Airspace Diameter Research Articles

Aerosol-derived lung morphometry: comparisons with a lung model and lung function indexes

This study evaluated the ability of aerosol-derived lung morphometry to noninvasively probe airway and acinar dimensions. Effective air-space diameters (EAD) were calculated from the time-dependent gravitational losses of 1-microns particles from inhaled aerosol boluses during breath holding. In 17 males [33 +/- 7 (SD) yr] the relationship between EAD and volumetric penetration of the bolus into the lungs (Vp) could be expressed by the linear power-law function, log (EAD) alpha beta log (Vp). Our EAD values were consistent with Weibel's symmetric lung model A for small airways and more distal air spaces. As lung volume increased from 57 to 87% of total lung capacity (TLC), EAD at Vp of 160 and 550 cm3 increased 70 and 41%, respectively. At 57% TLC, log (EAD) at 160 cm3 was significantly correlated with airway resistance (r = -0.57, P less than 0.0204) but not with forced expired flow between 25 and 75% of vital capacity. Log (EAD) at 400 cm3 was correlated with deposition of 1-micron particles (r = -0.73, P less than 0.0009). We conclude that aerosol-derived lung morphometry is a responsive noninvasive probe of peripheral air-space diameters.

Hyperoxic inhibition of newborn rat lung development: Protection by deferoxamine

Prolonged exposure to hyperoxia markedly inhibits normal lung development (alveolarization and respiratory surface area expansion) in immature animals. Since (a) hyperoxia results in excess hydroxyl radical (OH ⋅) formation, (b) (OH ⋅) is implicated in O 2-induced lipid peroxidation and DNA alterations, and (c) both OH ⋅ formation and its interaction with DNA are Fe ++ dependent; chelation of Fe ++ should act to protect against pulmonary O 2 toxicity and hyperoxic inhibition of lung development. We therefore treated litters of newborn rats with the iron chelator Deferoxamine mesylate (DES) (150 mg/kg/day) during a 10-day exposure to >95% O 2. Morphometric analysis demonstrated that compared to the mean airspace size in air control rat pups ( L m = 44.5 μm hyperoxic exposure resulted in a 34% larger mean air space diameter in O 2-saline rat lungs (59.5 μm) versus only an 11% enlargement in O 2-DES lungs (51.1 μ ∗). Lung internal surface area (cm 2) per 100-g body weight were air control = 4480, O 2- saline = 3750 (↓ 20.3%), and O 2-DES = 4125 ∗ (↓ 7.9%) ( ∗p<0.05 versus O 2-saline group ) . DES-treated animals also had significantly decreased lung conjugated diene levels during hyperoxic exposure and increased lung elastin content (reflective of preserved lung alveolar formation) compared to O 2-saline rats. These results indicate that DES treatment substantially ameliorated the inhibitory effects of neonatal hyperoxic exposure on normal lung development.

Changes in aerosol-derived airspace diameter induced by bronchoconstrictors and alterations in lung volume

Inhaled aerosols have been used to estimate the size of pulmonary airspaces, yet little is known regarding the sensitivity of this technique to detect changes. To evaluate this, we measured aerosol-derived airspace diameter (ADAD) in the lungs of four dogs at different volumes as well as before and after bronchoconstriction induced by intravenous methacholine (MCH) or prostaglandin F 2 α(PGF)

Oxygen toxicity in neonatal rats: The effect of endotoxin treatment on survival during and post-O 2 exposure

ABSTRACT: Neonatal rats were treated with low doses of bacterial ipopolysaccharide (endotoxin) to test for a protective effect of endotoxin against O2 toxicity and the severe inhibition of normal lung development which occurs during prolonged exposure to hyperoxia. The rationale for the prophylactic use of endotoxin included its marked protective effect against pulmonary O2 toxicity in adult rats and its lung growth-promoting effect in experimental pulmonary stress models. Neonatal rats (4-5 days old) survived a 14-day exposure to >95% O2 equally well whether treated with saline (39/51 = 76%) or with endotoxin (41/51 = 80%). However, during the following 24 h of gradual weaning to room air breathing, there was a marked difference in survival between the endotoxin group (32/41 = 78%) and the saline pups (14/39 = 36%) (p<0.001). Both groups showed inhibition of lung development (alveolarization) during O2 exposure, but endotoxin treatment compared to saline was associated with increased specific lung volume (5.33 versus 4.50 ml/100 g) (air control = 4.08), smaller mean airspace diameter (mean linear intercept = 49.0 versus 55.8 μm) (air control = 43.3), increased specific internal surface area (4393 versus 3232 cm2/100 g) (air control = 3753), and greater preservation of alveolar wall capillary patency (24.83 versus 18.52% “capillary density”) (air control = 27.70%). We conclude that endotoxin treatment resulted in significant protection against O2 toxicity in neonatal rats which was manifested during readaptation to room air breathing. The protective effect was likely due to a combination of reduced inhibition of lung growth and development and reduced hyperoxic damage to the respiratory membrane of the lung.

Oxygen toxicity in neonatal rats: the effect of endotoxin treatment on survival during and post-O2 exposure.

Neonatal rats were treated with low doses of bacterial lipopolysaccharide (endotoxin) to test for a protective effect of endotoxin against O2 toxicity and the severe inhibition of normal lung development which occurs during prolonged exposure to hyperoxia. The rationale for the prophylactic use of endotoxin included its marked protective effect against pulmonary O2 toxicity in adult rats and its lung growth-promoting effect in experimental pulmonary stress models. Neonatal rats (4-5 days old) survived a 14-day exposure to greater than 95% O2 equally well whether treated with saline (39/51 = 76%) or with endotoxin (41/51 = 80%). However, during the following 24 h of gradual weaning to room air breathing, there was a marked difference in survival between the endotoxin group (32/41 = 78%) and the saline pups (14/39 = 36%) (p less than 0.001). Both groups showed inhibition of lung development (alveolarization) during O2 exposure, but endotoxin treatment compared to saline was associated with increased specific lung volume (5.33 versus 4.50 ml/100 g) (air control = 4.08), smaller mean airspace diameter (mean linear intercept = 49.0 versus 55.8 microns) (air control = 43.3), increased specific internal surface area (4393 versus 3232 cm2/100 g) (air control = 3753), and greater preservation of alveolar wall capillary patency (24.83 versus 18.52% "capillary density") (air control = 27.70%). We conclude that endotoxin treatment resulted in significant protection against O2 toxicity in neonatal rats which was manifested during readaptation to room air breathing. The protective effect was likely due to a combination of reduced inhibition of lung growth and development and reduced hyperoxic damage to the respiratory membrane of the lung.

CT Assessment of the Adult Extrathoracic Trachea

A total of 40 neck computed tomographic (CT) scans in adult patients were retrospectively reviewed and absolute measurements made of the anteroposterior (TRAP) and transverse (TRTR) air spaces at the first tracheal cartilage. For each patient, ratio measurements were calculated of the anteroposterior (TRAP/TC) and transverse (TRTR/TC) tracheal air space relative to the glottic air space at the true cord level. Mean TRAP (2.01 cm) and TRTR (1.84 cm) measurements for normal patients agreed closely with figures reported in prior cadaver preparation studies. The lower normal limit found for absolute tracheal diameter was 1.5 cm (TRAP) and 1.4 cm (TRTR), whereas lower normal limits for relative tracheal to glottic air space diameters were 0.7 (TRAP/TC) and 0.6 (TRTR/TC).

A morphometric and morphological study of the lungs of rabbits after unilateral pneumonectomy

Boatman, E. S. (1977). Thorax , 32, 406-417. A morphometric and morphological study of the lungs of rabbits after unilateral pneumonectomy. A study was made to determine the changes occurring in the contralateral lung of adult rabbits as a result of left pneumonectomy. Stereological procedures for light microscopy and for electron microscopy were used to quantitate the changes. Lungs from control rabbits, ranging in body weight from 1·0 to 9·0 kg, were also analysed. Resin corrosion casts of left and right lungs were prepared. Left pneumonectomy causes the volume of the right lung to increase to the total paired lung volume in about four weeks. Total surface area, while increasing directly with lung volume in control rabbits, increased as two-thirds of the lung volume after pneumonectomy. In some right lungs there appeared to be an increase in the number of alveoli. Mean linear intercepts for control lungs were fairly constant, but the volume density of alveolar ducts increased with age. In pneumonectomised animals, mean air-space diameter of the right lung increased by about 25% and the volume density of alveolar ducts by 22-33%. The volume density of alveolar wall tissue decreased by about 30%. The average number of alveoli/cm 3 for whole lungs was 2·31±0·46×10 6 , whereas for right lungs eight weeks or more after pneumonectomy it was significantly less (1·70±0·38×10 6 ). Morphometry by electron microscopy revealed slight changes in the components of the alveolar septum and a reduction in the thickness of the air-blood barrier. The overall effect of left pneumonectomy was mainly one of a compensatory increase in the volume of the right lung with dilatation of alveoli and of alveolar ducts.

Mean air space diameter, lung surface area and alveolar surface tension.

Results from pressure-volume studies indicate that lung surface area is directly proportional to volume rather than to volume raised to the two thirds power as has been assumed previously. Mean air space diameter was found to decline with an increase in lung volume which is indicative of a significant degree of alveolar recruitment. Calculation of alveolar surface tension during 20-min inflation-deflation cycles reveals a minimum surface tension of 15.9 +/- 2.3 and a maximum surface tension of 42.7 +/- 4.2 dyn/cm (mean +/- SE). Comparison of surface tensions obtained from the surface balance and calculated alveolar surface tension reveals no significant difference between the means and a significant correlation between the two values.