Mid-lung Volumes Research Articles

Occupational asthma caused by IgE-mediated sensitization to multiple woods

Wood is a natural material that is able to trigger rhinitis and asthma in exposed subjects in occupational settings. This has been described with both soft and hard woods.1,2 Involvement of both low- and high-molecular-weight allergens has been reported, and the relevance of these is related with the wood type.1 There are cases where protein may be the responsible allergen. Crossreactivity between obeche and ramin woods3 and between obeche and latex4 has been shown. However, to the best of our knowledge, this is the first report of a multiple IgE-mediated sensitization to different woods that caused occupational respiratory symptoms in the same worker.

Intrabreath Diffusing Capacity of the Lung in Healthy Individuals at Rest and During Exercise

Traditional approaches to measuring the diffusing capacity of the lung for carbon monoxide (DLCO) treat the lung as a single, well-mixed compartment and produce a single value for DLCO to represent an average diffusing capacity of the lung (DL). Because DL distribution in the lung is inhomogeneous, and changes in the DL in diseased lungs may be regional, measuring regional DL, especially during exercise, may be more sensitive in detecting pulmonary vascular diseases. To characterize regional changes in DL in healthy individuals from rest to exercise, and to provide normal references for future studies in pulmonary vascular disorders. We reanalyzed DLCO and phase III CH(4) slopes that were obtained during a slow, single exhalation at rest and during exercise in our extended database of 105 healthy individuals. DLCO profiles between 20% and 80% of exhaled vital capacity (VC) (ie, the intrabreath DLCO) were analyzed by calculating the average DLCO measured at midlung volume (ie, 30 to 45% of exhaled VC [DLCOMLV]) and by fitting the whole curve with a third-order polynomial equation. DLCO decreased nonlinearly by approximately 30%, from 20 to 80% of exhaled VC at rest. DLCO during exercise was greater than that at rest, and the increase was similar at all lung volumes. The CH(4) slopes at rest and during exercise were similar. Prediction equations based on regressions on age, sex, and height were computed for resting and exercise DLCOMLV and the phase III CH(4) slope (an index of ventilation distribution). Capillary recruitment/dilation during exercise in healthy individuals is a uniform process throughout the lungs. Our analyses provide a database for a noninvasive method that can incorporate exercise to evaluate the volume-dependent distribution of DLCO in lung diseases.

Effect of an endurance triathlon on pulmonary function

We assessed the effect of an endurance triathlon consisting successively of a 3.8-km swim, a 180-km bicycle ride, and a 42-km run on the forced expiratory spirogram, indices of inspiratory and expiratory muscle strength (PImax and PEmax), and maximal voluntary ventilation (MVV). Twelve male participants were recruited from competitors in the Cape Cod Endurance Triathlon and underwent studies on the afternoon before the event, after each segment, and on the following morning. Participants averaged 32.9 yr of age. All completed the triathlon with an average finishing time of 12 h 45 +/- 90 min. Following completion of the triathlon, statistically significant declines occurred in FVC (7.1%), FEV1 (8.4%), FEF25-75% (15.2%), and FEF50% (18.6%), but not in MVV. On the morning after the triathlon, only FEV1 remained significantly below baseline. PImax was not significantly reduced after the swim, but significant reductions did occur after the bicycle and running events (26% and 25%, respectively); full recovery had occurred by the following morning. PEmax did not change significantly. We conclude that vital capacity, flow rates at mid-lung volumes, and inspiratory muscle strength decline as a consequence of participation in a triathlon.

Effect of alveolar pressure on single-breath CO diffusing capacity at mid-lung volume

The present study examines whether changes in the alveolar pressure (P a) affect the single breath diffusing capacity for carbon monoxide (D l CO) more strongly at mid-lung volume than at total lung capacity (TLC) in normal subjects. D l CO was measured at 60%, 80% and 100% of TLC, while P a was kept at +30, 0, or −30 cm H 2O by the subject's effort during the measurement of D l CO at each lung volume. The capillary blood volume (Vc) and the membrane diffusing capacity (Dm) were also determined. D l CO at zero P a was found to be higher at 100% TLC than at lower lung volumes. At P a = +30 cm H 2O D l CO at 100%, 80%, and 60% TLC decreased by 8%, 13%, and 13%, respectively, and the decreases in Vc were 2%, 10%, and 21%, respectively. However, negative P a did not cause any significant changes in D l CO or Vc at any lung volume. Also, Dm di not change at any P a. We conclude that D l CO is more affected by a positive P a at mid-lung volume than at a high lung volume, probably due to a greater decrease in Vc.

Connective tissue, mechanical, and morphometric changes in the lungs of weanling rats fed a low protein diet.

We studied the effect of low-protein diet (8% casein) on lung growth in rats from 3 to 7 weeks of age. Their diet was isocaloric with that of control animals fed a diet of 20% casein. The calorie intake of experimental animals was increased during the first 3 weeks of the experiment, but they increased less (about 10%) in body weight, had less protein and less water when the whole body was examined, and had lower serum proteins and decreased urinary hydroxyproline. The experimental animals remained in positive nitrogen balance by maintaining low urinary nitrogen excretion. The lungs of the experimental animals were abnormal, with decreased absolute amounts of hydroxyproline and desmosine and of these relative to unit lung weight. The lungs contained more air per gram of lung tissue, and the volume of air in the lung was increased at all transpulmonary pressures above zero. When corrected for increased total lung capacity, there was a loss of recoil at mid-lung volumes. Saline-filled volume-pressure curves, corrected for lung volume, showed similar loss of recoil. Alveolar multiplication was quantitatively normal, but the experimental animals had larger alveoli. We conclude that the protein deprivation in isocalorically fed animals has a specific effect on lung scleroprotein content, which may be due to diminished synthesis, and this results in both structural and functional abnormalities in the lung. Our results indicate the importance of dietary protein in lung development and possibly as one of the causes of emphysema. Further studies are needed to know whether this would be a problem in infants of Kwashiokor.

Effects of lung volume and alveolar surface tension on pulmonary vascular resistance.

Utilizing the arterial and venous occlusion technique, the effects of lung inflation and deflation on the resistance of alveolar and extraalveolar vessels were measured in the dog in an isolated left lower lobe preparation. The lobe was inflated and deflated slowly (45 s) at constant speed. Two volumes at equal alveolar pressure (Palv = 9.9 +/- 0.6 mmHg) and two pressures (13.8 +/- 0.8 mmHg, inflation; 4.8 +/- 0.5 mmHg, deflation) at equal volumes during inflation and deflation were studied. The total vascular pressure drop was divided into three segments: arterial (delta Pa), middle (delta Pm), and venous (delta Pv). During inflation and deflation the changes in pulmonary arterial pressure were primarily due to changes in the resistance of the alveolar vessels. At equal Palv (9.9 mmHg), delta Pm was 10.3 +/- 1.2 mmHg during deflation compared with 6.8 +/- 1.1 mmHg during inflation. At equal lung volume, delta Pm was 10.2 +/- 1.5 mmHg during inflation (Palv = 13.8 mmHg) and 5.0 +/- 0.7 mmHg during deflation (Palv = 4.8 mmHg). These measurements suggest that the alveolar pressure was transmitted more effectively to the alveolar vessels during deflation due to a lower alveolar surface tension. It was estimated that at midlung volume, the perimicrovascular pressure was 3.5-3.8 mmHg greater during deflation than during inflation.

Effects of airway tone and volume history on maximal expiratory flow in asthma.

We assessed the difference between isovolumic maximal expiratory flows (Vmax) using maneuvers begun at mid-lung volumes, so-called partial expiratory flow-volume curves (P), vs. those begun at full inflation, so-called maximal expiratory flow-volume curves (M), in 10 asthmatic subjects before and following obstruction induced by isocapnic hyperpnea with cold air and before and after bronchodilation with a beta-agonist or antimuscarinic agent. Volume history effects were quantitated as an M-to-P ratio of Vmax at 30% vital capacity (M/P V30). Although M/P V30 was variable among patients at base line, there was a uniform increase in M/P V30 during constriction and a consistent decrease below base line after dilation. Blunting of induced obstruction with beta-agonists also diminished the increase in M/P V30. Antimuscarinics, despite equivalent bronchodilation, failed to alter the degree of obstruction induced by cold air or the increase in M/P V30 seen during obstruction. The level of airway tone, as indicated by specific resistance, related directly to the M/P V30. We conclude that the response of the asthmatic lung to a deep inhalation is relatively predictable when acute changes in airway tone are produced.

A computational model for expiratory flow.

A mathematical model of maximal expiratory flow was developed. Coupled equations describing the pressure losses in the flow and the pressure-area behavior of the airway were integrated along the airway from the periphery to the flow-limiting site. Equations describing pressure losses in the flow were adapted from studied of bronchial casts. The bronchial anatomy utilized was that described by Weibel. Bronchial mechanical properties were obtained from measurements in excised human lungs for the central airways and by extrapolations of these data for the peripheral airways. The maximal flow for air and helium predicted by the model agrees with that of five lungs from which mechanical properties were obtained. The model predictions agree with published values of density and viscosity dependence of maximal flow. At high and midlung volumes, maximal flow is determined primarily by the wave-speed mechanism. At low lung volumes, maximal flow is primarily determined by the coupling of viscous pressure losses and airway mechanical properties.

The effect of the minimal deflation pressure on lung mechanics in isolated rabbit lungs.

Alterations in the PV relationships of isolated rabbit lungs which are dependent on the minimal deflation pressure (Pmin) have been studied. When Pmin remains positive both inflation and deflation limbs of the PV loop are shifted toward lower transpulmonary (P1) pressures throughout most of the cycle. In addition, Pmin(+) conditions eliminate the deflation inflection and increase deflation compliance at low and mid-lung volumes. Results from indicator washout and spontaneous deflation reveal that Pmin(+) conditions produce a more even inflation of the lung parenchyma and dilate airways at low lung volumes. These effects cause a stabilization of the parenchyma and a delay in airway closure resulting in the increased deflation compliance and a decrease in the trapped gas volume during Pmin(+) conditions. The relevance of Pmin(+) and (−) conditions are discussed for several clinical conditions.

The mechanisms that limit expiratory flow.

Recent progress in modeling expiratory flow is reviewed. Two idealized flow limitating mechanisms are described: flow limitation at wave speed and viscous flow limitation. In the lung, both convection acceleration and viscous dissipation contribute to the pressure distribution that determines airways compression, but the first dominates at high and mid lung volumes and the second dominates at low lung volumes. A computer model describes the combined effects. This quantitative modeling is consistent with long-standing qualitative concepts of flow limitation and provides a basis for future work on modeling expiratory flow limitation in abnormal lungs.

Effect of elastase and ventilation on elastic recoil of excised dog lungs.

The effect of porcine pancreatic elastase and mechanical ventilation on tissue elastic recoil was examined in excised dog lung lobes. Lobes incubated for one hour with an elastase-buffer mixture showed a significant (P less than 0.001) left shift of the liquid-filled pressure-volume curve at all pressures measured (0 to 12 cm H2O) when compared to lobes treated with buffer only. These results suggest that the contribution of elastin to the elastic properties of lung tissue is greatest at mid-lung volumes, but that it also contributes to delimiting maximal lung volume. Elastase and buff-treated lobes were inflated cyclically with humidified air to a pressure of 20 cm H2O 6 times per min during a 16-hour period. This mechanical ventilation caused no further decrease of tissue elastic recoil. Ventilation did cause an unexpected increase in the elastic recoil of liquid-filled lobes that was significant at pressures of 4 cm H2O (P less than 0.025) or more (P less than 0.001). Elastase and buffer-treated lobes showed an almost identical rightward shift of the pressure-volume curve after ventilation when compared to the respective nonventilated control lobes. This increased recoil cannot be attributed to altered surface tension.

Minimal Reaction Times for Phonatory Initiation

The maximum speed at which voluntary vocal and digital responses can be initiated was investigated in 15 male and 15 female neurologically normal adults using simple reaction time (RT) methodology. All subjects were pretrained to respond as quickly as possible to stimulus onset following a computer-controlled preparatory interval. Voluntary minimal RTs for phonation initiation were studied as a function of (1) stimulus type (auditory and somesthetic), (2) prephonatory vocal-fold position (abducted and adducted), and (3) subject's lung volume (75%, 50%, and 25% VC). The average minimal vocal RT across subjects was 195 msec, and the fastest recorded vocal RT was 120 msec. Although vocal responses to an auditory stimulus were somewhat shorter than to a somesthetic stimulus, neither these differences nor the RTs between sexes were statistically significant except that females had shorter vocal RTs from an abducted prephonatory vocal-fold position. Shorter vocal RTs were obtained when phonation was initiated at midlung volume than at the lung volume extremes, and for both sexes the average digital RTs were significantly shorter than vocal RTs.

The influence of lung volume on expiratory flow rates in diffuse interstitial lung disease.

This study evaluated maximum expiratory flow rates with respect to lung volume and maximum recoil pressure in selected patients with diffuse interstitial lung disease who had normal large airway function by standard technique. Coefficient of retraction was normal or greater than normal in all. Peak flow varied directly with lung volume as in normals. At 50% vital capacity (VC) and 25% VC, the absolute flow rates varied from higher to lower than normal. However, when flow was adjusted to volume, the flow/volume ratio was normal or high in all. Flow/volume ratio at mid-lung volume appeared to increase with increase in coefficient of retraction. Patients with frequency dependence of compliance had lower flow/volume ratios at 25% VC than those without, although still within normal range. Thus, despite recognized wide variations in normals, the flow/volume ratio is pertinent to the evaluation of reduced air flow rates in in interstitial lung disease to distinguish abnormal upstream airway resistance from volume-dependent reduction of flow rate. An effort-independent flow rate that yields a supernormal flow/volume ratio suggests increased recoil properties of the respiratory system.

Distribution of transpulmonary pressure and chest wall shape

After wide opening of the abdomen in paralysed supine dogs the changes of transpulmonary pressure (PI) on the costal surface for a given increase of lung volume were lower than those under normal conditions, whereas those on the diaphragmatic surface at the same height were greater. As a result pleural surface pressure on the diaphragmatic surface was still subatmospheric at large lung volumes. The difference between PI on the diaphragmatic and costal surface became marked (4 cm H 2O) only at the largest lung volume, suggesting a large parenchymal interaction between the two directions of expansion. When the lateral diameter of the caudal part of the rib cage was kept at the value occurring in the head-up posture at FRC, the difference between PI on the diaphragmatic surface and that on the caudal part of the rib cage, as well as the difference between PI on the cranial and caudal part of the rib cage were marked even at mid lung volume. In line with the author's previous work, these results show that the shape is an important factor in the distribution of transpulmonary pressure.

ANATOMICAL DEAD SPACE (VD) AND LUNG EMPTYING IN ASTHMA AND CYSTIC FIBROSIS (CF)

Ten normal, 10 CF and 10 asthmatic children were studied to assess the contribution of lung zones emptying at different rates to curvilinearity of the maximum expiratory flow-volume (MEFV) curve. Lung volumes, MEFV curves on air and on heliumoxygen mixture and single breath nitrogen washouts were measured. Partial forced expiratory maneuvers were performed to produce flow transients exceeding maximum flow at mid-lung volumes. Normal children and those with asthma and mild CF had small or no transients and normal VD. Those with severe CF had large transients (mean 150ml.) and large VD (mean, 155% pred.), and the volume of the transients corresponded closely to that of the VD. These large transient volumes were associated with increased curvilinearity of the MEFV curve and loss of helium response; whereas asthmatics with marked curvilinearity had small transients and helium responsiveness. In severe CF, the large transients suggest sequential emptying of fast and slow compartments which influences the shape of the MEFV curve. The fast component could correspond to emptying of an enlarged VD. Any time constant inequality present in asthma and mild CF does not appear to contribute to the shape of the MEFV curve.