabolism or less the
availability of O2 or nutrients to the tissue,
greater is the rate of formation of vasodilator
substances in the tissue cells.(adenosine, CO2,
histamine, phosphate ions, hydrogen ions)

 Vasodilatorsubstances diffuse to the arterioles,

meta-arterioles & pre-capillary sphincters to
dilate.

 Eg:i) Coronary blood flow decreases-Adenosine

ii) Heart activity increases
Oxygen lack theory/ oxygen demand theory:
 O2 is required for vascular smooth muscle contraction
 Absence relax the VSM  dilate the vessel

Vasomotion: The meta arterioles and pre- capillary

sphincters open & close several times per minute ,
duration of open phase being proportional to the
metabolic need of tissue O2. This cyclical opening &
closing is called vasomotion.
 Role of other nutrients.
 Lack of glucose

 Deficiency of vitamin B

Vit B  required to produce ATP in tissue cells

Deficiency decreased contractile ability  vasodilation.

 Special mechanism:
 Reactive hyperemia Blood flow is blocked for few
seconds or hours & then unblocked, blood flow
increases immediately 4-7 times the normal.

 Active hyperemia When tissue becomes highly active,

rate of blood flow to the tissue increases.
Eg: intense excercise , increased mental activity
Autoregulation:
 Ability of the organ to adjust its vascular resistance and
maintain a relatively constant blood flow over a wide
range of arterial pressure.

 2 theories:
Metabolic theory
Myogenic theory
 Metabolic theory :

When the arterial pressure becomes more , the excess

flow provides too much O2 and nutrients and washes

out vasodilators released by the tissue. This causes the

blood vessel to constrict.

 Myogenic theory:
An increase in the arterial pressure initially stretches the
smooth muscle fibers , in response to which VSM contracts
and returns the wall tension to control levels. The narrowed
lumen increases the resistance returning the blood flow to
normal level.

 Special mechanisms in kidney, brain, skin

ENDOTHELIUM DERIVED FACTORS
 Nitric oxide- vasodilator , healthy endothelial cell

 Endothelin- vasoconstrictor, damaged endothelium

(crushed injury)
 LONG TERM REGULATION
Important
 when the metabolic demands of tissue change.

 Tissue becomes chronically overactive

 O2 & nutrient demand increases

Both number and size of vessels increase.

Mechanism:
 Vascularity increases- angiogenesis

-New tissue growth is rapid

-Older tissue growth is slower
 Role of O2
 Role of Vascular endothelial growth factor
Fibroblast growth factor
Angiogenin
Eg: High altitudes
Premature babies-Retrolental fibroplasia

 Development of collateral circulation:

- Acute – rapid metabolic dilation
- Chronic – growth and enlargement of new vessels
- Eg: thrombosis in coronary artery
2. Humoral regulation:
 Vasoconstrictor agents- Nor epinephrine
Epinephrine
Angiotensin II
Vasopressin
 Vasodilators agents – Bradykinin
Histamine
 Ions-
Vasodilation: potassium , magnesium, H+ ion, CO2 ,
acetate, citrate
Vasoconstriction: calcium ion
3.NERVOUS REGULATION
 VSM is innervated by sympathetic nerve fibers
 VSM contain adrenergic receptors

 Noradrenaline  vasoconstriction

 Sympathetic fibers exert tonic effect at rest vasomotor tone in

blood vessels
 Stimulation  increases vasomotor tone vasoconstriction

 Inhibition  decrease vasomotor tone vasodilatation

 Adrenaline β 2 receptors vasodilatation

 Vasomotor centre: pressor area, depressor area
 APPLIED
 Aging: degenerative changes in windkessel vessels
Increase in SBP and Decrease in DBP
Increase in pulse pressure
Resulting in defective perfusion at periphery

 Atherosclerotic changes Hypertension

 Chronic hypertension

 Angina pectoris
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