week 9 Flashcards
at rest what is skeletal muscle primarily regulated by?
sympathetic innervation
what are the receptor types in vascular smooth muscle cells ?
a1 and b2 receptors
what are a1 receptors activated by?
NE from Sym neurons
what are b2 receptors activated by?
E fro sym neurons
what do a1 receptors lead to?
vasoconstriction
what do b2 receptors lead to?
vasodilation
what predominates vasoconstriction or vasodilation?
vasoconstriction predominates because sym adrenergic neurons primarily activate a1 receptors
what happens during exercise or fight or flight response?
epinephrine released from adrenal glands activates b2 receptors causing vasodilation to increase blood flow to the muscles
during exercise, what are the main regulators of blood flow in skeletal muscles and what do they promote?
local metabolites byproducts promoting vasodilation
what’s functional hyperemia?
increased blood flow to meet the metabolic demands of active tissue
what’s reactive hyperemia?
increased blood flow after a temporary reduction (ischemia), such as when a muscle temporarily compresses blood vessels during contraction
what are the key metabolic signals triggering vasodilation?
decreased pO2
increased pCO2
increased lactate (lower pH)
increased potassium (K+)
increased adenosine (from ATP metabolism)
mechanical compression*****?????
exercise-induced compression of blood vessels temporarily restricts flow, causing brief ischemia, followed by reactive hyperemia and vasodilation to restore blood supply
at rest, how much blood flows to skeletal muscles?
1L/min (20% of cardiac output)
during exercise, how much blood flows to skeletal muscles?
20-30 L/min (20-30x resting level)
what’s the arteriovenous difference in O2 at rest and during exercise?
rest - 60 mL O2/L
during exercise - 150 mL O2/L (due to increased oxygen extraction)
what’s considered dynamic exercise?
cycles of continuous muscle contraction and relaxation and contraction again
what does contraction do to arterial inflow?
inhibits arterial inflow due to vessel compression
what does relaxation do to arterial inflow?
increases arterial inflow as vessels are no longer compressed
what does contraction do to venous outflow?
increases venous outflow, enhancing venous return
what does relaxation do to
reduces venous pressure creating a larger pressure gradient supporting increased blood flow
what’s considered static exercise?
keeping the weight in 1 position when muscles are contracted
what’s the impact of muscle contraction in static exercise?
resistance in vessels increases and blood flow decreases
what happens to total peripheral resistance (TPR) in static exercise?
increases.
what happens to mean arterial pressure in static exercise?
increases (systolic and diastolic pressure increase)
with increased cardiac output and metabolic activity , what increases in consumption?
higher oxygen consumption
what are the metabolic changes leading to vasodilation?
decreased PCO2
increased pCO2
increased. H+ (lower pH)
increased K+
increased adenosine from ATP metabolism
effect of K+ channels
activation of k+ channels causes smooth muscle hyperpolarizatoin, reducing ca2+ influx leading vasodilation
effect of calcium reduction
increased adenosine raises cAMP levels, which further reduces IC ca2+, promoting muscle relaxation and vasodilation
from muscles when Ca increases what happens?
increase in ca, leads to NO synthase activation so NO produced by endothelial cells, leading to vsmr so also vasodilation
effect of NO release
muscle contraction raises Ca2+ which activates oxide synthase in endothelial cells, NO causes relaxation of VSMC further aiding vasodilation
what’s splanchnic circulation?
blood flow to abdominal organs, including GI tract, liver, spleen, pancreas
flow rate of splanchnic circulation?
1500 mL/min
blood supply origins
celiac artery, sup mesenteric artery, inferior mesenteric artery
splanchnic circulation functions? (2)
-site of adjustable resistance
-major reservoir of blood
–> extensive interconnections between arterial branches provide collateral pathways through which blood can reach different parts
–> decreases the risk of ischemia during arterial occlusion
type regulation in splanchnic circulation
autoregulation
postprandial circulation
an increase in blood flow through GI tract after a meal
what type of innervation do splanchnic blood vessels receive?
sympathetic innervation
during sympathetic contraction of splanchnic arterials, what happens to blood flow?
decreases blood flow to GI tract, which increases blood for organs/ muscles needed for exercise
effect of increase in TPR
increase blood to other organs
what controls blood flow in coronary circulation
local metabolites
most important local metabolite factors in coronary circulation
hypoxia
adenosine
coronary blood flow Qc at rest
amount of blood heart gets in a minute
Qc=200-250 blood/min, 5% of CO 5,6L/min
coronary blood flow Qc exercise
1250mL/min
ADVO2 value
120-130mL O2/L blood
ADVO2 during exercise
900-1200mL/min
O2 consumption
30 mL O2/min
formula for Qc
Qc = pp/R
LCA during systole
-wall tension increases
-aortic valve closed
-high pressure in myocardium compresses coronary vessels
increase in perfusion pressure on LCA during systole
increase in CO
increases Perfusion pressure
blood flow during diastole
-wall tension decreases
-resistance decreases
-bood flow increase
how is coronary blood flow regulated
myogenic, metabolic and neutral controls
myogenic mechanism role in in coronary blood flow
myogenic mechanism (Bayliss effect) provides autoregulation, maintaining stable flow during perfusion pressure (60-160 mmHg)
describe how Bayliss effect maintains coronary blood flow
increased arterial pressure causes vasoconstriction to limit blood flow, while decreased pressure causes vasodilation maintaining steady flow
mechanism of Bayliss effect at cellular level
increased pressure raises wall tension, activating non-selective cation channels, leading to depolarisation and VDCC activation which increases Ca2+ and causes vasoconstriction
what happens at cellular level in Bayliss effect when pressure decreases
decreased pressure reduces wall tension, decreasing activation of cation channels and VDCC leading to less Ca2+ and resulting in vasodilation
metabolic regulation
process where factors from metabolism cause vasodilation
what happens to o2 and co2 during exercise
o2 decreases, co2 increases which triggers vasodilation
what effects cause vasodilation
decreased PO2, increased Co2, increased H+, increased K+ and increased adenosine
how does increased heart rate indirectly cause vasodilation
higher heart rate increases CO leading to vasodilation
difference between abrupt and gradual occlusion in coronary vessels
-abrupt occlusion leads to necrosis
-gradual occlusion allows new vessels to form, reducing damage
what primarily controls cerebral circulation
local metabolites, auto regulation and hyperemia
most important local vasodilator in brain
increased co2 sensed by central chemoreceptors
what effect does increased co2 have on cerebral blood flow
causes vasodilation, increased blood flow to remove excess co2
what happens to cerebral blood flow during hyperventilation
Co2 level drop, causing vasoconstriction
blood flow in brain
750-800 mL/min & 15% of CO
what happens if brain blood flow stops for 5 secs, for 5 mins
loss of consciousness
irreversible brain damage
auto regulation in cerebral circulation
brains ability to maintain constant blood flow despite changes in pressure
what metabolic changes increase cerebral blood flow
increased pCO2, decreased pO2, increased H+, K+ and adenosine lead to vasodilation
key regulators of cerebral blood flow
pCO2 and EC K+
how do brain vessels respond to high pCO2 levels
they vasodilate to increase blood flow to remove co2
effect of hyperventilation on brain vessels
lowers pCO2, leading to vasoconstriction
role of astrocytes near neurons
are in close contact with synapses, take up K+ and release them to cause vasodilation
what happens if 1 volume component in brain increases
compresses brain tissue, which can cause damage
what is Cushing reflex
increased intracranial pressure (ICP) compresses arteries leading to increased blood pressure and decreased heart rate
what forms the blood brain barrier and function
capillaries with tight junction that restrict direct access to brain EC fluid, prevents harmful solutes in blood from reaching ec fluid
volume and daily production of csf
volume - 150mL
production rate - 550 mL/day
main functions of csf
provides mechanical protection , allows brain to float and maintains stable environment for neurons
where is csf produced
by ependymal cells in choroid plexus
how does csf compare to blood composition
csf has low k+, low protein concentration and slightly lower pH
how is csf absorbed
passively absorbed through arachnoid vili driven by csf pressure to sup saggital sinus
typical pressure of csf
100 mmH2O
what happens if csf pressure increases
absorption increases, which leads to brain damage
