Unit 1 Flashcards
(205 cards)
1
Q
Vascular bed anatomy
A
Vascular tress - branching progressively to become smaller vessels
2
Q
Capillary size among different species
A
Capillaries have an endothelial layer on the outside and the width is only one red blood cell across, therefore must pass individually through. Capillary and red blood cell size does not change between animals, does not scale. It is blood flow / output that meets the demands of the animal
3
Q
Conduit vessel
A
An artery that carries bulk flow, carries most of the blood in the body
4
Q
Feed artery
A
Branch off of the conduit artery, more narrow in diameter and more specific in location, continues to branch off into progressively smaller branches of arterioles. Quantity of branches is dependent on type and size of muscle
5
Q
Steady state conditions
A
Looks at an average of many values over time (different heat beats in the cardiac cycle) (averaging blood flow over time)
6
Q
Pulsatile flow / event
A
Looks at a more specific value at particular time (e.g. during cardiac cycle)
7
Q
Source of pulsatility in the system
A
The heart provides the constriction and dilation in a cyclic pattern of the vessels and the overall system
8
Q
Downward vasculature
A
Provides what blood pressure looks like, looses compliancy as you go down the vasculature system. Downward vasculature refers to the vessels onward, past starting point
9
Q
CO =
A
SV x HR
10
Q
What is cardiac output?
A
Cardiac output is the total blood output that your heart is sending out in L / minute
11
Q
What is stroke volume?
A
Stroke volum is the amount of blood ejected with each heartbeat
12
Q
What is mean arterial pressure?
A
MAP is the pressure on the arterial side of the cardiovascular system (venous side pressure is normally very close to zero)
13
Q
What is conductance?
A
How easily blood can flow through the vessels (good conductors - materials that easily allow electrons, blood or current to pass through)
14
Q
What is resistance?
A
Opposite to conductance. The opposition of movement through the vessels
15
Q
What is compliancy?
A
Different vessels of the vascular system have different levels of compliancy, it is dependent on elastin and muscle within the vessels. Compliancy is how well the vessel can alter diameter to account to the cardiac cyclic pattern of the heart, absorb energy and move blood forward
16
Q
Damping effect
A
The damping effect of elastic blood vessels is the capacity of absorption of energy by the vessels with the increase in diameter to temporarily store the blood
17
Q
What is required for movement of the blood?
A
Pressure gradient is required for flow in one direction
18
Q
Red blood cells
A
The main articulate of the blood that adds viscosity to the otherwise rather liquid plasma blood (adding some level of resistance)
19
Q
Effect of change in radius of blood vessel on pressure and resistance
A
Change in radius is to the power of four in the equation, therefore an even small change can cause a large impact on pressure
20
Q
Radius of blood vessel is impacted by …
A
Metabolic and neuronal control depending on the conditions of the internal and external environment
21
Q
Delta P =
A
8uLQ / pi r^4
Delta P is the pressure drop or gradient. It is influenced by the length of the vessel, viscosity of fluid, volumetric flow rate and the radius of the vessel
22
Q
R =
A
8uL / pi r^4
R is a measurement of vasoconstriction (the decrease in diameter of the vessel) due to the contraction of the muscular wall of the vessels. It is impacted by length of the vessel, viscosity of the fluid and radius of the vessel
23
Q
Difference between delta P and R
A
Delta P takes into account the volumetric flow rate
24
Q
What are two fundamental determinants of the R and pressure drop
A
Segment length and tube size
25
Ohm's Law =
I = V / R
I is total current
V is voltage gradient
R is resistance
Ohms = volts / amperes
26
Ohm's Law and the cardiovascular system
Voltage = potential difference across a conductor = delta P
Amperes = total current, blood flow (Q)
Ohms = vascular resistance (the resistance to the flow)
27
Ohm's Law and the cardiovascular system,
R =
R = delta P / Q
28
Ohm's Law and the cardiovascular system,
Q =
Q = delta P / R
29
Ohm's Law and the cardiovascular system
CO =
Cardiac output = mean arterial pressure / total peripheral resistance
CO = MAP / TPR
30
MAP =
MAP = CO x TPR
31
Ohm's Law and the cardiovascular system verbal explanation
Explains the relationship between pressure, flow and resistance.
Flow = Pressure / Resistance
32
What is MAP?
Mean arterial pressure is the average arterial pressure of the entire body
33
What is TPR?
Total peripheral resistance is the resistance of all of the vessels of the body, the heart has to pump against this, downstream resistance of all vessels
34
Typical CO
5-6 L / min
35
What impacts MAP?
Downstream resistance changes, vascular resistance changes, compliance of vessels
36
What impacts TPR?
Poiseuille's Law:
- viscosity changes (u)
- vessel length (L)
- radius change (r)
Main factor is the radius change ...
R = 8uL / pi r^4
37
Cardiovascular analogue to the electrical equation delta V = I x r
MAP = CO x TPR
38
If pressure was negative in the system equation, what would this indicate?
The flow of the fluid would be in the opposite direction
39
Average MAP in larger vessels
100 mmHg
40
MAP difference throughout vascular system
Begins at about 100 mmHg in the larger vessels and then large drop in blood pressure from arteries to arterioles because the mass of the blood is being divided into a much larger number of arterioles, even less with capillaries
41
Compliancy difference throughout vascular system
Vessels become less compliant as you go down the system (arteries more compliant than arterioles, which are more than capillaries)
42
Pressure drop in a series (no branching) system
In a single vessel, pressure will go down as the diameter of the vessel decreases. Same amount of blood in a small space, V / P relationship
43
Pressure drop in a parallel (branching) system
Large branching system of the vascular system as you go down and therefore the distribution of the volume of blood is so vast that the pressure will drop. Large increase in cross sectional distribution therefore large decrease in pressure
44
More compliant vessels ..
Contain more elastic and are larger in size
45
Vascular resistance (tone)
Describes how easily blood can flow through a vessel (blood flow easier in a vessel under low tone, rather than high tone)
46
Blood flows more easily through a vessel with ___ tone
Lower
47
Higher resistance =
Higher tone
48
Higher conductance =
Lower tone
49
Equation used for system (all vessels)
```
R = delta P / Q
MAP = CO x TPR
```
50
Equation used for vessel (one segment)
```
R = delta P / Q
R = 8uL / pi r^4
```
51
Why is it better calculating resistance with the other equation, not Ohm's for a single vessel?
Because in a vessel, you must consider viscosity, length and radius but viscosity and length don't change much in a segment, but radius is modulated
52
Rule for choosing equation for vascular tone
Whatever changes most (pressure or flow) should be in the numerator. If pressure changes but flow does not, we would use resistance, since that puts pressure in the numerator (R = delta P / Q)
53
Resistance = 1 / vascular conductance, therefore VC =
Vascular conductance = Q / delta P
VC = Q / delta P
54
Factors affecting pulsatile flow ...
compliance (elasticity), viscoelasticity and inertia
55
What is compliance (elasticity)?
Change in volume for a given change in pressure (inverse of stiffness), the more compliant vessels are the ones with the capacity to alter the pulsatility of the system, this is the main effector of pulsatile flow
56
What is viscoelasticity?
Resistance to the circumferential stretch, characteristic of a material that exhibits both viscous (not flowing freely) and elastic distended) properties, collagen doesn't allow elastin to do it's job
57
What is inertia?
Resistance to change or movement, related to the mass and viscosity of a) the blood being accelerated by the systolic blood pressure and b) the vessel wall that is being pushed out of the way of the moving blood. Greater inertial force in the more compliant, larger vessels - more ideal for back flow because walls of the arteries are more willing to move and change diameter
58
Equation for compliance
delta V / delta P
59
Role of compliance
A compliant vessel will descend during systole to absorb energy, a more stiff vessel will not, the more compliant vessel will expand over time during the systolic phase to absorb the volume of blood ejected from the heart (cycle of expansion and recoiling of the vessels relative to the heart's phase), temporarily stored during systole in the vessel
60
Compliance is determined by ..
Elastic properties of the vessel
61
Arterial pressure (2 conditions)
steady state - shown by MAP (averaged over time), pulsatile - accounts for oscillatory nature, within cardiac cycle
62
Where in the vascular system would we want to consider the pulsatile nature of blood pressure?
Figure out
63
Where in the vasculature would we not want to consider pulsatility?
Figure out
64
How does compliance affects both steady state and pulsatile aspects of pressure?
Figure out
65
Flow in compliant vessels
Flow is more constant in compliant vessels and they momentarily store blood within the vessels, providing opportunity for constant blood flow instead of intermittent flow in the smaller, less compliant vessel
66
Windkessel effect
Term used to describe the change of shape of the arterial blood pressure waveforms, seen in larger elastic arteries
67
Blood flow is ___ in elastic tubes
Pulsatile
68
As a damping feature, compliance is one determinant of the ___ and the ____
Flow pattern and the blood pressure waveforms downstream
69
Windkessel vessels provides a second kind of ___ by ...
Second pump by providing constant blood flow even with the heart is in diastole (relaxing)
70
During systole, compliant vessels ...
Change their size to store a greater volume of blood
71
During diastole, compliant vessels ...
Constrict to move on the blood flow to protect upstream vessels from high pressure and prevent intermittent blood flow
72
Pressure wave form downstream
As you go down the vasculature tree, the pressure wave form changes, more dull in the beginning because in the beginning of the system there are larger vessels and they absorb more of the pressure (greater damping effect) than in the smaller arteries
73
Flow in a stiff system
The flow would be faster than in a compliant system because this absorbs more energy which requires additional time
74
Pulse wave velocity
PWV - the shorter this time, the higher the pulse wave velocity, don't want this to be high because that would indicate a stiff system and more intermittent flow
75
Compliance = ..
Elasticity, distensibility
1 / stiffness
76
Crashing of waves (primary and secondary heart beats) is dependent on ...
Compliance of the vessels and how resistant the vascular is downstream
77
Resistance in the organs
Within the organs there is a high level of resistance, the vessels are a lot smaller in diameter than in the conduit arteries
78
Greater resistance results in ...
Greater reflected waveform
79
Hypertension and reflected waveform
With hypertension, the diameter and compliance of the vessels can be increased - higher resistance, higher tone of the vessels there more difficult to pump blood forward, the reflected pressure / waveform is greater
80
Reflected waveform in healthy individuals
Reflected waves will always exist no matter the person because of the large drop of pressure with the high distribution and small diameters, but the volume of the reflected wave back will be less for healthy individuals with lower resistance than someone with hypertension
81
Energy and waveforms
Some energy is absorbed in the arteries, but some energy is bounced back, this reflected wave form will tell you what is going on downstream
82
High resistance, high blood pressure =
More energy being bounced back and less energy going through
83
High resistive beds =
Reflected wave will have greater overlap with the forward wave, therefore greater summation and higher blood pressure (systolic blood pressure)
84
Less resistive beds =
Healthier vessels that are more compliant, there will be a greater spread between the two waves
85
Compliance and PWV with age and hypertension
Vascular compliance decreases and PWV increases (less time as less energy is absorbed), higher blood pressure from greater vascular stiffening and greater downstream resistance (plaque build up, lower diameter)
86
Difference of vessel diameter at old age
No significant difference between diameter during systole and diastole therefore energy is not being absorbed in the elderly patients due to high stiffness of the vessels (diminished capacity to descend - stiffer vessel, not as compliant)
87
Reflected wave overlap at older age
Reflective wave overlaps more due to greater stiffness and more constriction in smaller arterioles leads to summation of wave peaks (total peak is larger, therefore greater systolic blood pressure)
88
Wave velocity with older age
Higher velocity because of more stiff vessels in hypertensive and greater age therefore the crash of the waves is going to occur earlier resulting in a greater peak
89
Augmentation Index
How much does the reflected waveform increase the peak blood pressure (the systolic blood pressure through summation of waves)
90
Isolated systolic hypertension
It is mostly systolic pressure causing increase in MAP, with age, systole rises (greater than 120) due to less damping, less energy absorbed and this energy goes down the system and is read as a higher systolic value
91
Diastolic blood pressure with age
Blood pressure (during relaxation) rises with age until a certain point until it starts to decline, when the heart relaxes the vessels recoil and shoot the energy forward, recoil decreases because of stiffening of the vessels decreases (loose ability to store energy and vasodilation is lower therefore less to recoil)
92
Pulse Pressure
Difference between systole and diastole values, with age this increases, difference between these values increases
93
Exercise and compliance
Endurance-trained athletes have greater compliance of their vessels than sedentary individuals (significant difference seen only in older age). With training (brisk daily walking of about 20 minutes) increases compliance of vessels
94
Exercise hyperemia
Increased blood flow due to volitional exercise, because of something you've done, under volitional contraction
95
Reactive hyperemia
Increased blood flow due to muscle ischemia (without / lack of blood flow) - but no exercise, the reaction of lack of blood flow with a large rebound flow of blood
96
Flow mediated dilation
The conduit vessel dilation due to shear stress typically following an increase in blood flow
97
FMD order of events
Muscle ischemia, downstream dilation, downstream hyperemia with release of cuff, increase in blood flow in conduit vessel to satisfy downstream dilation, conduit shear stress, conduit dilation
98
Endothelial layer
Is the inside layer and can respond to stress, the endothelium is important for resting dilatory capacity
99
Sympathetic tone
There will always be a level of constriction and dilation - there is always some level of sympathetic control of resting constriction
100
Endothelium function with age and atherosclerosis
There is a hindered ability of the endothelium doing it's job (lines all of the blood vessels of the body including those in the brain). Dilation ability is lacking
101
Mechanical shear
Caused by increased blood flow and red blood velocity
102
FMD decrease
Will go down with age and atherosclerosis development as the endothelium does not respond as well to the stimulus (dilation capacity decreases)
103
Endothelium sensitivity to high fat or sugar meal
FMD will lower within a couple of hours, this will return to normal eventually if the individual is healthy, but overtime this can accumulate and be more chronic in nature
104
Acetylcholine Hypothesis
Ach diffuses from the neuromuscular junction and causes dilation via muscarinic receptor on smooth muscle cells
105
Blockers of Ach
Atropine binds to muscarinic receptor and prevent's ACh's ability to contribute to vasodilation
106
Duty cycle
Change of intensity of work load (local contraction of the muscle from electrical stimulation at different frequencies)
107
During light intensity exercise, role of atropine on order of vessels of hamsters
Atropine causes less of a diameter change than the control animals - Ach contributes to the dilation of the vessels (no matter the order at low exercise intensity)
108
During heavy intensity exercise, role of atropine on order of vessels of hamsters
Atropine causes less of a diameter change only in the feed artery, no significant change within the 2A and 4A arterioles (order does matter at high exercise intensity), therefore other redundant system may kick in
109
Atropine effect on rats
There are no significant differences between the diameter of the rats who received atropine and those who received saline (no dilation in this case)
110
Volitional exercise produces ..
Sub-maximal contraction strength
111
Low intensity exercise hand grip and atropine effect
Giving atropine while the person is contracting - there is no change in mean blood volume (MBV), if atropine did have an effect on preventing Ach's effect, it would cause a drop in the MBV because if Ach was a vasodilator and was inhibited, the vessel would constrict which causes a decline in MBV (but this is not the case therefore Ach likely does not play a large role in dilation in this muscle at this intensity level)
112
L-NMMA
Prevents nitric oxide from being produced, nitric oxide causes an increase in vasodilation so therefore preventing it should result in constriction
113
Muscarinic receptors exert ..
Important influence over baseline forearm blood flow but have little influence on submaximal exercise hyperemia
114
Blocking ACh receptors and nitric oxide
The only time you see an effect is at baseline levels, not during moderate intensity exercise
115
Exercise and endothelial dysfunction
Exercise can help to preserve, sometimes reverse and prevent endothelium dysfunction
116
Increase in RBC velocity ..
Should be sensed by the endothelium and cause it to increase diameter to balance this out again
117
Redundant pathways of dilation
There are other redundant systems that work together to get dilation (the effect of potassium in hyperpolarization)
118
Stimulus is shear stress
Gamma = (8 x MBV) / diameter
119
Oxygen offloading
Occurs in capillaries because the endothelial layer of the capillaries is only one cell thick and therefore diffusion is more efficient
120
Muscle's demands in exercising
Oxygen demand goes up and the oxygen offloading must increase to meet demand, when this happens, you must increase blood flow to increase oxygen need
121
Chain of command
Capillaries demand, upstream delivers
122
Increasing blood flow ___ TPR
Drops TPR (resistance has to decrease to allow for increase in blood flow)
123
Increasing blood flow ___ MAP
Drops MAP
124
Balance of blood flow during exercise
Balance between supplying muscles the nutrients and oxygen it needs while maintaining blood pressure for proper homeostatic levels
125
VO2
The volume of oxygen consumption, indicative of aerobic capacity
126
a-v (O2)
Arterial, venous oxygen difference, how much oxygen you have in the blood on arterial and venous side of the system
127
Most important determinant of exercise capacity
Total perfusion of exercising skeletal muscle - if you don't have enough blood flow, you won't be able to exercise
128
VO2 and exercise
The greater the intensity, the higher the oxygen consumption until VO2 max is reached at the plateau
129
VO2 max height extent
Governed mostly from genetics, can be increased with training to an extent
130
Q represents ..
Blood flow or cardiac output (L / minute)
131
VO2 =
Q * (aO2 - vO2)
OR
Q * (a-v) *O2
132
Local blood flow and workload
Local blood flow increases linearly with workload
133
Vascular conductance
How easily blood can flow through vessels, higher conductance = greater flow
134
Vascular resistance
Opposite to conductance, as resistance goes up, it is more difficult for blood to move through the vessels
135
Conductance =
1 / resistance
136
Cardiac output is at the ..
Heart level (systemic change)
137
Vascular conductance occurs ..
Locally at the tissue in the smaller vessels (local change)
138
Pericardium
Physical restraint of the heart, surrounds the heart like a jacket and puts a restraint on how much the heart can hold (therefore limiting cardiac output) (SV)
139
Removing the pericardium
VO2, CO and SV all increased when the pericardium is taken off, able to increase heart's capacity by removing the physical constraint
140
Recruiting muscle over and above that which requires the maximal CO would result in ..
Hypotension unless there was some limit to muscle vasodilation. Something has to kick in to prevent BP falling
141
Why can't we rely on CO alone?
The pericardium limits the amount of blood that the heart can eject and therefore the amount of blood that can be delivered to the muscle only from CO is limited, have to look at local factors of vascular conductance to distribute blood demand
142
How do we get the muscles enough blood by reducing resistance without sacrificing MAP?
Need a system to protect the levels of MAP so that we don't faint whenever we workout (when we faint, we fall horizontally as a protective mechanism to get the brain and heart on the same altitude level and eliminate effect of gravity)
143
The pattern of blood flow to muscle during exercise
Redistribution, rapid, ascending vasodilation
144
Ascending vasodilation
Capillaries signal upstream parent (larger) vessels to vasodilate to provide more blood to the vessels that follow in the working muscles because capillaries cannot dilate themselves
145
As intensity increases, CO ..
Increases - a lot of this blood is going to the muscle, demand in the heart increases as well but majority to muscles, less to viscera
146
Maximum voluntary contraction and blood flow
Hand grip strength test for 1 second - arterial pressure is fairly constant throughout the test, but mean blood flow locally in the hand shows a rapid increase
147
Electrical stimulation and blood flow
Involuntary, sudden increase in local blood flow and slow recovery (similar pattern)
148
Volitional contraction and blood flow
You are contracting under own terms, increase is a bit more gradual, but still sudden increase in blood flow with slow recovery
149
Changes in local blood flow can be ..
Very rapid even to a small stimulus
150
Rapid increase in blood flow related to several hypothesis ..
Mechanical (myogenic, muscle pump), endothelial factors, metabolic factors, red blood cell factors, neural
151
Vascular blood flow follows ..
Resistance or conductance gradient
152
Increasing blood flow to the muscle ..
Decrease resistance, increase vascular conductance or increase pressure gradient (P1 or P2)
153
VC =
1 / R
R is resistance
154
Q =
| In terms of blood flow
```
Q = (P1 - P2) / R
Q = VC x (P1 - P2)
```
155
Three different categories for changing vasodilation and vasomotor control
Mechanical, neural and biochemical (metabolic, endothelium, neural)
156
Upregulation of VC done by
ACh, PG, NO, K, Metabolites (Pi, La)
157
Down regulation of VC done by ...
Myogenic autoregulation
158
Upregulation / increasing pressure gradient done by
MP and P
159
Muscle pump
Mechanically changing the pressure gradient across the capillary bed, increases venous return. Compliant vessels allow for the movement of the blood, dictate direction with their mechanical pump actions. Progressively moving blood forward
160
Myogenic mechanical factor
Mechanically changing the transmural pressure across the vessel wall, mechanical compression of the vessel, as it it pressed the vessel will respond by dilating
161
Increasing perfusion pressure gradient by muscle pump mechanism
When you compress on the veins, you are moving blood forward to the heart (greater venous return) and you are leaving little blood in the veins and therefore lower pressure in the veins and pressure gradient between a-v will increase
Higher gradient = higher blood flow in the direction of the venous side (goes from 60 mmHg to 100 mmHg)
Greater venous return = greater CO
162
Myogenic mechanical - mechanism
Arterial pressure increases upstream causing momentarily larger diameter but then the arteriole actually constricts to prevent too much high pressure of the capillaries
163
Pressure summation of myogenic mechanism
With continuous trains of contractions, you will have consistent expansion / dilation of the vessels
164
Muscle fibre contraction and blood vessels
Muscle fibres contract and they are in close proximity to the small vessels within them - they provide this compressive force on the vessels which then dilate (maintains blood flow to the skeletal muscle and protects capillary pressure downstream)
165
Biochemical factors involved in exercise vasodilation
During exercise, the muscle uses more potassium which leaks out into the interstitial space. Leakage of ACh can cause vasodilation to decrease resistance
166
Tangenital stress
Sheer stress going along the vessel applied parallel - the opposite side of the vessel
167
Smooth muscle cells are placed ...
Circumferentially which is valuable in contraction inward and outward rather than if they were placed a long the muscles (like skeletal muscle cells)
168
Neural control of vasodilation and vasoconstriction
Neurons innervate smooth muscle cell layers of the vessel and will release NTM on to specific receptors and this will increase resistance of the vessels (vasoconstriction) (NE)
169
Metabolic hypothesis of rapid and sustained dilation
Direct vascular effect, indirect effect on NE release
170
Acetylcholine hypothesis of rapid and sustained dilation
ACh release from neuromuscular junction, direct vascular effect, indirect effect on NE release, endothelial effect
171
Endothelial hypothesis of rapid and sustained dilation
Shear stress mechanisms, productions of nitric oxide (NO) and prostaglandins (PGs), direct vascular effect, indirect effect on NE release
172
Red blood cells and rapid and sustained dilation
Red blood cells brush against the endothelial layer of the vessels - shear stress. Red blood cells are able to sense low levels of oxygen and they have this oxygen sensing capacity that allows them to release ATP to bind to receptors of endothelial (P2Y receptors) to cause the smooth muscle layer to relax and cause vasodilation which increases blood flow and in turn solve the low oxygen problem
173
Evidence for Metabolic Hypothesis
Potassium is part of the metabolic waste produced during muscle contractions, increase in venous plasma potassium with increased exercise intensity
174
Increase of potassium in interstitium
Rapid release of potassium from contracting muscle into the interstitium (not just plasma), gradient between local changes in the muscle (interstitium) and before getting into the venous blood (systemic circulation) is increased with workload
175
Potassium and vasodilation
Potassium causes vasodilation of blood vessels whether it is produced intrinsically through muscle contractions or extrinsically through injection. Therefore potassium increases blood flow
176
Potassium, membrane potential and vascular smooth muscle change
Increased potassium on outside of vessel will make it more positive and therefore inside will appear more negative - hyperpolarization - makes it more difficult for absolute threshold to be reached and vessel to constrict and therefore if vessel is not constricting it will be dilated
177
Gap junctions
Are used in ascending vasodilation - facilitates the communication across cells. Endothelial cells are going to be parallel to the vessel
178
Homeocellular communication
Communication among cells that are the same, allowing the endothelial cells to talk to each other
179
Heterocellular communication
Communication across different cell types (smooth muscle cells to endothelial cells)
180
Myoendothelial gap junctions
Pores that allow communication from endothelial to muscle cells
181
Sucrose and dilation
As you exercise and you use more oxygen, you need more and more blood flow. Vessels upstream (the arterioles) will dilate and get more blood to the downstream vessels. With sucrose - no dilation in the upstream arterioles, sucrose hinders effects of the gap junctions from functioning, getting rid of communication
182
Potassium movement through the gap junctions
Kicked out of the endothelial cells which makes the endothelial cells hyperpolarized and this signal travels along through the gap junctions up until it reaches the closes blood vessel (signal has to go from capillaries where it cannot dilate itself to a larger blood vessel) and gets to a smooth muscle cell
183
Increased calcium release in the endothelial cells causes..
The potassium channels to open and get kicked out
184
Electrical impulse travels through myoendothelial gap junctions to the ..
Smooth muscle cell layer - changes electrical charge of these cells and this blocks calcium entry into these cells therefore taking away its ability to contract - if the vessel cannot contract, the vessel will therefore have to be dilated
185
When Ach binds to the receptor on the endothelium, you get an increase in ..
Calcium this turns on nitric oxide synthase --> produces eNOS (endothelial nitric oxide) from O2 and L-citruline
186
Two molecules that block NOS production
L-NAME and L-NMMA
187
NOS leaves the endothelial cells and enters ..
The smooth muscle cell and this increases cyclic GMP levels in the smooth muscle cells and this causes dilation (relaxation) of the smooth muscle cells
188
Cyclic GMP
Prevents contractile units of the smooth muscle cell from working - inhibition
189
Shear
Mechanical, more blood flow, higher red blood cell velocity physically along the vessel this breaks down part of the phospholipid layer of the cells of the endothelium layer, blood glycoclyx breaks off, this leads to an increase in calcium and the pathway mechanism is the same from here on out
190
Shear causes ..
Phospholipid breakdown which increases arachidonic acid to accumulate. Cycloxygenase turns arachidonic acid into prostaglandins which will go into the smooth muscle cells and increase cyclic AMP
191
Cyclic AMP
Will prevent calcium increases in the vascular smooth muscle cells, lowering calcium layers therefore causing dilation
192
NSAIDS reduces ..
Inflammation by reducing too much blood flow, blocks cycloxygenase so that dilation does not occur as much anymore (throbbing feeling in this area will go down because of reduction in dilation and reduction in blood flow)
193
2 ways to cause dilation
Increase calcium --> eNOS
| Shear stress --> PG
194
FMD
Is a qualitative value received from the lab to measure the health of the endothelium, if the endothelium is working properly. Shear will cause dilation, if there is increased shear and no dilation occurs then there is something wrong with part of the mechanisms that cause dilation in either one of the two pathways
195
Flow-mediated vasodilation
Ultrasound probe looks at the diameter of the brachial artery at rest and the cuff is inflated on the forearm - this is supra-systolic (above systolic pressure), this causes little blood flow through the arm (turns slightly blue), when the cuff is released there is a large increase in blood flow going through the arm (whoosh sound heard as blood flow increases) - increases shear levels in the upper arm because of something that happened in the forearm
196
Increased calcium in smooth muscle layer
Will cause contraction
197
Increased calcium in endothelial cells
Will cause dilation of the smooth muscle layer
198
Shear mechanisms of using the cuff - time mechanism
The longer you have the cuff on, the greater the increase of blood flow in the brachial artery - because the longer you have the cuff on for, the greater the shear stress stimulus you will create, by creating a larger demand for blood downstream. There is a limit level of dilation that your arm can do to maximum shear stress in the brachial artery. To get enough shear to produce dilation effect you need to have the cuff on for about 5 minutes
199
Shear stress of the brachial artery requires ...
Increase in red blood cell velocity
200
Once the cuff is released there is a ..
Surge in blood flow velocity causing large increase in shear stress - eventually the vessel recovers and gets back to baseline
201
Shear stress change is the stimulus for ..
Diameter change in the brachial artery - because you need time to experience and build up enough shear stress to get dilation, the change in the brachial artery has a delay (about 90 seconds) (before peak effect of change in diameter) (takes time for molecular processes to summate and their effect to occur)
202
Healthy individuals vs. some level of endothelial dysfunction - FMD
Healthy individuals - your FMD (percentage brachial artery will dilate in response to shear stress) will be about 8-12%, with some level of endothelial dysfunction (high fatty meals, aging, atherosclerosis, etc..), this peaks of FMD value will drop, can produce the same shear stimulus in the vessel but the response will be less, not able to respond in the same way. Below 5% is a bad sign but there are ways to increase this value
203
Pre-ischemia
Before you put on the cuff, the diameter is about 0.4 cm of the brachial artery, forearm blood flow is normal
204
Ischemia
When cuff is on, the vessels in the forearm will drop in blood flow because you are in ischemia from the mechanical compression of the cuff
205
Mechanical compression during ischemia ..
The vessels in the forearm will dilate therefore blood flow greater increases post ischemia. Largest increase 10 seconds post, increase in blood flow rate. Matching th need of high blood flow in the forearm, the brachial artery will increase in dilation (increase in diameter) after about 90 second post ischemia (note the delay of this) - catches up
