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what type of transport do substances use to cross the PM?
simple diffusion or facilitated transport
the cell is a barrier to what?
small, non-polar molecules and hydrophilic molecules
how do small, non-polar molecules cross the PM?
they will follow a concentration gradient → simple diffusion
how do hydrophilic molecules cross the PM?
Unlikely to cross the hydrophobic interior unassisted → need facilitated transport
includes inorganic ions, sugars, amino acids, nucleotides (and others)
what do we mainly care about in PM transport?
the speed of crossing
How does size affect permeability?
The smaller the molecule → the faster the rate of diffusion
The larger the molecule → the slower the rate of diffusion
What are 2 factors relevant to permeability?
size and solubility in water
How does solubility affect permeability?
A proxy of charge
Uncharged molecules are not impeded by the lipid barrier
Polar molecules are slowed by the lipid barrier
Charged molecules are prevented by lipid barrier
What is the mathematical relationship between blood pH and H+ concentration?
Blood pH is an inverse logarithmic measure of H+ concentration
How does an increase in PCO2 within the normal range (35–75 mm Hg) affect alveolar ventilation?
An increase in PCO2 within the normal range between 35 and 75 mm Hg causes a marked increase in ventilation
How significant is the respiratory change across the normal blood pH range (7.3–7.5) compared to PCO2 changes?
The change in respiration within the normal blood pH range (7.3 to 7.5) is less than 10% as great as the change caused by PCO2
How do changes in O2 affect control of the resp. center?
changes in O2 have little direct effect on control of the resp. center
What direct effect do changes in O2 concentration have on the respiratory center?
They have virtually no direct effect on the respiratory center itself to alter respiratory drive.
Through what structure do O2 concentration changes indirectly influence breathing?
Through their effect on peripheral chemoreceptors.
At what threshold does the peripheral chemoreceptor mechanism respond to low blood O2?
It responds when blood O2 falls too low, mainly below a PO2 of 70 mm Hg.
Where are peripheral chemoreceptors located, and where are the majority found?
Most chemoreceptors are in the carotid bodies, with others located in the aortic bodies along the arch of the aorta.
What is the rate of blood perfusion to the peripheral chemoreceptor bodies?
They are highly perfused, receiving a blood flow equal to 20 times the weight of the bodies per minute.
Why are peripheral chemoreceptors continuously exposed to arterial blood rather than venous blood?
Because perfusion is so high, the percentage of O2 removed from the flowing blood is virtually zero, keeping the surrounding blood at arterial levels.
what stimulates the chemoreceptors?
decreased arterial oxygen.
How do different levels of arterial PO2 affect the carotid body?
they affect the rate of nerve impulse transmission from a carotid body
In what specific range of arterial PO2 is the impulse firing rate of the carotid body particularly sensitive?
The impulse rate is particularly sensitive to changes in arterial PO2 in the range of 60 mm Hg down to 30 mm Hg.
What cells detect low blood O₂ in the peripheral chemoreceptors?
Type I glandular-like cells (glomus cells) detect decreases in blood PO₂.
What happens to O₂-sensitive potassium channels in glomus cells when blood PO₂ decreases markedly?
The O₂-sensitive K⁺ channels are inactivated (close).
What is the effect of K⁺ channel inactivation in glomus cells?
Closure of K⁺ channels causes the cell to depolarize.
What occurs after glomus cell depolarization?
Voltage-gated Ca²⁺ channels open, allowing Ca²⁺ influx.
What is the role of calcium influx in glomus cells?
Ca²⁺ stimulates neurotransmitter release, which activates afferent neurons.
How does low blood PO₂ ultimately increase respiration?
Low PO₂ → K⁺ channels close → depolarization → Ca²⁺ channels open → neurotransmitter release → afferent neurons activated → signals sent to the CNS → respiration is stimulated.
Describe the glomus cell response to O₂ deficiency.
↓PO₂ → K⁺ channels close → depolarization → Ca²⁺ channels open → neurotransmitter release → afferent nerve activation → CNS stimulation → ↑ respiration.
How do increased CO₂ and H⁺ concentrations affect the chemoreceptors?
Increased CO₂ or H⁺ concentration excites peripheral chemoreceptors, which indirectly increases respiratory activity.
Do CO₂ and H⁺ stimulate respiration through peripheral chemoreceptors?
Yes. Increased CO₂ or H⁺ activates peripheral chemoreceptors, which send signals that increase respiration.
Which has a stronger effect on respiration: direct stimulation of the respiratory center by CO₂/H⁺ or stimulation through peripheral chemoreceptors?
The direct effects of CO₂ and H⁺ on the respiratory center are about 7x more powerful than their effects mediated through peripheral chemoreceptors.
Compare the direct and indirect effects of CO₂ and H⁺ on respiration.
Indirect effect: CO₂/H⁺ → peripheral chemoreceptors → increased respiration.
Direct effect: CO₂/H⁺ → respiratory center → increased respiration.
The direct effect is ~7× stronger.
How does the speed of respiratory stimulation via peripheral chemoreceptors compare to central stimulation?
Peripheral chemoreceptor stimulation occurs up to 5 times faster than central stimulation
When only low O2 is being considered, what ventilatory drive is active?
Only the ventilatory drive caused by low O₂ on the chemoreceptors is active.
What effect does hypoxemia have on ventilation when arterial PO₂ is greater than 100 mm Hg?
Almost no effect on ventilation occurs as long as arterial PO₂ remains above 100 mm Hg.
How does ventilation change as arterial PO₂ falls below 100 mm Hg?
Ventilation begins to increase; it approximately doubles when PO₂ falls to about 60 mm Hg.
How much can ventilation increase at very low arterial PO₂ values?
Ventilation can increase up to fivefold at very low PO₂ levels.
When does low arterial PO₂ become a strong driver of ventilation?
At low PO₂ values (especially below ~60 mm Hg), low arterial PO2 drives the ventilatory process quite strongly.
Which factors primarily regulate ventilation in healthy animals at sea level?
PCO₂ and H⁺ concentration are the primary regulators of ventilation because the effect of hypoxia is relatively modest when PO₂ is greater than about 60–80 mm Hg.
What happens to arterial PO₂, PCO₂, and pH during exercise?
Arterial PO₂, PCO₂, and pH remain almost exactly normal.
How does alveolar ventilation change during exercise?
Alveolar ventilation ordinarily increases almost exactly in step with the increased level of oxygen metabolism.
What is believed to stimulate the respiratory center during exercise?
The brain, on transmitting motor impulses to the exercising muscles, is believed to transmit collateral impulses into the brain stem at the same time to excite the respiratory center
•This action is analogous to the stimulation of the vasomotor center of the brain stem during exercise that causes a simultaneous increase in arterial pressure
How do direct nervous signals contribute to respiratory control during exercise?
They stimulate the respiratory center by almost the proper amount to supply extra O₂ for exercise and remove extra CO₂.
What happens when nervous respiratory control signals are too strong or too weak?
Chemical factors help make the final adjustment of respiration.
What happens to alveolar ventilation at the onset of exercise?
Alveolar ventilation increases almost instantaneously without an initial increase in arterial PCO₂.
What effect does the initial increase in ventilation have on arterial PCO₂?
It often decreases arterial PCO₂ below normal at first.
What is meant by "anticipatory" stimulation of respiration during exercise?
The brain increases ventilation at the onset of exercise
What happens about 30–40 seconds after exercise begins?
the amount of CO2 released into the blood from the active muscles approximately matches the increased rate of ventilation, and the arterial PCO2 returns essentially to normal, even as the exercise continues
Which change in arterial blood produces the greatest increase in alveolar ventilation within the normal physiological range?
a. A decrease in PCO₂
b. An increase in PCO₂
c. A decrease in H⁺ concentration
d. An increase in PO₂
b. An increase in PCO₂
Which statement best describes the direct effect of changes in arterial O₂ on the respiratory center?
a. Changes in O₂ have a strong direct effect on the respiratory center
b. Changes in O₂ have virtually no direct effect on the respiratory center
c. Increased O₂ directly stimulates the medullary respiratory centers
d. O₂ is detected primarily by central chemoreceptors
b. Changes in O₂ have virtually no direct effect on the respiratory center
A dog develops a substantial decrease in arterial PO₂. Which receptors are primarily responsible for detecting this change?
a. Central chemoreceptors in the medulla
b. Pulmonary stretch receptors
c. Chemoreceptors in the carotid and aortic bodies
d. Baroreceptors in the carotid sinus
c. Chemoreceptors in the carotid and aortic bodies
At approximately what arterial PO₂ does hypoxia begin to produce a substantially stronger ventilatory response?
a. 150 mm Hg
b. 100 mm Hg
c. 60 mm Hg
d. 30 mm Hg
c. 60 mm Hg