Journal of applied physiology
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The amount of urea produced in 60 min, [urea]t = 60, from intact guinea pig hepatocytes incubated in NH4Cl, oleate, lactate, NaHCO3, and ornithine at 37 degrees C at pH 7.1 is decreased by ethoxzolamide (EZ): Ki,EZ [urea]t = 60 +/- SD at 37 degrees C, pH 7.1 is 0.14 +/- 0.11 mM (10 Dixon plots). This value is in the same range as Ki,EZ for carbonic anhydrase (CA) activity of disrupted hepatocytes at 37 degrees C: 0.08 +/- 0.06 mM (2). [Urea]t = 60 is pH dependent whether external CO2 is supplied (25 mM HCO-3, 95% O2-5% CO2 and 5 mM HCO-3, 99% O2-1% CO2) or not [20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES), 100% O2]. Ki,EZ [urea]t = 60 is independent of both external pH and external total CO2. ⋯ This value was approximately 3,000-fold lower than the Ki,EZ [urea]t = 60 for intact hepatocytes or Ki,EZ (CA) for disrupted hepatocytes. These results support the general hypothesis that mitochondrial CA is involved in urea synthesis by intact hepatocytes and that cytosolic components raise the experimentally determined Ki,EZ [urea]t = 60. We also conclude that the value of Ki,EZ [urea]t = 60 is independent of the availability of the substrate HCO-3 from external sources.
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Gas exchange in avian lungs is described by a cross-current model that has several differences from the alevolar model of mammalian gas exchange [e.g., end-expired PCO2 greater than arterial PCO2 (PaCO2)]. Consequently the methods available for estimating effective ventilation and physiological dead space (VDphys) in alveolar lungs are not suitable for an analysis of gas exchange in birds. We tested a method for measuring VDphys in birds that is functionally equivalent to the conventional alveolar VDphys. ⋯ Bohr dead space, calculated by substituting end-expired PCO2 for PEiCO2, was insensitive to such inhomogeneity. Enghoff dead space, calculated by substituting PaCO2 for PEiCO2, is theoretically incorrect for cross-current gas exchange and was often less than anatomic dead space. We conclude that VDphys is a useful index of avian gas exchange and propose a standard definition for effective parabronchial ventilation (VP) analogous to alveolar ventilation (i.e., VP = VE--VDphys, where VE is total ventilation).
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Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). ⋯ Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.
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We examined the relationship between mucus rheology, depth of mucus layer, and clearance by simulated cough. A model trachea was constructed of rigid Plexiglas of rectangular cross section (1 X 2 X 35 cm). The bottom of the trachea was lined with mucus simulants, gels prepared from locust bean gum cross-linked with sodium borate. ⋯ For a given driving pressure and depth, CI decreased with increasing mucus cross-link density. For mucus samples with comparable levels of dynamic viscosity, samples with higher elasticity cleared less well. Mucus clearance was associated with transient wave formation in the lining layer.
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In 11 mechanically ventilated patients, respiratory mechanics were measured 1) during constant flow inflation and 2) following end-inflation airway occlusion, as proposed in model analysis (J. Appl. Physiol. 58: 1840-1848, 1985. ⋯ In all instances Ers and RT were higher than normal. RT(min) was lower in all patients than the corresponding values of RT, indicating that resistance was frequency dependent due to time constant inequalities. Changes in inflation rate did not affect Ers, while RT increased with increasing flow.