Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
mechanism of local control
|
perfusion is controlled by diameter of vessels via:
1. local effects 2. neural activity 3. hormonal signals |
|
Limitations of coronary BF
|
- Cardiac muscle (especially LV) is best supplied/ relieved at diastole
- shortening of diastole has a negative impact on supply/ relief - diastole limits max HR: shortens much more than systole |
|
acute and long term regulation of BF
|
-acute: compensated within a few sec to min, but some deviation remains
- long term: over hours to weeks, more precise - P changes between 50 and 250 cause only small changes in BF |
|
long term regulation through size and number of vessels
|
1. low P (eg 60) for many weeks increases the size and eventually number of vessels
2. high P has opposite effect 3. increase of metabolism has same effect as low P |
|
long term regulation through reconstruction of tissue vasculature
|
1. fast in young animals (days)
2. fast in cancerous tissue 3. slow in older tissues (months to years) |
|
long term regulation through angiogenesis
|
- release of angiogenic factors initiates angiogenesis
- rapidly growing tissues - tissues with a high metabolic rate |
|
three angiogenic factors
|
1. endothelial growth factor
2. fibroblast growth factor 3. angiogenin |
|
norepi and epi
|
-vasoconstricting agents
- Norepi more powerful - Epi may even cause mild vasodilation |
|
angiotensin
|
- one of the most powerful vasoconstricting agents known:
1microg increases BP more than 50 -renin (kidney) --> angiotensinogen (liver) --> angiotensin (lung) --> aldosteron (hypothalamus) |
|
ADH (vasopressin)
|
- even more powerful than angiotensin but only very small quantities released
- most likely, little role in P regulation - important fx in kidneys: reabsorption of fluid |
|
bradykinin
|
- vasodilator
- formed in tissue fluid: kallikrein converts kallidin to bradykinin - arteriolar dilation and increased capillary permeability |
|
histamine
|
-vasodilator
- released in all tissues: damage, inflammation, allergic rxn - arteriolar dilation and increased capillary permeability: fluid leaks out, leading to edema |
|
prostaglandins
|
- majority are vasodilators
- almost every tissue - importance in circulatory regulation not completely clear |
|
calcium
|
-increase causes vasoconstriction:
stimulation of smooth m |
|
potassium
|
-increase causes vasodilation: ability to inhibit smooth m contraction
|
|
magnesium
|
-increase causes powerful vasodilation: generally inhibits smooth m
|
|
sodium
|
-increase causes mild vasodilation: ability to inhibit smooth m contraction
|
|
hydrogen ions, carbon dioxide
|
vasodilation
- carbon dioxide also has powerful vasoconstrictive effect on the vasomotor center |
|
Intrinsic Control
|
-from inside= tissue itself
- critical tissues: brain, heart. working skeletal m |
|
extrinsic control
|
- from outside
- non- critical tissues: kidney, stomach, intestines, liver, resting skeletal m |
|
active hyperaemia steps
|
-intrinsic metabolic increases:
1. increase in waste products 2. release vasdilators: H+, CO2, ADP, AMP 3. supplying arteriole dilates 4. blood flow increases: supply of nutrients and relief of wastes returns to normal 5. tissue supplied but at a higher level: increased perfusion 6. negative feedback limits the blood flow |
|
active hyperaemia definition
|
increased perfusion caused by increased metabolism
|
|
reactive hyperaemia gen
|
-extrinsic factors (eg compression) causes metabolic changes
- vasodilators released which increase blood flow= hyperaemia - negative feedback limits blood flow |
|
reactive hyperaemia steps
|
1. interruption of blood flow (eg vascular compression) cause temporary cessation in supply/relief
2. release vasodilators: H+, CO2, ADP, AMP 3. when block removed blood flows through dilated arterioles until ICF [vasodilator] returns to normal 4. supply/relief normal also |
|
reactive hyperaemia definition
|
increased perfusion based on compensation for deficiency caused by a decrease in blood flow
|
|
sudden decreased in BP
|
1. perfusion P decreased steeply: 100 to 60
2. initiallly, BF decreases: 100 to 60 3. within a short period of time, blood flow returns almost to the initial value: 60 to 90 |
|
sudden increase in BP
|
1. perfusion P increases steeply: 100 to 140
2. initially, BF increases: 100 to 140 3. within a short period of time (seconds), BF returns almost to the initial value: 140 to 110 |
|
autoregulation in the brain
|
within a wide range of perfusion P (60 to 190), the corresponding changes in BF are very small
|
|
metabolic control of BF
|
increase or decrease of the ECF [vasodilator] changes the vascular resistance and thus BF
|
|
myogenic theory
|
1. increase of BP stretches the muscle fibers in the vascular wall
2. muscle fibers respond with contraction - protects capillaries from excessively high BP |