control of blood flow Flashcards
Acute (metabolic control)
response in seconds. finite response. Controlled mainly vasodilation / vasoconstriction of
arterioles, metarterioles, precapillary sphincters
Long-term
sow response – takes days / weeks
More permanent changes in metabolism; oxygen content; input
pressure
Almost infinite response
Controlled by increasing / decreasing physical size and
number of blood vessels within tissue
8 fold increase in metabolism results in
four fold increase in BF
Acute Control – Response to Decrease in oxygen
results in an increase in blood flow through the tissue. Increased flow almost makes up for decreased oxygen carrying capacity
causes of decraesed arterial oxygen saturation
High altitude Pneumonia Carbon monoxide poisoning Cyanide poisonin
Precapillary Sphincters
Open and close multiple times each minute
As duration of open phase increases, flow through the tissue increases
Duration of open phase inversely proportional to oxygen content and
directly proportional to concentration of metabolic waste
Theories for Acute Regulation
Oxygen (nutrient) lack theory
Oxygen & other nutrients needed for smooth muscle
contraction
Nutrients not available – muscle relaxes producing dilation
As metabolism increases local decrease in oxygen content
results in vasodilation
Theories for Acute Regulation Vasodialator theory
As metabolism increases production / concentration of
metabolic waste increases
Metabolic waste interacts with smooth muscle resulting in dilation
both Oxygen (nutrient) lack theory and Vasodialator theory
affect tone of smooth muscle mainly in metarterioles
and precapillary sphincters with some affect on arterioles
Overall tone of arterioles depends
on tone of autonomic nervous system
vasodilator factor release proportional to
tissue metabolism
on tone of autonomic nervous system
overall concentration of vasodilator factors. Factors cause direct dilation of metarterioles & precapillary sphincters.
Adenosine
vasodilator Released from tissue in response to decreased oxygen
concentration
Released by cardiac cells when coronary blood flow
inadequate, oxygen concentration has decreased, & stores of
ATP has decreased.
Carbon dioxide
potent vasodilator especially in the brain
Adenosine phosphate compounds
Result of increased ATP degradation. vasoldilator
histamine
potent vasodilator released from mast cells & basophils
Hydrogen ions
vasodilator Released from tissue in form of lactic acid in response to decreased oxygen concentration
potassium
vasodilator
Active Hyperemia
Response to increased metabolic demand with a tissue
Example
Increased metabolic activity of skeletal muscle
Reactive Hyperemia
Response of tissue to period of no flow (ischemia)
Flow can increase 4 to 7 times normal
Longer the ischemic period the longer the reactive hyperemic period
How long it takes to repay the oxygen debt
Autoregulation: Response to
Changes in Mean Arterial
Pressure
Local control mechanisms are only functional as long as MAP doesn’t change If MAP changes then all tissues will be affected by a change in flow – All tissues would see some type of local control response Able to keep flow through tissue close to normal over autoregulatory range Metabolic theory / Myogenic theory
Myogenic Theory
Sudden stretch of small blood vessels causes
surrounding smooth muscle of vessel wall to contract
Increased blood pressure stretches small blood
vessels triggering reactive constriction thus reducing
blood flow
Decreased blood pressure results in decreased stretch
of small blood vessels triggering reactive relaxation
and increased blood flow
Only allows vessels to respond to changes in
pressure, not changes in flow
Endothelial-Derived Control Factors
Nitric oxide: important direct vasodilator
Endothelin: potent vasoconstrictor
nitric oxide
Lipophilic gas released in response to variety of chemical
(increased calcium, angiotensin II) & physical stimuli (increased
shear stress due to increased flow)
nitric oxide location of action
Acts mainly in larger vessels upstream of metarterioles &
precapillary sphincters –When flow through capillary increases
release of NO causes corresponding dilation of the larger upstream
vessels
Decreased NO release is one consequence of chronic hypertension
or atherosclerosis
Arginine + Oxygen in presence of nitric oxide synthase (NOS)
Has a half-life of 6 seconds – move into smooth muscle quickly
Activates soluble guanylate cyclase (SGC)
SGC mediates conversion of cyclic guanosine triphosphate (cGTP)
to cyclic guanosine monophosphate (cGMP)
cGMP activates cGMP-dependent protein kinase (PKG)
PKG ultimately leads to relaxation of the smooth muscles
Endothelin
Large amino acid peptide
Small quantities produce significant vasoconstriction
Present in all endothelial cells but concentration
increases with vessel injury
Released from damaged cells
Can close arterial vessels as large as 5 mm in diameter
Local control is very quick but
not complete
Not able to completely compensate and return blood flow to
normal level
Chronic increase in metabolism
– flow will increase close to
actual need – long-term changes would bring total tissue
flow up to actual flow needed
increase pressure from 100 to 150 mmHg (no change in
metabolism) would cause
Quick increase in blood flow – Within 30
seconds to 2 minutes local constriction occurs producing
slow decrease in flow through tissue – When compensation
complete, flow will still be 10 to 15% higher than needed
If change in pressure was permanent,
flow would slowly
decrease over the next few weeks until total flow back to
original value
Short-term changes able to attenuate
changes in flow over pressure range of 75
mmHg to 175 mmHg
Long-term changes able to keep flow
normal over pressure range of 50 to 250
mmHg
long term control-change vascularity caused by
changes in metabolism or pressure. increase metabolism increase vascularity. decreases pressure increase vascularity. occurs in days chronic lox oxygen also increases vascularity. total change depends on max blood flow needed by tissue which allows response to exercise
Vascular Endothelial Growth Factors
Small peptides that promote new vessel growth from
existing vessels
Vascular endothelial growth factor (VEGF)
Fibroblast growth factor
Angiogenin
Decrease of tissue oxygen leads to production by
affected cells
Antiangiogenic Substances
Block the growth of new vessels
Angiostatin
Endostatin
Not sure what they do within the body, BUT receiving
a lot of interest as anticancer agents
Cancer cells cannot grow into tumors unless they are
able to develop an adequate blood supply
Collateral Circulation
Development of new vascular vessels to reestablish
blood flow to tissue affected by blocked arteries or
veins
Involve opening of existing but closed pathways and
generation of new pathways
If vessel blockage occurs slowly, then collateral
development could ensure adequate distal flow
Norepinephrine
Potent constrictor – released via ANS and adrenal medullae
Epinephrine
Not as potent as norepi
Angiotensin II
1/1,000,000 gram can increase arterial pressure 50 mmHg
Part of the overall regulation of blood pressure
Vasopressin (Antidiuretic hormone)
More powerful than Angiotensin II
Released from posterior pituitary
Major role is to increase water reabsorption by the kidneys
May play vasoactive role during acute hypovolemia
Bradykinin
Kinins are small peptides split from alpha2-globulins by
proteolytic enzymes
Kallikrein is proteolytic enzyme in the blood – inactive
Activated by damage to blood, inflammation
Activated kallikrein interacts with alpha2-globulin to release kallidin
Kallidin is converted by tissue enzymes to bradykinin
Causes powerful vasodilation & increased capillary
permeability – important responses during inflammation
Histamine
Released by mast cells and basophils located in damaged or
inflamed tissue
Potent vasodilator & increases capillary permeability
Can result in significant edema formation
Common component of allergic reactions
calcium
vasoconstriction
potassium
vasodilation
magnesium
vasodilation
hydrogen ions
increases cause constriction and decreases cause dilation
acetate citrate
cause mild vasodilation
