Control of Blood Flow Flashcards
What is the vasodilator theory for acute local blood flow control?
Acute control (short-term): vasodilator theory is a theory that when we have an increase in metabolism that leads to a decrease in oxygen availability this causes the formation of vasodilators.
What are the 6 vasodilators?
1)adenosine 2)carbon dioxide 3)adenosine phosphate compounds 4) histamine 5) potassium ions 6) hydrogen ions
What is the oxygen (nutrient) lack theory acute local blood flow control?
Acute control (short-term): oxygen (nutrient) lack theory is a theory stating that low oxygen concentrations and lack of oxygen to the vessels depletes their energy to maintain the baseline constricted state and therefore causes them to vasodilate.
What is vasomotion:
Cyclical opening and closing of pre capillary sphincters. The number of pre capillary sphincters open at any given time is roughly proportional to nutritional requirements of tissues.
What is hyperemia?
Hyperemia is increased blood flow.
What is the reaction when blood flow has been blocked from tissue for an extended period of time (seconds to hours or more)?
When blood flow is blocked for an extended amount of time and then allowed to flow back, the blood flow to that tissue is increased above the normal baseline. This is called reactive hyperemia.
What is reactive hyperemia?
Reactive hyperemia is when the blood flow is increased from baseline because the tissue was just deprived of blood flow. This increase can be 4-7x the normal blood flow.
What is active hyperemia?
Active hyperemia is when blood flow is increased simply because there is increased metabolism in the tissue (ex: exercise).
What happens to the rate of blood flow when there is an increase in the rate of metabolism?
When the rate of metabolism increases there is also an increase in the rate of blood flow.
What happens to the rate of blood flow when arterial oxygen saturation decreases?
When arterial oxygen saturation decreases there is an increase in the rate of blood flow to that tissue
What is autoregulation?
It is the fact that in any tissue…
- rapid increase in arterial pressure leads to increased blood flow
- within minutes, blood flow returns to normal even with elevated pressure
The metabolic theory and the myogenic theory are two theories to explain how autoregulation works.
What is the metabolic theory of autoregulation when the arterial pressure becomes too great?
The metabolic theory of autoregulation is a theory stating that when the arterial pressure becomes to great there is an increase in blood flow and delivers an overabundance of oxygen and nutrients “washes out” the vasodilators. This causes the vessels to constrict and return flow to nearly normal despite increased pressure.
What is the myogenic theory of autoregulation?
The myogenic theory of autoregulation states that stretching of vessels causes reactive vasculature constriction (stretch induced depolarization of smooth muscle cells).
Describe the mean arterial pressure vs blood flow line graph representing the acute and long-term autoregulation of arteries.
The solid red line depicts the acute autoregulation of blood flow as arterial pressure increases. Between 70 and 175mmHg, blood flow only increases 20 to 30 percent even though the arterial pressure increases 150%
The dashed line represents the long-term autoregulation of blod flow as arterial pressure increases over a period of many weeks. The blood flow only increases slightly because of increase in number and size of capillaries and arterioles.
What are the special acute blood flow control mechanisms?
The special acute blood flow control mechanisms are controlled by the:
- kidney
- tubuloglomerular feedback: involves the macula densa/juxtaglomerular apparatus (regulates fluid volume)
- brain
- (See attached figure) during increased metabolism there is a buildup of carbon dioxide and hydrogen ions and decreases oxygen concentration in the brain. This is why cerebral vessels would want to dilate.
- skin
- blood flow linked to body temperature, sympathetic nerves via CNS, blood flow to skin varies considerably
What is the mechanism for endothelial-derived control of tissue blood flow?
Healthy endothelial cells secrete nitric oxide, which converts cyclic GTP to cyclic GMP. In return, cyclic GMP activates protein kinases and cause vasodilation.
What is the mechanism by which damaged endothelial cells cause hypertension?
Damaged endothelial cells secrete a higher concentration of endothelin than normal. Endothelin is a 21 amino acid peptide, effective in only nanog. Endothelin is responsible for vasoconstriction as endothelin is really helpful during a crushing injury. In an inappropriate response, endothelin causes hypertension and potentially more damage to endothelial cells.
Presence of nitric oxide in healthy endothelial cells causes vasoconstriction or vasodilation?
Presence of nitric oxide in healthy endothelial cells causes vasodilation.
What two reactants do endothelial cells use to synthesize NO?
Endothelial cells use oxygen (o2) and L-arginine to synthesize NO by reduction of inorganic nitrate.
What molecule does nitric oxide (NO) activate and what does this molecule move on to accomplish?
nitric oxide (NO), from endothelial cells, activates guanylate cyclase which goes on to convert cyclic GTP to cyclic GMP in the smooth muscle, which then causes vasodilation.
What are the 4 signalling molecules that cause vasoconstriction?
The four signaling molecules that cause vasoconstriction are:
1) norepinephrine
2) epinephrine
3) angiotensin II
4) vasopressin
What are 2 signaling molecules that cause vasodilation?
The two signaling molecules that cause vasodilation are:
1) bradykinins - also causes increased capillary permeability
2) histamine - from mast cells and basophils
Where is the vasomotor control center in the brain?
bilaterally mainly in the reticular substance of the medulla. Transmits parasympathetic impulses through vagus nerve to heart and sympathetic impulses through spinal cord and peripheral nerves to all arteries, arterioles, and veins of body. There is also a center for receiving sensory input form the vagus and glossopharyngeal nerves.
What is vasomotor tone?
The baseline contraction of blood vessels. There is constant sympathetic firing causing this tone.
The graph attached shows what happens to the arterior blood pressure when a spinal anesthetic blocks sympathetic signals to the arteries.
What is the signaling pathway when baroreceptor in aortic arch senses a blood pressure greater than 30mmHg?
- aortic baroreceptor >30mmHg
- signal to sensory area
- sensory area stimulates the vasodilator area
- vasodilator inhibits vasoconstrictor area
- this allows slight relaxation of the vessels
What is the signaling pathway when baroreceptor in carotid arch is stimulated by blood pressure greater than 60mmHg?
- carotid >60mmHg
- stimulates Hering’s nerve
- stimulates CN IX (glossopharyngeal)
- relays sensory information to sensory area of brain
- sensory area activates vasodilator area
- vasodilator area inhibits vasoconstrictor area.
Do baroreceptors control arterial pressure minute-by-minute or over long period of time?
Baroreceptors are super sensitive and adjusts arterial pressure minute-by-minute.
The graph shows the normal regulation of arterial blood pressure in healthy dog while the bottom graph shows complete denervation of baroreceptors causing the dog’s arterial blood pressure to fluctuate a lot.
True or False. When total peripheral resistance increases arterial pressure increases too.
True.
True or False. Changing total peripheral resistance in a patient will effect the long-term arterial pressure.
False. In individuals with healthy kidneys the long-term arterial pressure will always remain at 100mmHg because the kidneys will adjust pressure diuresis and pressure natriuresis.
However, it is true that arterial pressure=cardiac output x total peripheral resistance. So this reveals that the cardiac output will adjust over a long-term span to compensate for the difference in total peripheral resistance.
How does an increase in nitric oxide production lead to decreased peripheral resistance and decrease in blood pressure?
Nitric oxide is released from endothlial cells and converts cyclic GTP to cyclic GMP which activates protein kinases causing vasodilation.
Increase in vasodilation decreases peripheral resistance and decreased blood pressure.
How does increased release of prostacyclin decrease peripheral resistance and lead to decreased blood pressure?
prostacyclin causes the muscles of the vessels to relax decreasing the peripheral resistance and therefore decreasing the blood pressure.
