Exam 8 - Blood Flow Control Flashcards
1
Q
3 principles of blood flow
A
- Local flow depends on local need
- VR/CO is the sum of flow through all local tissues
- Control of BP is independent of local flow and VR/CO
~Pressure drop kept constant across tissues….R changes
2
Q
When does external contractility change
A
- In times of emergency / out of ordinary situations
3
Q
Types of flow control
A
- Acute: moment to moment situations
can’t compensate 100% - Chronic: long term mechanism
4
Q
What tissues need from blood flow
A
- Oxygen
- Nutrients (glucose, amino acids, fatty acids)
- Waste removal
- Maintain [ion]
- Supply hormones
5
Q
Demand between tissues
A
- Tissues have different functions, thus, different demands
- Demand varies over time (local flow adjusts for this)
- Ensure that each tissue gets its needs without overworking heart
- EXCEPTION: some organs get flow based on function…not need
- Kidneys, liver, adrenal glands
6
Q
Distribution of flow
A
- Heart: 4%
- Brain: 14%
- Muscle: 15% (can go up to 80%)
- Bone: 5%
- Liver: 27% (6% arterial / 21% GI and Spleen)
- Kidney: 22%
- Skin: 6%
- Other: 8%
7
Q
Flow range on skeletal muscle
A
750 - 16,000 mls/min
8
Q
Acute (metabolic control)
A
- Response within seconds
- Not 100% compensation
- Control via dilation/constriction of metarterioles/pre-cap sphincters
- Arterioles can be overridden by sympathetic tone/ANS
9
Q
Long-term (chronic control)
A
- Slow response…days to weeks
- More permanent changes in metabolism/O2 content/input pressure
- Infinite response…close to 100% compensation
- controlled via increase/decrease # and/or size of vessels
10
Q
Acute Control response to metabolism
A
- 8x increase in metabolism causes 4x increase in flow
- achieved by decreasing venous sat (taking out more O2) and increasing flow
11
Q
Acute control response to Oxygen
A
- decrease in arterial sat results in increase blood flow
~ high altitude
~ Pneumonia
~ CO poisoning (HgB can’t carry O2)
~ Cyanide poisoning (tissues can’t use O2) - Increased flow almost makes up for decreased O2
~ Acute cannot fully compensate
12
Q
Branching in capillary bed
A
- Arterioles: flow to whole bed
- Metarterioles: flow to branches
- Pre-cap sphincters: flow to individual vessels in bed
- No ANS innervation….acute response is innate to vessels
13
Q
Precapillary Sphincters
A
- Either completely closed or open
- Open/Close multiple times/min (vasomotion)
- If open more….flow increases
- Time open proportional to waste…inversely to O2 content
~ Waste = CO2 and H+ (in form of Lactic Acid)
14
Q
Two theories that explain response to O2/metabolism
A
- Oxygen Demand Theory (Nutrient demand theory)
- Muscles use O2 to contract (other nutrients as well)
- More O2/less metabolism -> more contraction -> less flow
- As O2 decreases/metabolism increases -> less contraction -> more flow
- Vasodilator theory
- Metabolism increase -> waste formation increase
- Waste interacts with smooth muscle and causes vasodilation
- Mostly affects metarterioles and precap sphincters
- tone of arterioles depends on tone of ANS
- Control probably a mixture of both theories
15
Q
Vasoactive substances
A
- Adenosine: released when [O2] down
- released when flow is down, ATP is down too - CO2: Vasodilator especially in brain
- Adenosine phosphate compounds:
- released when ATP broken down or Adenosine released - Histamine: vasodilator from mast cells/basophils
- K ions: vasodilator in brain and heart (causes hyperpolarization)
- makes it harder to contract - H ions: released from tissue in form of lactic acid when [O2] down
16
Q
Active Hyperemia
A
- Internal change
- response to increased metabolic demand in a tissue
- like in skeletal muscle - Plateau flow determined my local need/demand
17
Q
Reactive Hyperemia
A
- Response of tissue to period of ischemia
- Flow can bump to 4-7x normal after ischemic period
- Longer the ischemic period….longer reactive Hyperemia period
- bigger oxygen debt to repay to tissue
18
Q
How does cardioplegia help?
A
- Keeps the O2 debt down while we have no flow through heart
- Lessens the O2 debt
19
Q
Autoregulation and MAP
A
- Local control only function if MAP is constant
- If MAP changes…ALL tissues/flow will change
- If MAP up…constrict to try and keep flow through tissue normal
- Gets close to 100% compensation but not quite
- Can autoregulate only over a range of BP
20
Q
Myogenic Theory
A
- Sudden stretch of small vessels -> SM contract -> flow down
- stretch will happen if BP increases
- If BP down…stretch down…triggers SM relax…flow up
- Only allows vessels to respond to changes in P….not flow
21
Q
Special acute flow control
A
- Kidney: tubuloglomerular feedback control
- Brain: CO2 and H+ [ ] sensitivity as well as normal control
- Skin: control linked to temperature regulation
22
Q
Tubuloglomerular feedback in Kidneys
A
- Macula Densa monitor filtrate in distal tubule
- If flow of filtration increases…Na increases…trigger afferent arterioles to constrict….reduce flow
- Opposite is true if too little flow/filtration
23
Q
Brain and CO2/H+
A
- If either increase…vasodilation…increase flow to remove them
- ideal level of cerebral activity requires fixed CO2 level
- essentially operates at an optimal pH
24
Q
Endothelial derived control factors
A
- endothelial cells release and interact directly with SM
- NO (vasodilator) and Endothelin (vasoconstrictor)
25
Q
NO
A
- Lipophilic gas that acts on SM
- 6 second half-life
- released if increase in Ca or Angiotensin II
- released if increase in shear stress sue to increase in flow
- dilates larger vessels upstream (not metarterioles and precaps)
- decrease in NO if hypertension or atherosclerosis
26
Q
NO formation
A
O2 + L-Arginine —-> NO + L-Citruline
-NOS must be present to catalyze reaction
27
Q
NO activation cascade
A
- NO activates SGC
- SGC turns cGTP into cGMP (cyclic guanosine monophsphte)
- cGMP activates PKG
- PKG relaxes SM
28
Q
Endothelin
A
- Large amino acid peptide
- Very potent (small amount causes large constriction)
- can close vessel 5mm in diameter - Increases [ ] if injury to vessel
- released from damaged cells
29
Q
Chronic flow control
A
- Long-term
- If BP increase…acute control makes changes quickly
- flow still 10-15% above normal - If BP change permanent…chronic control would bring flow back to normal over course of a couple weeks
- Long-term has control over larger range of MAP (50-250)
- versus 75-175 for acute control MAP range
30
Q
Long term control and vascularity
A
- Chronic increase in metabolism / decrease in pressure will increase vascularity (and visa versa)
- # of arterioles and caps would increase
- size of existing arterioles and caps increase
- happens in days for young…weeks/months for old
- chronic low O2 can also increase vascularity
- total change depends on MAX blood flow needed to tissue
31
Q
Vascular endothelial growth factors
A
- small peptides that promote growth from existing vessels
- stimulated by decrease in O2 in affected cells
- VEGF
- Fibroblast growth factor
- Angiogenin
32
Q
Antiangiogenic substances
A
- Block growth of new vessels
- Angiostatin
- Endostatin
- possible anti-cancer agents
33
Q
Collateral circulation
A
- existing (closed) vessels open up to create new path for flow
- happens when normal pathway is blocked or clogged
- if blockage happens slowly…collateral flow can be adequate
34
Q
Inward Eutropic (chronic)
A
- in small arteries/arterioles
- respond to increase in BP by increase in wall thickness only
- radius of vessel decreases so no change in x-sec diameter
35
Q
Hypertrophic (chronic)
A
- Large vessels
- respond to increase in BP w/ increase in wall thickness AND diameter
- radius stays same so x-sec area goes up with increase in wall
36
Q
Outward (chronic)
A
- Large vessels
- respond to increase in flow with increase in radius
- radius bigger (stretch) but not much extra wall thickness
37
Q
Outward hypertrophic
A
- Large vessels
- respond to increase in flow AND BP by increase in wall thickness and vessel radius
- overall x-sec diameter increases
38
Q
Humoral control - Vasoconstrictor agents
A
- Norepi: from ANS and adrenal medulla
- Epi: not as strong as Norepi / short term
- Angiotensis II: VERY potent / regulates overall BP / renal function
- Vasopressin: ADH / stronger than Angio II / from post pit. / increases H2O reabsorption in kidneys / helps when hypovolemic
39
Q
Humoral control - Vasodilator agents
A
- Bradykinin: small peptide spilt from alpha2-globulins
- Kallikrien is inactive form….activated by damage to blood…
- activated kallikrien interact w/ a2-globulin to make kallidin
- Kallidin converted to bradykinin by tissues
- dilates and increases cap permeability…helps w/ inflammation
- Histamine: from mast cells and basophils in damaged tissue
- dilates and increases cap permeability
- causes edema
- component in allergic reactions
40
Q
Vascular control via ions
A
Ca - increase causes SM contraction (constricts)
K - increase inhibits SM contraction (dilates)
Mg - increase inhibits SM contraction (dilates)
H - increase dilates / slight decrease causes arteriole constriction
Acetate/Citrate - increase causes mild dilation
