Chapter 15a: Blood Flow単語カード | Quizlet

endothelium

inner lining of all blood vessels

artery

- diameter: 0.1-10+ mm

- Mean wall thickness: 1.0 mm

- Endothelium: minimal

- Elastic tissue: medium

- Smooth muscle: lots

- fibrous tissue: little

arteriole

- diameter: 10-100 um

- Mean wall thickness: 6.0um

- Endothelium: minimal

- Elastic tissue: none

- Smooth muscle: little

- fibrous tissue: none

capillary

- diameter: 4-10 um

- Mean wall thickness: 0.5 um

- Endothelium: minimal

- Elastic tissue: none

- Smooth muscle: none

- fibrous tissue: none

venule

- diameter:10-100 um

- Mean wall thickness: 1.0 um

- Endothelium: minimal

- Elastic tissue: none

- Smooth muscle: none

- fibrous tissue: little

vein

- diameter: 0.1-100+ mm

- Mean wall thickness: 0.5 mm

- Endothelium: minimal

- Elastic tissue: little

- Smooth muscle: little more

- fibrous tissue: little

conducting or elastic arteries

- smooth muscle

- proportionally high elastic content

allows for stretch and elastic recoil

- maintains driving force for blood during ventricular diastole

distributing or muscular arteries

- proportionally high smooth muscle content

- vasoconstriction and vasodilation

arterioles

- progress from all three tunics: externa, media and intima to only thin media and intima

- most regulation of vasoconstriction and vasodilation

- vasomotor tone

Metarterioles

- little smooth muscle

- precapillary sphincters

- supplies blood to capillaries

- acts as a bypass for white blood cells

capillaries

Endothelium

- with basal lamina or basement membrane

- surrounded by pericytes w/ contractile properties

continuous capillaries

most common type of capillary

intercellular clefts

- blood-brain barrier has tight junctions

fenestrated capillaries

intercellular clefts with fused vescile clefts

sinusoids or discontinuous capillaries

incomplete endothelial lining and basement membrane

capillary beds

sites of chemical exchange between the blood and interstitial fluid

can be regulated by pre-capillary sphincters

venules

small vessels that gather blood from the capillaries into the veins

progress from only thin media and intima tunics to all three tunics: externa, media, and intima

- smallest venules allow some exchange

veins

- one way valves

- work w/ skeletal muscle and respiratory pumps

- Do you need valves in the jugular veins? YES

blood reservoir: about 60% in veins and venules

more veins and larger diameter than arteries

Angiogenesis

formation of new blood vessels

Promote: mitogenic (mitosis) growth factors

- vascular endothelial growth factors

- fibroblast growth factor

- potential treatment for artery diseases

- development of collateral blood vessels

- inhibit: cytokines

- angiostatin: stasis

- endostatin: stasis

- potential treatment for some cancer

- block development of blood vessel growth and access to nutrients

relationships among pressure, flow and resistance

Recall:

- pressure gradient

- resistance to flow

- velocity and cross-sectional area

- Flow = ∆P/R

- MAP = CO x R

Blood pressure basics

arterial pressure

The pressure of the blood against the arterial walls.

systolic pressure

pressure resulting from ventricular systole - contraction

diastolic pressure

pressure resulting from ventricular diastole - relaxation

pulse or pressure wave

- vibration in the arteries

- alternation between ventricular systole and diastole

- travels 10x faster than the blood

- pulse is the direct reflection of the ventricular action

- pulse deficit

Pressure: decreases the further away it gets from the heart

Effect of distance and friction on pressure and pressure waves

Pulse pressure (PP)

- strength of the pressure wave

PP = SP-DP

- mmHg 160/120 vs 120/80 vs 100/60

MAP

driving force for arterial blood flow

- effect on perfusion of organs and tissues

- DP + 1/3 PP or (SP + 2DP)/3

- mmHg

- 160/120 vs 120/80 vs 100/60

- 133.33 vs. 93.33 vs. 73.33

PP = systolic - diastolic

How do you find pulse pressure?

MAP = DP + 1/3 PP

How do you find MAP?

Syphygmomanometry

laminoar flow vs. disrupted flow

1st Korotkoff sound: systolic pressure

2nd Korotkoff sound: diastolic pressure

less than 120/80 mm Hg

normal blood pressure

120-129/less than 80

elevated BP/ pre- hypertension

130-139/80-89

hypertension stage 1

140 + / at least 90

hypertension stage 2

Health risks

- hemorrhagic strokes

- aneurisms

- kidney failure

- heart failure

over 180 and/or / over 120

hypertensive crisis

ineffective flow against gravity

- below 90/60 mmHg

MAP = 70mmHg

MAP = below 60 is problematic = ineffective ciruclation

Hypotension

1. blood volume

2. cardiac output (HRxSV)

3. volume of blood into vs volume of blood out of arteries

4. volume of blood in venous reservoir

What can influence MAP?

Mass balance of water: volume into body vs. volume out

increase volume = increase pressure

How does blood volume influence MAP?

CO = HR x SV

HR increases = SV increases = CO increases

Heart rate: parasymp vs symp input

Stroke volume:

- EDV: venous return, frank starling law of the heart

- heart contractility: ejection fraction

How does cardiac output affect MAP?

CO vs. peripheral resistance

- ∆ CO → ∆ flow into arteries

- CO affected by heart rate & stroke volume

- ∆ R → ∆ flow out of arteries

- R affected primarily by arteriole diameter

How does volume of blood into vs volume of blood out of arteries affect MAP?

venous vasoconstriction

- ∆ in distribution of blood in arteries vs. veins

- Affected by venous vasoconstriction or vasodilation

- EDV

- Venous return

- Frank-Starling law of the heart

How does volume of blood in venous reservoir affect MAP?

1. Local control of arteriolar resistance: matches tissue blood flow to the metabolic needs of the tissue. In the heart and skeletal muscle, these local controls often take precedence over reflex control by the CNS

2. Sympathetic reflexes mediated by the CNS maintain MAP and govern blood distribution for certain homeostatic needs, such as temperature regulation.

3. Hormones - particularly those that regulate salt and water excretion by the kidneys - influence BP by acting directly on the arterioles and by altering autonomic reflex control

What are some influences on arteriole resistance?

Local or intrinsic control

local regulation to adjust to local needs

Myogenic autoregulation: on-off regulation

- arteriole smooth muscle stretch and mechanically gated Ca channels

- increase blood flow, increases muscle stretch --> opens mechanically gated Ca channels

- intracellular Ca increases, blood flow increases, diameter increases, arteriole resistance decreases

- decrease blood flow, decrease muscle stretch, close mechanically gated Ca channels, opposite effects

Active hyperemia

response to increased metabolic need

- increased metabolic activity → vasodilation → increased blood flow

- stimuli for arteriole dilation

- accumulated metabolic byproducts: CO2, adenosine, H, K

- Paracrine agents: CO2, bradykinin, NO

- after increasing blood flow: remove vasodilators and return to tonic state

Reactive hyperemia

Response to lack of flow

occlusion: decreased blood flow and accumulate metabolic byproducts

stimuli for arteriole dilation

- accumulate metabolic byproducts: CO2, adenosine, H, K

- paracrine agents: CO2, bradykinin, NO

after increasing blood flow

- remove vasodilators and return to tonic state

Active

increase tissue metabolism → increase release of metabolic vasodilators into ECF → arterioles dilate → decreased resistance creates increase in blood flow→ O2 and nutrient supply to tissue increases as long as metabolism is increased

Reactive

decrease tissue blood flow due to occlusion → metabolic vasodilators accumulate in ECF → arterioles dilate, but occlusion prevents blood flow → remove occlusion → decrease resistance creates increase blood flow → as vasodilators wash away, arterioles constrict and blood flow returns to normal

occlusion = close up

when occluded for a few seconds to a few mins. O2 levels fall and metabolic paracrine signals such as CO2 and H accumulate in the interstitial fluid

Active vs. reactive hyperemia

Arteriole pressure autoregulation: on-off regulation

decreased arterial pressure → vasodilation→ increased blood flow

stimuli for arteriole dilation

- same as for active hyperemia

- but different in that metabolic activity is constant but blood flow can't keep pace

- increased arteriole pressure → vasoconstriction → decreased blood flow

stimuli for arteriole constriction or return to tonic state

- increased O2 and removal of vasodilating chemicals

Sympathetic influence on arteriole resistance

Tonic control: vasomotor tone

- sympathetic system regulates most changes

- parasympathetic input is not necessary for vasodilation

- NE NT and E neurohormone with a1 adrenergic receptors

- vascular sm. muscle

- increased symp. input → increased vasoconstriction

- decreased symp. input → decreased vasoconstriction (return to tone or allow to vasodilate)

- E neurohormone with B2 adrenergic receptors

- vascular smooth muscle of liver and cardiac and skeletal muscle

- increased symp. input → decreased vasoconstriction (allow to vasodilate)

- decreased symp. input → increased vasoconstriction (return to tone)

Why mixed responses? Fight or flight

Hormone influence on resistance

extrinsic control

Atrial Natriuretic peptide (ANP)

- vasodilation

- influences function of kidney for water regulation → blood volume (more water in blood)

Angiotensin II (ANG II)

- potent vasoconstriction

- influences function of kidney for water regulation → blood volume (less water in blood)