Regulation of Vascular Function 1 and 2 (Ramchandra) Flashcards
What Law is relavent when it comes to stretching of the blood vessels?
Frank Starling Law (more blood goes in- more stretch- more blood comes out)
Post capillary vessels have ________________________- than pre-capillary vessels of
similar vascular generation
Post capillary vessels have smaller
proportion of vascular smooth muscle in
their walls than pre-capillary vessels of
similar vascular generation
______________nerves supply all
vascular beds in the body.
Veins are more sparsely
innervated than _______________, but innervation increases as the vessels get larger.
Sympathetic adrenergic nerves supply all
vascular beds in the body.
Veins are more sparsely
innervated than equivalent pre-capillary vessels, but innervation increases as the vessels get larger.
Blood vessel dimensions are determined by…..
Vascular smooth muscle activity
Describe the dsitribution of cardiac output in different situations
After eating, you distribute your blood so your GI tract receives more blood
After drinking, you distribute your blood so that your kidneys receive more blood (to excrete water)
When exercising, you distribute more blood to skin and muscles.
Describe the movement of water between circulation and interstitial space with changes in the pre-capillary diameter.
Hydrostatic pressure moves fluid out (red)
When the pressure in the tissue is higher than the venous system/post-capillaries, fluid is reabsorbed. (Blue)
If you increase the pre-capillary resistance (e.g. a clamp), the pressure post-that clamp will fall, which will favour reabsorption. (Blue line)
If you reduce the precapillary resistance (e.g. dilation of pre-capillary), the pressure post-that area will increase, which will favour extrusion.
Describe the Autoregulation of the blood vessel diameters. (one of the mechanisms that allow changes in blood flow to different organs)
Definition: the intrinsic tendency of an organ to maintain constant blood flow despite of changes in perfusion pressure.
In the presence of changes in perfusion pressure, you might acutely get increases or decreases in flow, but over time the blood vessel autoregulates so it goes back to approx the same.
- This autoregulatory response occurs in the _absence of neural and hormonal influence_s and therefore is intrinsic to the organ, although thesse influences can modify the response. When perfusion pressure (arterial minus venous pressure, PA-PV) initially decreases, blood flow (F) falls because of the following relationship between pressure, flow and resistance:*
- When blood flow falls, arterial resistance (R) falls as the resistance vessels (small arteries and arterioles) dilate. Many studies suggest that metabolic, myogenic and endothelial mechanisms are responsible for this vasodilation. As resistance decreases, blood flow increases despite the presence of reduced perfusion pressure.*
Muscle blood flow ~ perfusion pressure
- Initially it’s around 100mmHg and blood flow is around 2ml/min.
- If the perfusion pressure increases, initially there will be an increase in flow, but after time, the flow returns to the similar level.
- If you decrease the perfusion pressure, the flow intiitally falls but eventually will come back up.
However if you drop your perfusion pressure enough (nothing goes in), the flow does drop off.
The ability of an organ to display reactive hyperemia is similar to its ability to display autoregulation.
The link between blood flow and metabolism is demonstrated by phenomenon of autoregulation.
- As perfusion pressure (arterio-venous pressure difference) is increased, there is initial increase in blood flow which then returns towards the previous level (vice versa). This recovery of blood flow can occur within a few seconds.
The level at which blood flow is regulated typically depends on metabolic requirements of the tissue. Effectiveness of autoregulation varies between vascular beds:
- Cutaneous circulation exhibits almost no autoregulation, while cerebral circulation is tightly autoregulated.
- Even in circulations where autoregulation is well-developed, there are limits to range of perfusion pressures over which blood flow is regulated, e.g. in the cerebral circulation, autoregulation is maintained from 50 to 180mmHg.
Different organs display varying degrees of autoregulatory behavior. The renal, cerebral, and coronary circulations show excellent autoregulation, whereas skeletal muscle and splanchnic circulations show moderate autoregulation. The cutaneous circulation shows little or no autoregulatory capacity.
If the perfusion pressure increases to 140mmHg, what happened to the diameter of the blood vessels such that flow was restored?
The pre-capillary vessels constricted
Describe the concept of reactive hyperaemia
One of the examples of autoregulation is Reactive Hyperaemia
If you occlude a BV for a short period of time, when you release the BV, blood flow through the vessel increases for a period of time. And this is proportional to the duration of the occlusion.
- Reactive hyperemia is the transient increase in organ blood flow that occurs following a brief period of ischemia (e.g., arterial occlusion). Reactive hyperemia occurs following the removal of a tourniquet, unclamping an artery during surgery, or restoring flow to a coronary artery after recanalization (reopening a closed artery using an angioplasty balloon or clot dissolving drug).In general, the ability of an organ to display reactive hyperemia is similar to its ability to display autoregulation.*
- In this example, blood flow goes to zero during arterial occlusion. When the occlusion is released, blood flow rapidly increases (i.e., hyperemia occurs) that lasts for several minutes. The hyperemia occurs because during the period of occlusion, tissue hypoxia and a build up of vasodilator metabolites (e.g., adenosine) dilate arterioles and decrease vascular resistance. Then when perfusion pressure is restored (i.e., occlusion released), flow becomes elevated because of the reduced vascular resistance.*
- During the hyperemia, the tissue becomes reoxygenated and vasodilator metabolites are washed out of the tissue. This causes the resistance vessels to regain their normal vascular tone, thereby returning flow to control. The longer the period of occlusion, the greater the metabolic stimulus for vasodilation leading to increases in peak reactive hyperemia and duration of hyperemia. Depending upon the organ, maximal vasodilation as indicated by peak flow, may occur following less than one minute (e.g., coronary circulation) of complete arterial occlusion, or may require several minutes of occlusion (gastrointestinal circulation). Myogenic mechanisms may also contribute to reactive hyperemia in some tissues. By this mechanism, arterial occlusion results in a decrease in pressure downstream in arterioles, which can lead to myogenic-mediated vasodilation.*
Describe the concept of Myogenic Hypothesis
- Increased perfusion pressure increases vascular preesures throughout the circulation.
- Increased transmural pressur eleads to veascular distension
- Stretch elicits smooth muscle contraction.
- (so it says that if you have change in pressure in the BV and this pressure is sensed, it reflexively tries to hold the shape. It tries to maintain blood flow).
- This isn’t really responsible for re-distribution of blood flow (unlike autoregulation).
- The myogenic hypothesis (increase in pressure causes vasoconstriction) is offset by the vascular endothelium hypothesis (increases in pressure by shear stress causes release of NO- which causes it to vasodilate)
What are the different Hypotheses of Local Control/Autoregulation?
1) Myogenic Hypothesis/Control
* Maintain blood flow (when it senses changes in stretch of BV)
2) Metabolic Hypothesis/Control
- Predominantly responsible for skeletal and cadiac muscles.
- BV dilates as we go from normal resting conditions to active phase - to supply blood the muscles
3) Vascular Endothelial Control
Describe the Metabolic Hypothesis
Predominantly responsible for skeletal and cadiac muscles.
BV dilates as we go from normal resting conditions to active phase - to supply blood to the muscles
The reason why we get vasodilation is because you have metabolites (e.g. adenosine, K+, CO2, H+) which are released by exercising muscles, that act on the BV to cause it to vasodilate (to increase the supply to meet the demands of the muscle).
Does not explain co-ordinated vasodilation throughout pre-capillary distribution circuit.
What are the effects of metabolites - Metabolic hypothesis.
What does this hypothesis not explain?
- Cause vasodilation in nearby BV
- Greatest in terminal pre-capillary vessels
- Limited in post-capillary vessels
- Does not explain coordinated vasodiatlion throughout pre-capillary distribution circuit.
Describe the concept of Vascular Endothelium hypothesis
- The vascular endothelium release Nitric Oxide which acts as a vasodilator
- I_ncreased blood flow_ increases shear stresses acting on the endothelium, which leads to the release of NO synthetase (and NO)
- The myogenic hypothesis (increase in pressure causes vasoconstriction) is offset by the vascular endothelium hypothesis (increases in pressure by shear stress causes release of NO- which causes it to vasodilate)
Describe the distribution of sympathetic innervation of the Blood Vessels
Each individual organ has different demand for blood/oxygen when it works harder, it has mechanisms in place to demand more. Some organs _(_e.g. heart) this is easier, but others (e.g. kidney) that _don’t release as much metabolite_s, this is harder. So in these need more sympathetic innervation- these can redistribute blood.
Most smypathetics nerves are in the arterial and pre-capillary side. These change BV diameter.
I_ncrease in sympathetic drive to organs_ that do not require as much blood cause vasoconstriction.