Continuous measurement of blood pH with an indwelling arterial glass electrode.

Band, David; Semple, S. J. G.

doi:10.1152/jappl.1967.22.4.854

Cited by 42 publications

(5 citation statements)

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“…The lag time to the end ofthe acid shift in abdominal aortic pH was 4-1 + 0-15 s (range 2-1-4-9 s). Typically, the pulmonary venous oscillations had a less sinusoidal shape than those in the aorta, while both had the added oscillations in time with heart rate as previously described by Band & Semple (1967 amplitude of the aortic oscillations became attenuated to a much greater degree than those in the pulmonary vein (Fig. 4).…”

Section: Dog Experimentssupporting

confidence: 61%

Measurement of pulmonary venous and arterial pH oscillations in dogs using catheter tip pH electrodes.

Chakrabarti¹,

Cobbe²,

Loh³

et al. 1983

The Journal of Physiology

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SUMMARY1. Respiratory pH oscillations were studied in 8itu in the aorta and superior vena cava of rabbits, and in the pulmonary vein and aorta of open-chested dogs, using catheter tip pH electrodes.2. Preliminary experiments on two spontaneously breathing rabbits showed pH oscillations of 0006-0010 pH units in the ascending aorta at a respiratory rate of 40/min. No oscillations were apparent in the superior vena cava.3. In anaesthetized, ventilated dogs, the delay from the upstroke in airway pressure to the onset of the alkaline limb of the pH oscillation was 1 15 + 0 9 s in the pulmonary vein and 441+0-1 s in the descending aorta (mean+S.E. of mean, n = 28 tracings in four dogs).4. Pulmonary venous oscillations were equal to or larger in amplitude than those in the aorta. Aortic oscillations became proportionately smaller at shorter respiratory cycle lengths, although both were related to tidal volume.5. Stop flow experiments were performed using a pH electrode placed in situ in the left atrium inside a wide-bore tube. A small fall in pH occurred when flow was stopped (-0-0036 + 0-0012, mean + S.E. of mean, n = 22 recordings in four dogs). The findings were not dependent upon the phase of the oscillation at which flow was stopped. Mean plasma free haemoglobin was very low (1 6 mg/dl), indicating minimal haemolysis of the blood withdrawn past the electrode.6. It is concluded that the plasma CO2 hydration reaction is virtually at equilibrium by the time blood reaches the pulmonary vein.

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Section: Dog Experimentssupporting

confidence: 61%

Measurement of pulmonary venous and arterial pH oscillations in dogs using catheter tip pH electrodes.

Chakrabarti¹,

Cobbe²,

Loh³

et al. 1983

The Journal of Physiology

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“…For this information to effect alterations in ventilation the Pco, oscillations would firstly have to persist in the blood after it had flowed through the lungs, and secondly to reach and be detected by a suitable receptor. Arterial Pco2 (Pa, co2) oscillations have been recorded, albeit indirectly, by means of fast-responding pH electrodes in vivo (Band & Semple, 1967;Le Blanc, Brown, Klebe, Niedrach, Slusarczuk & Stoddart, 1976).…”

Section: Introductionmentioning

confidence: 99%

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

Cochrane¹,

Newstead²,

Nowell³

et al. 1982

The Journal of Physiology

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SUMMARY1. The purpose of the study was to see whether the rate of rise of alveolar Pco, (PA, co2) in expiration was directly proportional to the rate of pulmonary elimination of C02 ( Vco2) in man in the steady state.2. Alveolar ventilation at rest and during exercise in man was calculated from the difference between total ventilation and dead space ventilation, and from the ratio of the rate of pulmonary C02 elimination to the mean expired alveolar C02 (total) fraction. The results were indistinguishable. In agreement with other workers' findings alveolar ventilation changed in direct proportion to the rate of carbon dioxide elimination, confirming the isocapnia of exercise ventilation in man.3. The rate of rise of expiratory alveolar PCO2 in individual breaths has been obtained by two methods. In the first, a pattern of respiration with constant expiratory flow in each breath brought expiratory alveolar profiles to the outermost end of the airway. In the second method, the early part of the alveolar PCO2 during normal expiration was calculated from airway PCO2 and expired volume.4. The data obtained with both methods show that, in the steady state, expiratory alveolar PCO2 rises at a rate which is directly proportional to the rate of C02 production.

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“…Yamamoto and Edwards (38) increased the apparent metabolic rate of rats by venous infusion of CO 2 -rich blood; the rats sustained PCO 2 homeostasis. Furthermore, PCO 2 oscillations of respiratory frequency have been demonstrated indirectly in the arterial blood of man and animals by Band and Semple by means of a fast-response pH electrode (4). There is little, if any, attenuation of the oscillations during transit in the arterial blood.…”

Section: Consideration Of Mechanismsmentioning

confidence: 99%

Alveolar Pco₂ oscillations and ventilation at sea level and at high altitude

Nickol¹,

Milledge²,

Ruiten³

et al. 2008

Journal of Applied Physiology

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This study examines the potential for a ventilatory drive, independent of mean PCO2, but depending instead on changes in PCO2 that occur during the respiratory cycle. This responsiveness is referred to here as "dynamic ventilatory sensitivity." The normal, spontaneous, respiratory oscillations in alveolar PCO2 have been modified with inspiratory pulses approximating alveolar PCO2 concentrations, both at sea level and at high altitude (5,000 m, 16,400 ft.). All tests were conducted with subjects exercising on a cycle ergometer at 60 W. The pulses last about half the inspiratory duration and are timed to arrive in the alveoli during early or late inspiration. Differences in ventilation, which then occur in the face of similar end-tidal PCO2 values, are taken to result from dynamic ventilatory sensitivity. Highly significant ventilatory responses (early pulse response greater than late) occurred in hypoxia and normoxia at sea level and after more than 4 days at 5,000 m. The response at high altitude was eliminated by normalizing PO2 and was reduced or eliminated with acetazolamide. No response was present soon after arrival (<4 days) at base camp, 5,000 m, on either of two high-altitude expeditions (BMEME, 1994, and Kanchenjunga, 1998). The largest responses at 5,000 m were obtained in subjects returning from very high altitude (7,100-8,848 m). The present study confirms and extends previous investigations that suggest that alveolar PCO2 oscillations provide a feedback signal for respiratory control, independent of changes in mean PCO2, suggesting that natural PCO2 oscillations drive breathing in exercise.

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Continuous measurement of blood pH with an indwelling arterial glass electrode.

Cited by 42 publications

References 0 publications

Measurement of pulmonary venous and arterial pH oscillations in dogs using catheter tip pH electrodes.

Measurement of pulmonary venous and arterial pH oscillations in dogs using catheter tip pH electrodes.

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

Alveolar Pco₂ oscillations and ventilation at sea level and at high altitude

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Continuous measurement of blood pH with an indwelling arterial glass electrode.

Cited by 42 publications

References 0 publications

Measurement of pulmonary venous and arterial pH oscillations in dogs using catheter tip pH electrodes.

Measurement of pulmonary venous and arterial pH oscillations in dogs using catheter tip pH electrodes.

The rate of rise of alveolar carbon dioxide pressure during expiration in man.

Alveolar Pco2 oscillations and ventilation at sea level and at high altitude

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Product

Resources

About

Alveolar Pco₂ oscillations and ventilation at sea level and at high altitude