Journal of applied physiology
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The occurrence of upper airway obstruction during sleep and with anesthesia suggests the possibility that upper airway size might be compromised by the gravitational effects of the supine position. We used an acoustic reflection technique to image airway geometry and made 180 estimates of effective cross-sectional area as a function of distance along the airway in 10 healthy volunteers while they were supine and also while they were seated upright. We calculated z-scores along the airway and found that pharyngeal cross-sectional area was smaller in the supine than in the upright position in 9 of the 10 subjects. ⋯ Because changing from the upright to the supine position causes a decrease in functional residual capacity (FRC), six of these subjects were placed in an Emerson cuirass, which was evacuated producing a positive transrespiratory pressure so as to restore end-expiratory lung volume to that seen before the position change. In the supine posture an increase in end-expiratory lung volume did not change the cross-sectional area at any point along the airway. We conclude that pharyngeal cross-sectional area decreases as a result of a change from the upright to the supine position and that the mechanism of this change is independent of the change in FRC.
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Previous work by Lehnert et al. (J. Appl. Physiol. 53:483-489, 1982) has demonstrated that adequate alveolar ventilation can be maintained during apnea in anesthetized dogs by delivering a continuous stream of inspired ventilation through cannulas aimed down the main-stem bronchi. ⋯ Reducing CFV flow rate to 1 l X kg-1 X min-1 at constant lung volume improved R-E* and log SD Q, but significant VA/Q inequality compared with that at IPPV remained and arterial PCO2 rose. Comparison of IPPV and CFV at the same mean lung volume showed a similar reversible deterioration in gas exchange efficiency during CFV. We conclude that CFV causes significant VA/Q inequality which may be due to nonuniform ventilation distribution and a redistribution of pulmonary blood flow.
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Tracheobronchial blood flow increases two to five times in response to cold and warm dry air hyperventilation in anesthetized tracheostomized dogs. In this series of experiments we have attempted to attenuate this increase by blockade of the autonomic nervous system. Four groups of anesthetized, tracheostomized, open-chest dogs were studied. ⋯ Five minutes before the end of each 30-min period of hyperventilation, measurements of vascular pressures, cardiac output, arterial blood gases, and inspired, body, and tracheal temperatures were measured, and differently labeled radioactive microspheres were injected into the left atrium to make separate measurements of airway blood flow. After the last measurements had been made animals were killed and their lungs were excised. Blood flow to the airways and lung parenchyma was calculated.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tracheobronchial blood flow increases with cold air hyperventilation in the dog. The present study was designed to determine whether the cooling or the drying of the airway mucosa was the principal stimulus for this response. Six anesthetized dogs (group 1) were subjected to four periods of eucapnic hyperventilation for 30 min with warm humid air [100% relative humidity (rh)], cold dry air (-12 degrees C, 0% rh), warm humid air, and warm dry air (43 degrees C, 0% rh). ⋯ After the last measurements had been made, all dogs were killed, and the lungs, including the trachea, were excised and blood flow to the trachea, left lung bronchi, and parenchyma was calculated. Warm dry air hyperventilation produced a consistently greater increase in tracheobronchial blood flow (P less than 0.01) than cold dry air hyperventilation, despite the fact that there was a smaller fall (6 degrees C) in tracheal tissue temperature during warm dry air hyperventilation than during cold dry air hyperventilation (11 degrees C), suggesting that drying may be a more important stimulus than cold for increasing airway blood flow. In group 2, the 15-micron microspheres accurately reflected the distribution of airway blood flow but did not always give reliable measurements of parenchymal blood flow.
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We have investigated the mechanism of alveolar liquid filling in pulmonary edema. We excised, degassed, and intrabronchially filled 14 dog lung lobes from nine dogs with 75, 150, 225, or 350 ml of 5% albumin solution, and then air inflated the lobes to a constant airway pressure of 25 cmH2O. By use of micropipettes, we punctured subpleural alveoli to measure alveolar liquid pressure by the servo-null technique. ⋯ We attribute this finding, on the basis of the Laplace equation, to an air-liquid interface of constant radius in all the lobes. In fact, we calculated from the Laplace equation an air-liquid interface radius which equalled morphological estimates of alveolar radius. We conclude that in the steady state, alveoli that contained liquid have a constant radius of curvature of the air-liquid interface possibly because they are always completely liquid filled.