Lecture 2 - Carotid And venous Chemoreceptors Key Papers

Question 1

What did Dripps and Comroe (1947) find?

Answer 1

They found that a PaO2 fall during exercise barely stimulates ventilation (it’s not sensitive to hypoxia)
Concluding no consistent fall in PaO2 has ever been mentioned.

Question 2

What did Sun (2001) find??

Answer 2

Evidence for no fall in PaO2 or no rise in PaCO2 during exercise
Evidence that PvO2 does fall by 50% and that PvCO2 rose enormously!

Question 3

What was the design of Sun(2001) and what were the limitations present??

Answer 3

Had 5 participants perform bike ergo to max (1.3KW- good)

Limitations

• Only 5 p’s
• measured o2 concentration rather than partial pressure, and no time on the X axis

Question 4

What evidence is there that PaCO2 does not rise during exercise ?

Answer 4

Sun (2001)
Forster (1986)
Hickam (1951)
Stringer (1992)

Question 5

What did Lambertsen (1953) show?

Answer 5

Highlighted the sensitivity of PaCO2. Just a 10mmhg increase (40-50) is needed for Ve to rise from 5L/min to 20L/min.

Question 6

What did Forster (1986) do and then show?

Answer 6

Had 9 subjects exercise for 5 mins at either 10-18Ve or 50Ve and showed no hypo/hypercapnia in phase 1 or phase 3

Question 7

We know Stringer (1992) showed no hypercapnia, how did he show this??

Answer 7

8 participants ergo on a bike to max (1.1kw), found PaCO2 actually fell during heavy ex

Question 8

We know from the literature that arterial PO2 or PcO2 doesn’t change during ex and hence carotid chemoreceptors are’nt stimulated and don’t drive breathing during ex, but whAt literature suggests that mixed venous pCO2 and mixed venous PO2 change?

Answer 8

Sun (2001) both
Edwards (1972) both
Casaburi (1989) mvpCO2 rise

Question 9

What did Edwards show (1972)?

Answer 9

Looked at 3 individuals performing ex at 150w equated work.
MvPCO2 increased from 46+/-3 at rest and to 62+/-3 after 5 mins
MvPO2 fell from 35+/-4 to 23+/-3 mmhg

Question 10

What did Casaburi (1989) find??

Answer 10

6 subjects using a pulmonary artery catheter,at 140-200w

MvPCO2 rose from 42-59 mmhg at 90s during steady state

Question 11

Describe the Cropp and Comroe (1961) study??

Answer 11

Looked at unaesthetized cats and dogs. Made them spontaneously breath CO2 sat blood. In 24/25 occasions infusion failed to increase respiratory frequency or Tv until PaCO2 rose

Question 12

Slyvester et al (1973)?

Answer 12

Looked at 12 unaes dogs. Had a co2 saturated saline infused in ascending aorta of SVC just above RA.

The results showed there’s no obvious role of aortic chemoreceptors in dogs either but do show there must be an additional chemoreceptors somewhere - looking in the wrong place, just as cropp was.
Remember negative results -‘absence of evidence not evidence of absence’

Question 13

Banner and Guz(1988) looked in transplant patients at phase 1+2 of exercise (first 2 mins), found what?

Answer 13

No increase in HR, SV, CO but again looking in the wrong place

Question 14

Describe the key stimulation experiment disregarding venous chemoreceptors ?

Answer 14

Dejours (1955) claimed no existence in man (n=4).

300mmhg leg cuffs for 2 mins after leg ex raising metabolic rate, release of the cuff caused deoxygenated blood to reach the carotid region a mean of 17s later.
But, breathing never rose until after the blood passed here, due to the negative result, all we can conclude is that if they do exist and stimulate breathing, their latency must be over 20s

Question 15

Describe Mills (1994)?

Answer 15

Injected cyanide to stimulate the carotid chemoreceptors, the hyperpnoea was too fast to be fully explained by carotid chemoreceptors - first evidence eluding to venous existence

Question 16

Describe Wassermans (1975) ablation experiment?

Answer 16

Had 6 asthmatics vs 11 similar aged controls with CBX

• showed after carotid chemoreceptor denervation, breathing still increases and matches met rate
• never been repeated at this or higher ex intensities
• either carotid chemoreceptors are redundant or they are irrelevant, were the results jut due to the fact they were asthmatic?

Question 17

What Shea (1993) find??

Answer 17

5 children needing mech vent vs 5 controls with CCx

• no difference in the rapid Ve responses at the onset of treadmill exercise
• not slower to reach steady state
• did however confirm an inability to hyperventilate above the lactate threshold

Question 18

Discuss the idea that CC contribute to hyperventilation during lactic acidosis??

Answer 18

Hagberg (1982) had 4 mcArdles patients fail to produce lactic acid yet do hyperventilate during exercise (0.4kw)

Supposedly may be due to increased brain temperature
- Chappius et al (1976) and Macdougall (1974)

• wasserman (1975) didn’t measure brain temperature and didn’t ex the asthmatics very hard, so perhaps that’s why the temp didn’t rise enough to cause hypervenitlation

Question 19

What evidence exists for the CO2 oscillation hypothesis ?

Answer 19

Band (1980) only had 1 subject and barely exercised him
Murphy (1987) had 4 dialysis patients and showed spontaneous oscillations in Ph at rest and in recovery that disappear during exercise .
So if they were important , they must be sensed by carotid chemoreceptors but from Wasserman 1975 peripheral chemoreceptor not needed for phase 1