Mechanisms of gas exchange in bird lungs.
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Biomedical subjects
Publications and source records attributed to P Scheid.
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Air flow resistance in the parabronchial lung of the duck was measured at various pressure differences between the lung and the body surface (Prs) using a body plethysmograph. One lung of the anesthetized animal was ventilated at a steady flow rate, from trachea, through the parabronchial lung, and out via a cannula in the caudal thoracic air sac (Tr leads to CS flow), or vice versa (CS leads to Tr flow), all flow being directed over the parabronchi (Pb) by blocking the main bronchus between the medioventral (MV) and mediodorsal secondary bronchi (MD). Pressure differences were measured between MV and MD (Ptot), and between the clavicular air sac and MD giving the pressure drop along the parabronchial tubes (PPb). The pressure drop along MV, PVb, was derived as Ptot-PPb. Air flow resistances, Rtot, RPb, RVb, were calculated from the ratio of the corresponding pressure difference to the flow rate. Results show: (1) All resistances decreased with increasing distending pressure (Prs) from -20 to +20 cm H2O this change being most pronounced around Prs = 0; (2) The flow resistance of these structures depended on the flow direction, being smaller with Tr leads to CS flow during distension than in the opposite direction; (3) Arterial blood gases did not significantly change with varying distending pressure, suggesting unimpaired gas exchange even when the lung is significantly compressed. The results indicate that the parabronchi and the secondary bronchi of the duck lung have a finite compliance but that changes in intrapulmonary pressure, compression of the lung, do not result in significant collapse of the air capillaries with ensuing impairment of gas exchange.
Pulmonary exchange of O2 and CO2 was measured in unidirectionally ventilated ducks in an attempt to determine lung O2 diffusing capacity, DO2. Perfusion shunt (= venous admixture) was estimated from O2 exchange in hyperoxia, and the ventilation shunt (ventilation of non-perfused parallel lung units) was estimated from exchange of the highly soluble inert gas, chloroform. Differences in the ventilation/perfusion ratio of parallel lung units were assessed from measurement of CO2 exchange using a parallel two-compartment model. DO2 values were calculated accounting for ventilation shunt, perfusion shunt, and inhomogeneity. Perfusion shunt averaged 2.7% and ventilation shunt, 9.4%. The ventilation/perfusion ratio in the two compartments differed on the average by a factor of 2.6. The uncorrected values of DO2, not accounting for lung inhomogeneities, progressively declined with increasing inspired PO2, but this dependence was less pronounced after correcting for lung inhomogeneities. The corrected value of DO2 averaged 100 mumol . min-1 . torr-1 for ducks of 1.8 kg mean body weight. DO2 did not differ when nitrogen was replaced by helium in the ventilatory gas indicating that diffusion within the air capillaries did not contribute a significant resistance to O2 uptake. The results suggest that neither functional inhomogeneities nor diffusion between lung gas and blood limit O2 uptake of the resting duck. Under conditions of elevated metabolism, however, these parameters may become rate-limiting for O2 supply.
The lung boundaries exhibit a tight barrier for any insoluble gas; hence boundary conditions for lung gas mixing have to account for the absence of both diffusive and convective fluxes across the lung walls. Scrimshire et al. (1978) have, in contrast, used the less rigid boundary condition that only the net flux be zero. As we believe this boundary condition to be inappropriate for the study of insoluble gases, the results derived appear to have no physiological significance.
A recent report (J. Appl. Physiol. 38: 382-388, 1975) suggests that negative blood-gas CO2 partial pressure (PCO2) differences exist in the dog during hypercapnia, as mean expired PCO2 exceeded arterial PCO2 by more than 10 Torr when the CO2 fraction in inspired gas (FICO2) was 0.1. We have reinvestigated this problem in anesthetized dogs breathing spontaneously room air or hypercapnic mixtures (FICO2 = 0.05 or 0.10). During steady state, arterial blood samples were analyzed with electrodes, care being taken to keep the electrode temperature within +/- 0.2 degrees C at the actual aortic temperature of the animal. Respired gas was measured at the tracheostomy by a sensitive low-noise respiratory mass spectrometer. During room air breathing, the arterial-end-expired PCO2 difference, P(a-E')CO2, averaged +5 Torr and decreased to +0.9 Torr and to +0.1 Torr with FICO2 = 0.05 and 0.1, respectively. Hypoxia (FIO2 = 0.10) had no apparent effect on the P(a-E')CO2 difference. We ascribe the decrease in P(a-E')CO2 with hypercapnia to the diminishing effects of alveolar dead space, whereby end expired PCO2 approached arterial PCO2. We then conclude that in blood-gas equilibration lungs, PCO2 in end-capillary blood comes close to alveolar PCO2, and that the negative blood-gas PCO2 differences reported earlier are probably caused by deficiencies in the techniques used.
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The Bohr factor, phi = delta log Po2/deltapH, was determined at various levels of hemoglobin O2 saturation (SO2) in fresh whole blood of the duck. Plasma pH was varied by either changing PCO2 of the blood at constant base excess (CO2 Bohr factor, phiCO2) or by addition of NaHCO3 and HCl at constant PCO2 (fixed acid BOHR factor, phiAH). No differences were found between phiCO2 and phiAH at SO2 levels between 20 and 85%, and there was no saturation dependence of the Bohr factor, its average value being -0.44. It is concluded that in whole blood of this bird species CO2 exerts no direct effect on the O2 affinity of hemoglobin.
Ventilation and blood gases were measured in unanesthetized ducks at various levels of inspired CO2 partial pressure (PICO2). Ventilation was markedly augmented with increasing PICO2, whereas arterial and mixed venous PCO2 stayed essentially constant up to a PICO2 of about 20 torr and changed only slightly between that and the highest level tested (34 torr). After carbonic anhydrase had been blocked, blood PCO2 was elevated at all levels of PICO2 but the ventilatory response to increases in PICO2 were attenuated. The response to CO2 in the normal bird (before administration of acetazolamide) shows similarities to that in mammals. Qualitative differences between both classes of vertebrates after blockade of carbonic anhydrase may, however, suggest differences in their systems that control ventilation.
The CO2 sensitivity of intrapulmonary CO2 receptors (IPC) in the duck was studied, before (Control) and after blockade of carbonic anhydrase by Diamox, by recording single unit afferent activity in the vagus nerve. During Control, IPC activity decreased with increasing airway CO2 concentration. After Diamox administration, the discharge from IPC was higher at all levels of airway PCO2, and the receptors' CO2 sensitivity was markedly attenuated. Comparing these results with measurements on ventilation and blood gases of the duck under similar experimental conditions (Powell et al., 1978b) suggests that IPC play a role in the adjustment of ventilation to altered concentrations of inspired CO2; IPC may thus be a significant component in the control of breathing under physiological conditions.
We have estimated the relative importance of changes in blood PCO2 and pH in determining activity of intrapulmonary chemoreceptors (IPC) in the unidirectionally ventilated duck. The response of single unit vagal afferents from IPC to changing lung gas PCO2 was tested before and after changing blood pH by intravenous infusion of NaHCO3. Using multiple linear regression analysis, we calculated how much of the change in IPC activity for a given change in PCO2 was due to the changing PCO2 at constant pH (CO2 sensitivity) or to the change in pH concomitant with the change in PCO2 (H+ sensitivity). For 10 IPC, the CO2 sensitivity was on the average 2.3 times larger than the H+ sensitivity. Changes in pH as well as PCO2 of lung blood should be considered in assessing the role of IPC in control of breathing.
The difference in gas exchange performance between continuous and intermittent ventilatory flow is theoretically studied in the alveolar lung model. When measurements obtained with intermittent flow are analyzed assuming continuous flow, an apparent diffusing capacity. Dapp, results which is an underestimate of the true value, D. This true value, D, may be assessed from measurements at continuous flow. With decreasing effective lung gas volume, Veff, Dapp increasingly deviates D. The dependence of Dapp/D on Veff in the parabronchial lung seems to be similar to that in the alveolar lung. Experimental data of Dapp/D (Scheid et al., 1977) are used to assess Veff for the duck lung. The average value of Veff thus obtained, 93 ml, exceeds the anatomical estimate of parabronchial gas volume. Gas transfer across the open parabronchial ends may contribute in enlarging the parabronchial gas volume to the volume, Veff, that is effective as gas capacity in conditions of non-steady ventilatory flow.
A number of models is analyzed to study gas exchange between blood capillaries and air capillaries in the avian parabronchial wall when diffusion is the only transport mechanism in the air capillaries. The existing anatomical arrangement of blood capillaries that traverse the periparabronchial tissue from peripherally located arterioles to draining venules at the luminal surface appears to provide a particularly high gas exchange efficiency. Application of the theory to measurements in the hen using histological estimates suggests that substantial concentration gradients exist inside the air capillary gas whose magnitude vary along the parabronchus. Thus at the gas inflow end of the parabronchus the partial pressure drop within the air capillaries could amount, for both O2 and CO2, to about 10--15 torr at rest and to 30--40 torr during exercise. Due to the peculiar arrangement of capillary blood flow to the air capillaries the effects of these gradients on gas exchange are very slight during rest. During exercise, however, the diffusional resistance inside the air capillaries may become limiting for the over-all gas exchange, and other mechanisms may be needed to secure respiratory gas transfer.
Blood flow to subunits of the lung was studied in the duck by use of radioactive microspheres. In spontaneously breathing, unanesthetized animals (series I) neopulmo was slightly better perfused than the average lung and along the paleopulmonic parabronchi, blood flow was found to decrease in the direction of ventilatory gas flow and thus of decreasing PO2 and increasing PCO2 in lung gas. The effects of respiratory gases on regional lung perfusion were investigated in unidirectionally ventilated animals (series II) in which gas mixtures offered to both lungs could be controlled independently. Local hypoxia resulted in reduction of local blood flow, whereas effects from hyperoxia or CO2 could not be substantiated. Reversal of the direction of unidirectional ventilatory flow (series III), and thus reversal of the profiles of respired gas concentrations along the parabronchi, suggest that the inhomogeneity in blood flow observed in spontaneously breathing animals of series I can only in part be explained as an acute adjustment to the local hypoxia. Calculations show that this inhomogeneity of blood flow constitutes an only minor impairment of the overall gas exchange efficacy of the parabronchial lung.
In the mixing technique for study of oxygen-hemoglobin equilibrium, the O2 saturation (SO2) of a blood mixture is calculated from the volume ratio at which an oxygenated sample is mixed with a deoxygenated sample, and the PO2 in the mixture is measured polarographically. Any predetermined level of SO2 may be obtained by proper choice of the volume ratio. It is shown that the volume and oxygen saturation of the mixed samples are by far the most critical parameters in calculating SO2, and a method is suggested by which the volume ratio is accurately measured by weighing the blood samples before mixing. Other parameters that influence determination of SO2, e.g., the O2 capacity of the blood, are much less important. The method has been applied to establish the O2 dissociation curve in human blood, and good reproducibility and agreement with standard curves were obtained. Measurements in rabbit blood yielded similarly satisfactory results. The technique is particularly applicable to problems that require exact adjustment of SO2 to a predetermined value, such as determination of the half-saturation pressure or of the Bohr effect at various levels of O2 saturation.
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Half saturation partial pressure of O2,P50, was determined in domestic Muscovy ducks (Cairina moschata) both by in vivo and in vitro techniques. For in vivo determination, blood samples were drawn from the anesthetized, artificially ventilated animals and analyzed both for O2 content, Co2, and O2 partial pressure, Po2. O2 capacity was detemined in arterial samples during hyperoxic ventilation (arterial Po2 about 180 torr). P50 was calculated from measurements in venous blood samples (O2 saturation near 50%). For in vitro determinations, Co2 was measured in blood samples equilibrated with Po2 close to P50. No significant difference was found between P50 values determined by both techniques. At 41 C and pH 7.50, P50 averaged 41.7 torr when analyzed by in vivo technique and 41.4 torr when determined in vitro. The variability between animals was less than 1 torr (SD) and could be explained by the experimental error. The partially discordant literature data on P50 of duck blood are reviewed and critically discussed.