Effects of oscillating and intermittent ventilatory flow on efficacy of pulmonary O2 transfer in the duck.
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Biomedical subjects
Publications and source records attributed to P Scheid.
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Single unit vagal recordings from intrapulmonary receptors were obtained in decerebrate, paralyzed lizards both during pump ventilation and during unidirectional ventilation on the cannulated, sack-shaped lung. Two types of receptors were identified: (1) CO2-receptors, which increased their discharge frequency as intrapulmonary CO2 concentration decreased but were not sensitive to stretch of the lung. (2) Mechanoreceptors, which rapidly increased discharge frequency when the lung was stretched. These receptors' CO2 sensitivity varied. Lungs of lizards thus appeared to possess both CO2 receptors, which have functional characteristics similar to those in birds, and mechanoreceptors with properties similar to stretch receptors in mammals.
Intrapulmonary receptors identified in the Tegu lizard by single-unit vagal recording (Fedde et al., 1977) were subjected to a number of stimuli and localized within the lung. Some carbon dioxide receptors could follow periodic changes in intrapulmonary CO2 concentrations as rapidly as 1.3 Hz; No oxygen sensitivity was observed with this receptor type, and halothane markedly depressed the discharge frequency. In response to intravenously injected acetazolamide they increased their discharge frequency and became almost totally insensitive to CO2, suggesting molecular per se is not the direct controller of receptor discharge; These receptors show many of the functional characteristics described for those in the avian lung. Afferent activity from both CO2 and mechanoreceptors could be elicited by electrically stimulating the lung surface. The CO2 receptors appeared to be organized in a receptive field covering more than 1 cm2 of lung surface, multiple receptors being innervated by a single afferent fiber. Activity in afferent fibers from mechanoreceptors could be evoked from only one distinct spot on the lung surface. Conduction velocities of afferent fibers from CO2 receptors ranged from 1 to 3 m-sec-1; from mechanoreceptors, from 1.9 to 5.2 m-sec-1.
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Krogh's diffusion constant for CO2, KCO2, was determined in respiring muscle tissue at various levels of tissue PCO2, between 10 and 160 torr, using a technique described previously (Kawashiro et atl, 1975). With increasing mean tissue PCO2, KCO2 declined towards an apparently asymptotic value. The relationship between KCO2 (10(-9) mmol-cm(-1)-min(-1)-tor(-1)) and PCO2 (torr) at 37 degrees C could be approximated by the equation KCO2 = 17.3 [1 + 1.72 - exp(--0.027 - PCO2)]-At PCO2 = 0 torr KCO2 exceeded the asymptotic value, which was virtually attained at PCO2 = 100 torr, by more than a factor of two. Thus CO2 diffusion in muscle appears to be facilitated in the low PCO2 range. Specific CO2 production rate of tissue, which was determined simultaneously, did not vary with CO2 in the PCO2 range studied. Effects of facilitated CO2 transport on CO2 exchange in muscle are assessd using simple models. In the presence of CO2 facilitation muscle PCO2 is reduced, particularly during exercise.
No appreciable errors are expected in determination of blood gas values and pH using classical techniques provided time of anaerobic storage is kept small and is, if unavoidable performed on ice. In particular, dissociation curves may safely be analyzed with the Van Slyke technique which is in disagreement with the conclusions of Lutz et al. (1973). For measurement of PO2 and PCO2, delay time is mainly dictated by response time of the electrodes; measurements may have to be corrected for metabolism, particularly in high PO2 range.
The method described is apt to measure, at the same time, Krogh's diffusion constant and specific metabolic rates for O2 and CO2 in intact, respiring tissues. Due to metabolism tissue thickness for this method is limited to about 500 mum unless hyperbaric conditions are used. The results suggest that both KO2 and KCO2 are similar in alive and in dead tissue. Due to tissue inhomogeneity and to possible facilitation of O2 or CO2 transport our values of K have to be considered as effective mean values for the physiological range of PO2 and PCO2 in muscle at rest and at exercise.
The technique described allows in vivo placement of a blocking balloon in the avian primary bronchus between the origins of the two sets of secondary bronchi, the medioventrals and mediodorsals. With caudal air sacs cannulated the animal may then be ventilated with a constant flow of gas passing entirely through the gas-exchanging parabronchi. This technique has been found useful particularly in studies of pulmonary gas exchange in birds.
Effects of CO2 on pulmonary smooth muscle were assessed by measuring the air flow resistance of secondary bronchi and parabronchi in ducks unidirectionally ventilated with a constant gas flow through the parabronchial lung, the bypass of the primary bronchus being occluded by a blocking catheter. Pressure differences across the blocking balloon (deltaP), corresponding to the pressure drop in the gas flowing through the mediodorsal and medioventral secondary bronchi (MD and MV) and parabronchi, were measured at flow rates (V) varied from 0.5 to 3 L-min-1 and at CO2 concentrations of ventilating gas (FICO2) varied from 0 to 10%. 1) deltaP increased more than linearly with V. The resulting flow resistance R(= deltaP/V) averaged 43 and 95 cm H2O-L-1-sec at V = 0.5 and 3 L-min-1, respectively. 2) Step changes in FICO2 at constant V were followed within 0.5 to 5 sec by changes in R. 3) Lowering FICO2 from 5% resulted in marked increases in R, the value at FICO2 = 0% being more than twice the average value at 5%. Raising FICO2 from 5% up to 10% was followed by only slight changes in R. 4) Vagotomy did not consistently change R at any level of CO2; it did, however, slightly increase the delay time for changes in R on step changes of FICO2. 5)The medioventral secondary bronchi and their orifices into the primary bronchus appeared to be mainly responsible for the resistance measured and its changes with CO2. The resistance offered by the parabronchi appeared to be much smaller and much less dependent on CO2. The results suggest importance of lung gas CO2 in aerodynamic valving of respiratory flow in avian lungs during normal breathing and particularly during thermal panting to prevent alkalosis.
Air sac gas exchange was studied in ducks by measuring the rates of inert gas uptake and of O2 and CO2 equilibration in caudal thoracic air sac whose ventilation was prevented by surgival sealing of the ostia. The data were analyzed on a model incorporating three possible routes by which air sac gas could be exchanged with the surrounding tissue: (1) into the blood perfusing the air sac walls; (2) into the adjoining air sac via tissue membranes; (3) into the bronchial system of the lung via diffusion through lung tissue bordering upon the caudal thoracic air sac. Exchange rates of gases via the two latter paths were found to be small as compared with the first route. From application of model parameters to O2 and CO2 exchange in air sacs under physiological conditions the following conclusions were drawn: (1) the caudal thoracic air sac makes the major contribution to total gas exchange between air sacs and blood; (2) this exchange can account for less than 5% of total respiratory gas exchange; (3) the exchange is too small to account for the O2 and CO2 partial pressures in caudal thoracic air sacs of ducks. Other mechanisms like gas exchange in neopulmonic parabronchi, which conduct air to the caudal air sacs during inspiration or re-inspiration of dead space appear to play a more significant role in the deviation of O2 and CO2 partial pressures in the caudal air sacs from those in inspired air.
Single unit activity was recorded in the cat vagus in order to detect possible receptors firing in response to changing lung CO2 concentration. The cats were ventilated at a high rate (60-120 breaths per min) and inspired CO2 concentration was altered between 0 and 8% in a step-like fashion, each phase consisting of about 10 breaths. Thus the effects of changing intrapulmonary CO2 concentration could be differentiated from the effects of stretch of lung tissue. Activity was recorded in 7 cats from 120 units firing in phase with ventilation. Many receptors showed some CO2 sensitivity, but no fiber was found discharging in response to CO2 exclusively. The results provide no evidence for the occurence of specific CO2 receptors in the feline lung with vagal afferents functionally similar to those reported for the avian lung.
Equilibration of inspired with lung residual gas was studied by a single-breath technique for varying breath-holding time with He, Ar, and SF6 as test gases. The ratio of end-expired (FE') to mean lung concentration after expiration (FL) was always below unity, indicating imperfect mixing of gas in the lung. The ratio of FL/FE' for all gases increased with tB, for any tB the ratio was smallest for SF6 and greatest for He. Similarly, Bohr dead space (VD) at any given tB was greatest for SF6 and smallest for He, with VD decreasing toward an asymptotic value common for all gases as tB increased. The results were analyzed quantitatively on a serial three-compartment model of the lung. Model analysis suggests that both diffusion and convection are effective in equilibrating test gases in the lung during breath holding. Further, stratified inhomogeneities in the absence of convective gas mixing in the alveolar space would seriously limit alveolar respiratory gas exchange; with convection, however, stratification is likely to impose only moderate constraints on resting gas exchange.
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.
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Gas transfer rates for O2 and CO2 through freshly excised respiring rat abdominal muscle were measured. The tissue separated as a thin membrane two chambers, one of which was ventilated with a constant gas mixture. The other chamber was closed and the time course of changes of PO2 and PCO2, initially set at varied levels, was followed by electrodes. A plot of rate of change of PO2 and PCO2 in the closed chamber against the partial pressure difference across the tissue yielded both Krogh's diffusion constant, KO2 and KCO2, and metabolic rate of tissue, i.e. specific O2 consumption and CO2 production, mo2 and mco2. The mean values at 37 degrees C, KO2 = 1.31 x 10(-9) mMol-cm-1-min-1-torr-1 and KCO2 = 28.0 x 10(-9) mMol-cm-1-min-1-torr-1, did not differ significantly from values determined by other authors in various tissue preparations in which metabolism had been suppressed. Average O2 consumption, mo2 = 0.87 mMol-min-1-L-1, was not different from the values obtained in the same tissue by the Warbung manometric method, 0.74 mMol-min-1-L-1. The mean respiratory quotient, calculated as the ratio of mean CO2 production and mean O2 consumption, was 0.85.
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