Blood Flow Flashcards
each tissue control its own
blood flow in proportion to its needs
tissues blood flow is closely related to its
metabolic rate
as metabolic rate increases,
tissue blood flow increases
skeletal muscle blood flow
don’t get much even though make up a lot of body weight
every day exercise will do what to skeletal muscle
increase the blood flow to the skeletal muscles
why not just give all the blood flw all they might ever need?
heart can’t keep up with that, so it jsut gives tissues what they need
what is acute control
local control within tissues: rapid, seconds to minutes
vasoconstriction and vasodilation is acute or long term control?
acute
what is long term control
increases/derease in size and number of blood vessels
how long does long term control take
ours, days, weeks -takes awhile
how long does acute control take
not long - imediate
for us students, where should a lot of blood flow be going right now?
brain
what factor is most important for blood flow control
oxygen
as oxygen saturation decreases, blood flow
increases
locally in interstitial fluid, the cells are eating up oxygen which is what causes
blood flow to increase
physiological examples where blood flow increases
high altitudes
pneumonia
carbon monoxide poisoning
cyanide poisoning
high altitudes pneumonia carbon monoxide poisoning cyanide poisoning the common theme in all of these, that cause blood flow to increase is:
lower oxygen throughout body
cyanide poisoning
doesn’t allow oxygen to bind in body
vasodilator theory
when the cell is using up oxygen it releases substances like adenosine, CO2, lactic acid ,postassium ions, histamine, and the local substances diffuse back to the arterioles and dilate them, the dilation causes increase in blood flow to the tissue that is releasing the chemicals
adenosine is biproduct of
ATP
why is adenosine high when cells are using oxygen
adenosine is biproduct of ATP
adenosine in heart
dilator
when heart is oorking hard puping oxygen, what is a local dilator that causes blodo vessels going to heart to dilate
adenosine
oxygen demand theory, how do we know its a thing
you can block all of the mediators from going out and you still have local control, so will still have increased blod flow
describe oxygen demand theory
when oxygen is high precapillary sphincters contract and blood won’t go through where there is high oxygen. if oxygen is low the precapilary sphincter sense low oxygen and open up and blood goes through the area and brings oxygen to it
reality, what theory is it?
combination of both theories
the way we increase blood flow the two theories: oxygen demand & vasodilator theory are independent of
nerves
all the capilaries arent always
open
the oxygen demand and vasodilatory theory are more powerful than
nerve control
active hyperemia
increased blood flow, occurs when tissue metabolic rate increases
reactive hyperemia
Occurs after the Tissue Blood Supply Is Blocked for a Short Time
look at graphs on pg 11
11
if you occlude artery going to muscle, then you release occulsion, describe what happens to blood flow
blood flwo goes higher than normal to resupply and then iwill come back down
the longer you occlude an artery the higher the
reactive hyperemia is
autoregulation, what is it
if you increase the pressure gradient to a tissue the flow goes up to that tissue but then blood flow will go back down, so the tissue is autoregulating its own blood flow
maintainign a constant bloodf low to a tissue regardless of arterial pressure
all tissues have
autoregulation
what two mechanisms are involved in autoregulation
metabolic & myogenic mechanism
metabolic theory
when you increase blood flow it will wash away the stuff (like adenosine) that caused the increase in blood flow, causing it gto go back down
myogenic theory
just property f blood vessels
Based on fact that sudden stretch of small blood vessels and arterioles will cause smooth muscle cells of vessel to contract (they don’t really understand why)
review graph pg 13
13
factors released from endothelial cells of blood vessels help control
blood flow
two important things released from endothelial cells in blodo vessels
nitric oxide
endothelin
nitric oxide synthase does what
converts arginine into gas: nitric oxide
nitric oxide is a gas and is diffusible, it can do what
go wherever, can go into smooth muscles
NO does what
stimulates guanylate cyclase which converts cGTP to cGMP which causes relaxation
NO is a (generally)
vasodilator
what is one thing that causes blood to release NO
shear stress
when is endothelin released frm blood cells
when there is damaged endothelium
endothelin causes
vasoconstriction
long term control changes what about blood vessels
number r size
angiogenesis:
growth of new blood vessels
angiogenesis occurs in respnse to angiogenic factors released from:
ischemic tissue
rapidly growing tissue
tissue with high metabolic rate (like cancer)
when heart hypertrophies, what long term effects happen
angigenesis - more blood vessels occur but they don’t increase in size
Collateral Circulation:
development of small channels around some particular block
how long dos Collateral Circulation take
a long time
if a blood vessel is blocked, what will grow to help
Collateral Circulation
BY THE TIME SOMEONE IS 60 OR 70 have a lot of
microchannels in heart
whahow does Collateral Circulation work
Dilation of vascular loops that already connect a vessel above and below the block.
why wuld it cause more damage for young person to have MI than an old
b/c old ppl have more collateral circulation, young people haven’t had the time the develop the collateral circulation
if you plant vein into arterial system what happens
it will hypertrophy to be able to withstand the new high pressure
blood vessels themselves can change depending on
what situation they are in
AV fistula
connect artery and vein, like pts undergoing dilaysis with renal failure
what happens to artery in AV fistula
gets bigger b/c its not in as much pressure
what happens to vein in AV fistula
vein gets bigger also
name three humora vasoconstrictors
Norepinephrine
Angiotensin II
Vasopressin
name two vasodilator humroal
Histamine
Nitric oxide
NE activate what in blood vessels
alpha 2 and alpha 2 reeptors and beta 1 in heart
NE activates alpha 1 and alpha2 and causes
vasoconstriction
EPI activates
alpha 1, alpha 2, beta 1, beta 2
EPI in blood vessels activates alpha 1 and alpha 2 and causes
vasoconstriction
EPI acting on Beta 2 causes
vasodilation
in kidney blood vessels only have what receptors
alpha1 and alpha 2
epi and NE in kidney what do you see
constriction
blood vessels in skeletal muscle have what receptors
alpha 1, alpha 2, beta2 receptors
infuse NE into skeletal muscle what happens
vasoconstriction
infuse EPI into sekeletal muscle what happens
vasodilation, because of the beta 2 receptor
dog infused with EPI vs NE which will have highest blood rpessure
the one with NE
Angiotensin II is pathway what inhibitors work on
ACE
Angiotensin is released in response to what enzyme
REnin
anytime there is fall in BP kidneys release
renin
draw angiotensin II pathway
pg 22
what does Angiotensin II do
constricts arterioles in body
what does Angiotensin II do to kidney
releases aldosterone and increases sodium reabosption
if you gave ACE inhibitor what would it do
blocks angiotensin II from being prduced, so high levels of angiotensin I, less constriction of bloodv essels, decreased sodium reabsorption
when might renin be released in kidney
hemorrhage
vasopressin is also known as
antidiuretic hormone
vasopressin is peptide produced where
hypothalamus
where is vasopressin released from
posterior pituitary
vasopressin is released in response to:
- Decrease in arterial pressure
2. Increase in plasma osmolarity
alcohol inhibits the release of
vasopressin
what does vasopresin do
Potent vasoconstrictor
Increases renal reabsorption of water
- Concentrated urine
histamine is a vaso:
dilator
histmaine is released from what cells
mast cells
histamine does what to capillary
increases its permeability
histamine is very powerful
vasodilator
histimen increasing capillary permeability, what is example he used
bee sting, it gets red and swolen
antihistamine is taken to block the effects of
histamine
Bradykinin is an _____ mediator
inflammatory
when is Bradykinin released
tissue damage
Bradykinin is very similar to
histamine
Bradykinin causes arterial
dilation
bradykinin does what to capillary
increases its permeability
what breaks Bradykinin to inactive fragments
kininase II or angiotensin converting enzyme
inhibition of angiotensin converting enzyme decreases production of angiotensin II but allows what to stay around longer
bradykinin
look at pg 26
26
