Respiration physiology
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Respiration physiology · May 1980
A comparison between carbon dioxide inhalation and increased dead space ventilation in chickens.
We compared the ventilatory response to elevated PICO2 with the response to elevation of dead space volume (delta VD) in anesthetized, hyperoxic chickens. In the first experimental series (I), PICO2 was varied between 0 and 26 Torr. In a second series (II), delta VD was raised between 0 and 17 ml by placing lengths of tubing between the bird and the source of inspired gas. ⋯ When changes in PaCO2 and ventilation were expressed as a function of the change in CO2 load reaching the lungs (delta L), the change in ventilation was greater, and that in PaCO2 less in Series I than in Series II at all levels of delta L below 25 ml (STPD) . min-1. The differences in ventilatory response to PICO2 and delta VD may qualitatively be explained by the distinct time patterns of CO2 concentration in the lungs which result in different discharge frequencies of CO2-sensitive intrapulmonary chemoreceptors and, possibly, by effects on ventilation resulting from differences in the timing of receptor discharge. Thus, these data provide additional evidence that avian intrapulmonary chemoreceptors may play a significant role in the chemical control of ventilation and regulation of PaCO2.
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Respiration physiology · Jan 1980
ReviewBlood/gas equilibrium of carbon dioxide in lungs. A critical review.
(1) The scope of this review is to examine the experimental evidence for the existence of negative PCO2 differences between pulmonary capillary blood and lung gas, [delta PCO2(b-G)], which have been observed both during rebreathing, when CO2 was at equilibrium, and during steady state gas exchange, particularly in hypercapnia. (2) The mechanism that have been invoked to explain negative delta PCO2(b-G) include (i) slow equilibration of the system CO2/HCO3-/H+ in blood, and (ii) effects of a negatvely charged surface of the pulmonary capillary endothelium. While the first postulated mechanism appears to be quantitatively insufficient to explain the results, the second seems to lead to serious qualitative difficulties. (3) Existence of negative delta PCO2(b-G) in CO2 equilibrium would invalidate the basis of the conventional analysis of alveolar gas exchange. (4) A critical analysis of the experimental evidence for the existence of negative delta PCO2(b-G) is presented. It includes the identification of directional experimental errors leading to spurious negative delta PCO2(b-G), and a critical review of the literature data in this regard. (5) Results of own experiments, conducted in an attempt to consider all possible sources of error, are reported, revealing (i) perfect PCO2 equality between alveolar gas and blood in rebreathing equilibrium of CO2; (ii) absence of negative delta PCO2 (b-G) during steady state gas exchange in hypercapnia. (6)Both experiments and model calculations show that negative delta PCO2 between mixed venous blood and end-expired gas observed in birds at steady state of gas exchange are explained by a particular action of the Haldane effect in avian parabronchial lungs with cross-current arrangement of gas and blood flow. (7) It is concluded that the negative delta PCO2(b-G) reported in the literature are probably artifactual and that there is no adequate evidence to invalidate the traditional view according to which blood/gas CO2 equilibration in lungs leads to equal PCO2 in both media.
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The influence of regional alveolar oxygen and carbon dioxide tensions on the distribution of lung blood flow and gas exchange was studied in unanaesthetised sheep. Right apical lobe (RAL) hypoxia, induced by administering nitrogen or nitrogen/oxygen mixtures to the lobe, stimulated a prompt, graded and well sustained reduction in lobar blood flow. Maximum hypoxia was accompanied by an approximate 65% reduction in perfusion, a significant fall in RAL carbon dioxide tension and output, a reversal of lobar oxygen flux and an average 13 Torr fall in arterial oxygen tension. ⋯ Mild RAL hypercapnia potentiated the hypoxia-induced change in perfusion and gas exchange. During lobar hypoxia RL blood flow and gas exchange increased to maintain total pulmonary gas exchange at an essentially constant level. RAL hyperoxia did not significantly alter the distribution of perfusion or gas exchange.
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Respiration physiology · Aug 1976
O2 transport in the alpaca (Lama pacos) at sea level and at 3,300 m.
Five male alpacas native to high altitude, of approximately 40 kg, were studied first at 3,300 m and again after a 3-month sojourn at sea level. Measurements were made with the animals standing, unsedated and breathing air. Cardiac output was measured by the dye dilution technique. ⋯ The values of PvO2 were lower than those reported for other mammals but similar to those of the llama. A higher PvO2 was measured in the alpacas at sea level. The alpaca under conditions of chronic hypoxia presents only minor cardiorespiratory adjustments suggesting the possibility of tissue characteristics well suited for life at high altitude.
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The effects of acute lobar obstruction on pleural surface pressure in supine dogs were examined. The right lower lobes (RLL) were obstructed at FRC in some dogs while in others the left lung and RLL were both obstructed at FRC. ⋯ In most dogs elastic recoil increased at the lateral costal margin of the obstructed RLL implying the application of a deforming pressure to the obstructed lobes. The tendency to inflate and deform the obstructed RLL was greater during spontaneous breathing than during artificial ventilation.