KNES 506 Practice Qs

Cerebral Blood Flow (CBF) Regulation. The test includes multiple-choice, true/false, and short-answer questions.

Cerebral Blood Flow Regulation Practice Test

Multiple Choice (10 Questions)

1. Which of the following is the strongest acute regulator of cerebral blood flow (CBF)?
a) Arterial oxygen pressure (PaO₂)
b) Partial pressure of arterial carbon dioxide (PaCO₂)
c) Mean arterial pressure (MAP)
d) Cerebral metabolism

2. Mayer waves, which represent oscillations in blood pressure, occur at a frequency of:
a) 0.01 Hz
b) 0.05 Hz
c) 0.10 Hz
d) 1.00 Hz

3. What happens to CBF when PaCO₂ increases?
a) CBF decreases
b) CBF increases
c) CBF remains unchanged
d) CBF stops completely

4. The neurovascular unit consists of which of the following components?
a) Neurons, glia, and microvasculature
b) Neurons, cerebrospinal fluid, and glia
c) Glia, dura mater, and vascular smooth muscle
d) Neurons, white matter, and pial arteries

5. Which part of the brain’s vascular system is most sensitive to changes in PaCO₂?
a) Middle cerebral artery (MCA)
b) Posterior cerebral artery (PCA)
c) Pial vessels
d) Basilar artery

6. The lower limit of autoregulation (LLA) is traditionally thought to be around what MAP value?
a) 40 mmHg
b) 50 mmHg
c) 60 mmHg
d) 70 mmHg

7. During hypoxemia, significant increases in CBF are observed when arterial oxygen saturation drops below:
a) 95%
b) 80%
c) 50%
d) 30%

8. Which of the following byproducts of neuronal activity contributes to vasodilation?
a) CO₂
b) Nitric oxide (NO)
c) Arachidonic acid metabolites
d) All of the above

9. Which of the following is NOT a key regulatory mechanism of cerebral blood flow?
a) Cerebrovascular reactivity
b) Neurovascular coupling
c) Cerebral autoregulation
d) Barometric pressure changes

10. Which of the following statements about squat-stand maneuvers is true?
a) They help demonstrate differences in cerebral autoregulation across the cardiac cycle
b) They increase blood pressure without affecting cerebral blood flow
c) They show that diastolic oscillations are extensively buffered
d) They prove that cerebral autoregulation is the same in all individuals

True/False (5 Questions)

11. CBF regulation is more responsive to CO₂ levels than to O₂ levels. (T/F)

12. Pial vessels are less sensitive to CO₂ changes compared to the middle cerebral artery (MCA). (T/F)

13. Cerebral autoregulation allows the brain to maintain constant blood flow despite changes in blood pressure. (T/F)

14. Hypercapnia (excess CO₂) leads to cerebral vasoconstriction. (T/F)

15. The lower limit of autoregulation (LLA) is fixed at 50 mmHg for all individuals. (T/F)

Short Answer (5 Questions)

16. Explain how cerebrovascular reactivity is influenced by changes in PaCO₂.

17. Describe the concept of neurovascular coupling and its role in CBF regulation.

18. What happens to cerebral autoregulation in cases of severe hypotension?

19. How does the brain respond to hypoxemia when arterial O₂ saturation drops below 50 mmHg?

20. List and briefly describe the three main factors that regulate cerebral blood flow.

Answer key for your Cerebral Blood Flow Regulation Practice Test:

Answer Key

Multiple Choice (10 Questions)

1. b) Partial pressure of arterial carbon dioxide (PaCO₂)

• CO₂ is the most potent acute regulator of CBF.

2. c) 0.10 Hz

• Mayer waves are oscillations in blood pressure occurring every 10 seconds.

3. b) CBF increases

• Higher PaCO₂ causes vasodilation, increasing blood flow.

4. a) Neurons, glia, and microvasculature

• The neurovascular unit links neuronal activity to blood flow.

5. c) Pial vessels

• These vessels are more sensitive to PaCO₂ changes than deeper arteries.

6. b) 50 mmHg

• The LLA is commonly cited as 50 mmHg, though it varies between individuals.

7. b) 80%

• Hypoxemia doesn’t significantly affect CBF until O₂ saturation drops below 80%.

8. d) All of the above

• CO₂, NO, and arachidonic acid metabolites all contribute to vasodilation.

9. d) Barometric pressure changes

• CBF is not regulated by atmospheric pressure, but by metabolic and vascular factors.

10. a) They help demonstrate differences in cerebral autoregulation across the cardiac cycle

• Squat-stand maneuvers test how blood pressure fluctuations affect CBF regulation.

True/False (5 Questions)

11. True

• The brain is far more sensitive to CO₂ than to O₂ changes.

12. False

• Pial vessels are more sensitive to CO₂ than MCA/PCA.

13. True

• Cerebral autoregulation maintains stable CBF despite blood pressure fluctuations.

14. False

• Hypercapnia (high CO₂) causes vasodilation, not vasoconstriction.

15. False

• The LLA is not fixed at 50 mmHg; it varies between individuals.

Short Answer (5 Questions)

16. How does cerebrovascular reactivity respond to PaCO₂ changes?

• Increased PaCO₂ (hypercapnia) = vasodilation = ↑ CBF

• Decreased PaCO₂ (hypocapnia) = vasoconstriction = ↓ CBF

17. Describe neurovascular coupling and its role in CBF regulation.

• Neurovascular coupling ensures that blood flow increases to active brain areas.

• Astrocytes and metabolic byproducts (CO₂, NO, arachidonic acid) trigger local vasodilation.

18. What happens to cerebral autoregulation during severe hypotension?

• Below the LLA (~50 mmHg MAP), vessels lose the ability to compensate, leading to ischemia.

19. How does the brain respond to hypoxemia when arterial O₂ saturation drops below 50 mmHg?

• CBF increases sharply to compensate for reduced oxygen availability.

20. List and briefly describe the three main regulators of cerebral blood flow.

• PaCO₂: Strongest acute regulator; ↑ CO₂ → vasodilation → ↑ CBF.

• Cerebral metabolism: Blood flow increases in active brain regions (neurovascular coupling).

• Autoregulation: Maintains constant CBF despite blood pressure changes.

Explanations:

1. Excitatory (activating) and inhibitory (suppressing) neurons communicate with astrocytes (star-shaped support cells) and GABAergic interneurons (neurons that release GABA, an inhibitory neurotransmitter).

• Astrocytes' "end-feet" surround blood vessels, specifically cortex-penetrating arterioles (small arteries leading into the brain).

• This positioning allows astrocytes to act as middlemen, translating neural activity into blood vessel changes.

What this means: When neurons are active, astrocytes detect this and help adjust blood flow to meet the energy needs of the neurons

2. Astrocytes Promote Vasodilation via Arachidonic Acid

• When neurons become more active, they require more oxygen and glucose.

• This increased oxidative metabolism (energy production) in astrocytes triggers the release of arachidonic acid metabolites, which help dilate blood vessels.

Why this matters: More blood flow means more oxygen and nutrients for the busy neurons.

3. Endothelial Cells & Nitric Oxide (NO) → Vasodilation

• Endothelial cells (which line the inside of blood vessels) experience shear stress as blood flows past them.

• In response, they release nitric oxide (NO), which relaxes smooth muscle cells in the blood vessel walls, leading to vasodilation.

Why this matters: This process helps maintain proper circulation and prevents excessive resistance in blood vessels.

4. Prostaglandins & Smooth Muscle Activation

• Prostaglandins (lipid molecules involved in inflammation and blood flow regulation) are released in response to various signals.

• They trigger smooth muscle activation, helping regulate vessel diameter by promoting either constriction or relaxation depending on the situation.

Why this matters: Smooth muscle in vessel walls must adjust continuously to ensure stable brain perfusion.

Vessel dilation: Arachidonic Acid & COX Pathway Activation

• Arachidonic acid (a fatty acid) is released from cell membranes in response to signals like increased neural activity or metabolic demand.

• This activates the cyclooxygenase (COX) enzyme, which converts arachidonic acid into prostaglandins (specifically PGE₂).

• Prostaglandins Trigger cAMP Release

  • PGE₂ binds to receptors on smooth muscle cells in blood vessels.

  • This activates a signaling pathway that increases cyclic AMP (cAMP) levels inside the muscle cells.

• cAMP Inhibits Myosin Light Chain Kinase (MLCK)

  • Normally, MLCK helps contract muscle cells by phosphorylating myosin, the protein responsible for muscle contraction.

  • When cAMP increases, it inhibits MLCK, preventing myosin from contracting the muscle.

• Smooth Muscle Relaxes → Vessel Dilates

  • Since MLCK is blocked, the smooth muscle relaxes, and the blood vessel expands (dilates).

  • This allows more blood to flow through, delivering oxygen and nutrients to active tissues.