Gas-blood CO2 equilibration in parabronchial lungs of birds

1976 ◽  
Vol 41 (3) ◽  
pp. 302-309 ◽  
Author(s):  
M. Meyer ◽  
H. Worth ◽  
P. Scheid
Keyword(s):  
Steady State ◽  
Venous Blood ◽  
Blood Perfusion ◽  
Co2 Exchange ◽  
Mixed Venous Blood ◽  
O2 Uptake ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Mixed Venous ◽  
Haldane Effect

We have conducted two experimental series in the chicken in order to study CO2 exchange in the parabronchial lungs of birds.In the first series, the animals were artifically ventilated and end-expired PCO2, PE'CO2,was measured and compared with mixed venous PCO2, PVCO2. On the average, PECO2 exceeded PVCO2 by 2.8 Torr. In the second series, rebreathing was used to investigate the mechanism of this positive (PE'-PV)CO2 difference.Lung gas PCO2 was found to equilibrate with PVCO2 if both CO2 and O2 exchange in the lung was abolished during rebreathing. Only if O2 uptake continued, we observed a positive gas-to-mixed venous blood PCO2 difference. The results suggest that positive gas-blood PCO2 differences both during rebreathing and steady-state ventilation are brought about by the Haldane effect.Model calculations show that in the homogeneous avian lung, unlike in the alveolar lung, the Haldane effect can produce positive (PE'-PV)CO2 differences during steady-state breathing due to the peculiarities of the crosscurrent arrangement and parabronchial ventilation and blood perfusion.

Dependence of Middle Ear Gas Composition on Pulmonary Ventilation

1997 ◽  
Vol 106 (4) ◽  
pp. 314-319 ◽  
Author(s):  
Haya Mover-Lev ◽  
Moshe Harell ◽  
Dalia Levy ◽  
Amos Ar ◽  
Michal Luntz ◽  
...  
Keyword(s):  
Steady State ◽  
Middle Ear ◽  
Pulmonary Ventilation ◽  
Venous Blood ◽  
Blood Gases ◽  
Mixed Venous Blood ◽  
Gas Composition ◽  
Blood Gas ◽  
Ventilation Perfusion Ratio ◽  
Mixed Venous

The middle ear (ME) steady state gas composition resembles that of mixed venous blood. We changed arterial and venous blood gases by artificially ventilating anesthetized guinea pigs and measured simultaneous ME gas changes during spontaneous breathing, hyperventilation, and hypoventilation. During hyperventilation, PaCO2 and PvCO2 (a = arterial, v = venous) decreased from 46.0 and 53.0 mm Hg to 17.9 and 37.5 mm Hg, respectively, while PaO2 and PvO2 (85.6 and 38.2 mm Hg) did not change. This was accompanied by an ME PCO2 decrease from 70.4 to 58.8 mm Hg and a PO2 decrease from 36.8 to 25.4 mm Hg. During hypoventilation, PaCO2 and PvCO2 increased to 56.8 and 66.4 mm Hg, while PvO2 decreased to 21.8 mm Hg. The ME PCO2 increased simultaneously to 88.8 mm Hg and the ME PO2 decreased to 25.4 mm Hg. The ME PO2 decrease during hyperventilation may be explained by a 33% decrease in ME mucosa perfusion, calculated from the ME ventilation-perfusion ratio. This study shows that ME gas composition follows fluctuations of blood gas levels and thus may affect total ME pressure.

Mechanism of pulmonary gas exchange and CO2 transport during breath holding

1959 ◽  
Vol 14 (5) ◽  
pp. 706-710 ◽  
Author(s):  
John C. Mithoefer
Keyword(s):  
Gas Exchange ◽  
Lung Volume ◽  
Venous Blood ◽  
Volume Shrinkage ◽  
Breath Holding ◽  
Mixed Venous Blood ◽  
Co2 Transport ◽  
Arterial Blood ◽  
Mixed Venous ◽  
Haldane Effect

Experiments describe the changes in PaCOCO2 and lung volume shrinkage during breath holding with O2 in man and the PaCOCO2, pH and CO2 content of arterial and mixed venous blood during breath holding in the dog. An explanation is offered for the aberrations in CO2 transport and exchange which occur during apnea. A self-perpetuating cycle is established during breath holding which is initiated by the arrest of the ventilatory output of Co2. The arterial PaCOCo2 rises rapidly as a result of decreased clearance of Co2 from venous blood, the concentrating effect of lung volume shrinkage and the Haldane effect from oxygenation of hemoglobin. The venous PaCOCO2 rises more slowly because of the uptake of Co2 by the tissues and the Haldane effect from reduction of oxyhemoglobin. By this mechanism the Co2 output into the lungs progressively falls and eventually stops. The cycle then is reversed and Co2 moves from lungs to arterial blood. Submitted on March 2, 1959

A New Open-Circuit Method for Estimating Carbon Dioxide Tension in Mixed Venous Blood

1977 ◽  
Vol 52 (4) ◽  
pp. 377-382 ◽  
Author(s):  
Reiah Al-Dulymi ◽  
R. Hainsworth
Keyword(s):  
Carbon Dioxide ◽  
Venous Blood ◽  
Carbon Dioxide Tension ◽  
Open Circuit ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Venous Pco2 ◽  
Rebreathing Methods ◽  
Mixed Venous ◽  
Good Agreement

1. A new open-circuit respiratory method was developed to estimate mixed venous Pco2 more rapidly and accurately than is possible with rebreathing techniques. 2. The subject breathes a mixture of CO2 in air from an open circuit. Carbon dioxide is added to the air flowing through the circuit at a rate such that the Pco2 in the inspired and expired gases (recorded continuously with a CO2 analyser) are almost identical. 3. Results from respiratory and cardiac patients showed that equilibrium occurred in less than 10 s. There was good agreement between the tensions of CO2 in the respiratory plateaux and in mixed venous and arterial blood withdrawn during equilibrium. 4. During exercise, the tensions of CO2 of the plateaux and arterial blood at equilibrium also showed good agreement. 5. It is suggested that the new method represents an improvement over rebreathing methods as equilibrium is achieved rapidly before the mixed venous tension rises from recirculation.

scholarly journals Arterial and Mixed Venous Blood Gas Status during Apnoea of Intubation — Proof of the Christiansen-Douglas-Haldane Effect in Vivo

1989 ◽  
Vol 17 (3) ◽  
pp. 325-331 ◽  
Author(s):  
F. O. Mertzlufft ◽  
L. Brandt ◽  
M. Stanton-Hicks ◽  
W. Dick
Keyword(s):  
Partial Pressure ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Rapid Adjustment ◽  
Venous Blood Gas ◽  
Clinical Conditions ◽  
Lung Capillaries ◽  
Mixed Venous ◽  
Haldane Effect

The Christiansen-Douglas-Haldane effect, in short the Haldane effect, describes the dependence of the CO2 binding of blood on the degree of oxygenation of haemoglobin. Under the physiological conditions of an ‘open’ system between blood and alveoli the partial pressure of arterial C02 (PaCO2), must be less than that of mixed venous blood (P[Formula: see text]CO2). During the unphysiological conditions of a ‘closed’ system, e.g. hyperoxic apnoea, i.e. continuous oxygen uptake without CO2 delivery by the lungs, the Paco2 will not only approximate the P[Formula: see text]CO2 but will even exceed it. Without the Haldane effect, rapid adjustment of Paco2 to P[Formula: see text]CO2 would be expected during apnoea due to the lack of CO2 excretion. If however, as undertaken in this study, ongoing oxygenation (high alveolar Po2 (PACO2) with concomitant lack of C02 delivery (apnoea, i. e. the C02 concentration remains constant) lead to a continuing sufficient oxygenation of blood during its passage through the lung capillaries, then this leads to a rightwards shift of the CO2 binding curve — the Haldane effect. The resulting increase in Pco2 as shown here actually leads to an arterial-mixed venous CO2 partial pressure difference (a[Formula: see text]DPco2) of 2.8±1.8 mmHg. The results described substantiate for the first time the existence of the Haldane effect under clinical conditions.

Shivering and cardiorespiratory responses during normocapnic hypoxia in the pigeon

1990 ◽  
Vol 68 (1) ◽  
pp. 84-87 ◽  
Author(s):  
G. M. Barnas ◽  
W. Rautenberg
Keyword(s):  
Defense Mechanism ◽  
Minute Ventilation ◽  
Venous Blood ◽  
Inhibitory Effect ◽  
Emg Activity ◽  
Mixed Venous Blood ◽  
Venous Pco2 ◽  
Arterial Po2 ◽  
Shivering Thermogenesis ◽  
Mixed Venous

To study the inhibitory effect of hypoxia on the cold defense mechanism, pigeons were exposed at low ambient temperature (5 degrees C) to various inhaled gas mixtures: normoxia [0.21 fractional concentration of O2 (FIO2)], hypoxia (0.07 FIO2), and normocapnic hypoxia (0.07 FIO2 + 0.045 FICO2). Electromyographic (EMG) activity indicative of shivering thermogenesis was inhibited during hypoxia, and body temperature (Tre) fell by 0.09 degrees C/min. Respiratory frequency (f) and minute ventilation (VE) increased by 143 and 135%, respectively, compared with normoxia, but tidal volume (VT) was not changed. PO2, PCO2, and O2 contents in the arterial and mixed venous blood were decreased and pH was enhanced. During normocapnic hypoxia, shivering EMG was present at approximately 50% of the normoxic intensity; Tre fell by only 0.04 degrees C/min. Arterial and mixed venous PCO2 and pH were the same as during normoxia, but VE increased by 430% because of twofold increases in both f and VT. During normocapnic hypoxia, arterial PO2 and O2 content were higher than during hypoxia alone. We conclude that the persistence of shivering during normocapnic hypoxia is due to maintenance of critical levels of arterial PO2 and O2 content.

Influence of Bohr-Haldane effect on steady-state gas exchange

1982 ◽  
Vol 52 (5) ◽  
pp. 1330-1337 ◽  
Author(s):  
B. J. Grant
Keyword(s):  
Steady State ◽  
Gas Exchange ◽  
Venous Blood ◽  
Gas Composition ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Venous Blood Gas ◽  
Mixed Venous ◽  
Haldane Effect

The influence of the Bohr-Haldane effect (BH) on steady-state gas exchange has previously been described by its effect of gas transfer from the blood when arterial and venous blood gas tensions were held constant. This report quantifies by computer analysis the effects of BH when either or both arterial and venous blood gas tensions are subject to change. When mixed venous blood gas composition is held constant, elimination of BH from a single lung unit typically reduces CO2 output by 6.5% and O2 uptake by 0.5%. Similar effects occur in a two-compartment lung model whether alveolar ventilation-perfusion (VA/Q) mismatch occurs in a parallel or series ventilatory arrangement. When arterial blood gas composition is held constant, elimination of BH increases systemic venous CO2 partial pressure, but O2 partial pressure is hardly affected in the absence of metabolic acidosis. When both mixed venous and arterial blood gas tensions vary and gas exchange is stressed by VA/Q inequality, altitude, anemia, or exercise, elimination of BH predominantly affects mixed venous rather than arterial blood gas tensions. it is concluded that BH may act primarily to reduce tissue acidosis.

Operation Everest II: oxygen transport during exercise at extreme simulated altitude

1988 ◽  
Vol 64 (4) ◽  
pp. 1309-1321 ◽  
Author(s):  
J. R. Sutton ◽  
J. T. Reeves ◽  
P. D. Wagner ◽  
B. M. Groves ◽  
A. Cymerman ◽  
...  
Keyword(s):  
Sea Level ◽  
Blood Lactate ◽  
Venous Blood ◽  
Blood Gases ◽  
Work Load ◽  
Open Circuit ◽  
Mixed Venous Blood ◽  
O2 Uptake ◽  
Fourfold Increase ◽  
Mixed Venous

A decrease in maximal O2 uptake has been demonstrated with increasing altitude. However, direct measurements of individual links in the O2 transport chain at extreme altitude have not been obtained previously. In this study we examined eight healthy males, aged 21-31 yr, at rest and during steady-state exercise at sea level and the following inspired O2 pressures (PIO2): 80, 63, 49, and 43 Torr, during a 40-day simulated ascent of Mt. Everest. The subjects exercised on a cycle ergometer, and heart rate was recorded by an electrocardiograph; ventilation, O2 uptake, and CO2 output were measured by open circuit. Arterial and mixed venous blood samples were collected from indwelling radial or brachial and pulmonary arterial catheters for analysis of blood gases, O2 saturation and content, and lactate. As PIO2 decreased, maximal O2 uptake decreased from 3.98 ±0.20 l/min at sea level to 1.17 ± 0.08 l/min at PIO2 43 Torr. This was associated with profound hypoxemia and hypocapnia; at 60 W of exercise at PIO2 43 Torr, arterial PO2 = 28 ± 1 Torr and PCO2 = 11 ± 1 Torr, with a marked reduction in mixed venous PO2 [14.8 ± 1 (SE) Torr]. Considering the major factors responsible for transfer of O2 from the atmosphere to the tissues, the most important adaptations occurred in ventilation where a fourfold increase in alveolar ventilation was observed. Diffusion from alveolus to end-capillary blood was unchanged with altitude. The mass circulatory transport of O2 to the tissue capillaries was also unaffected by altitude except at PIO2 43 Torr where cardiac output was increased for a given O2 uptake. Diffusion from the capillary to the tissue mitochondria, reflected by mixed venous PO2, was also increased with altitude. With increasing altitude, blood lactate was progressively reduced at maximal exercise, whereas at any absolute and relative submaximal work load, blood lactate was higher. These findings suggest that although glycogenolysis may be accentuated at low work loads, it may not be maximally activated at exhaustion.

Carbon Dioxide Equilibration in Canine Lungs during Rebreathing and Acute Alkalosis

1979 ◽  
Vol 57 (5) ◽  
pp. 385-388 ◽  
Author(s):  
R. D. Latimer ◽  
G. Laszlo
Keyword(s):  
Whole Blood ◽  
Base Excess ◽  
Venous Blood ◽  
Main Pulmonary Artery ◽  
Mixed Venous Blood ◽  
Arterial Blood ◽  
Significant Difference ◽  
Venous Pco2 ◽  
Pulmonary Arterial ◽  
Gas Pressures

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.

Effects of cocaine on incremental treadmill exercise in horses

1993 ◽  
Vol 75 (6) ◽  
pp. 2727-2733 ◽  
Author(s):  
K. H. McKeever ◽  
K. W. Hinchcliff ◽  
D. F. Gerken ◽  
R. A. Sams
Keyword(s):  
Right Ventricular ◽  
Blood Lactate ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Ventricular Pressure ◽  
Mixed Venous Blood ◽  
Work Intensity ◽  
Venous Blood Lactate ◽  
Mixed Venous

Four mature horses were used to test the effects of two doses (50 and 200 mg) of intravenously administered cocaine on hemodynamics and selected indexes of performance [maximal heart rate (HRmax), treadmill velocity at HRmax, treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l, maximal mixed venous blood lactate concentration, maximal treadmill work intensity, and test duration] measured during an incremental treadmill test. Both doses of cocaine increased HRmax approximately 7% (P < 0.05). Mean arterial pressure was 30 mmHg greater (P < 0.05) during the 4- to 7-m/s steps of the exercise test in the 200-mg trial. Neither dose of cocaine had an effect on the responses to exertion of right atrial pressure, right ventricular pressure, or maximal change in right ventricular pressure over time. Maximal mixed venous blood lactate concentration increased 41% (P < 0.05) with the 50-mg dose and 75% (P < 0.05) with the 200-mg dose during exercise. Administration of cocaine resulted in decreases (P < 0.05) in the treadmill velocity needed to produce a blood lactate concentration of 4 mmol/l from 6.9 +/- 0.5 and 6.8 +/- 0.9 m/s during the control trials to 4.4 +/- 0.1 m/s during the 200-mg cocaine trial. Cocaine did not alter maximal treadmill work intensity (P > 0.05); however, time to exhaustion increased by approximately 92 s (15%; P < 0.05) during the 200-mg trial.(ABSTRACT TRUNCATED AT 250 WORDS)

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