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Annual decline of lung function in pulmonary emphysema: influence of radiological distribution.

Fifty-six male patients with pulmonary emphysema and normal serum alpha 1-antitrypsin were followed for a minimum period of three years (range 3-13 yr) to observe the effects of the radiological distribution of emphysema on the annual rate of change of lung function indices. The subjects were placed in three categories--upper zone (UZ), lower zone (LZ), and generalised (G). The influence of smoking was taken into account with subjects in each radiographic category being divided into ex-smokers (group EX-S) and continuing smokers (group S). The rate of decline of FEV1, VC, TCO, and KCO was greater in group S than EX-S in all three x-ray categories. In group S, FEV1, VC, TCO, and KCO declined significantly faster in UZ emphysema than in G emphysema. In group EX-S, FEV1, TCO, and PaO2 declined significantly faster in UZ than G emphysema but VC remained unaltered. KCO and PaCO2 did not change significantly in any radiographic category in either group S or EX-S. Patients with G and LZ emphysema underwent very similar physiological changes over the course of time. Those with UZ emphysema, however, complained of exertional dyspnoea at an earlier age; a number of their lung function indices deteriorated at a faster rate than in patients from the other two categories, suggesting that UZ emphysema is a different disease entity.

Adult↗

Lung transfer factor and KCO at cardiac frequency 100 beats/min as a guide to impaired function of lung parenchyma.

Transfer factor (TL) and KCO have been measured by the single breath carbon monoxide method in 39 patients with confirmed or suspected lung disease, mostly of occupational origin, and 37 healthy subjects. TL and KCO at an exercise cardiac frequency of 100 beats/min (TL100 and KCO100) and the slopes of the regression of exercise transfer factor and KCO on exercise cardiac frequency (delta TL/delta fC and delta KCO/delta fC) were obtained. The discriminatory performance of these indices in detecting defective gas transfer was compared with that of TL and KCO at rest (TLrest and KCOrest). The slope indices did not distinguish between healthy subjects and patients with emphysema or conditions of the lung parenchyma, including asbestosis. The slope indices also failed to distinguish between individuals with normal and abnormal gas transfer at rest. The indices TL100 and KCO100 contributed additional information not contained in the indices at rest and they merit further study.

Adult↗

Strenuous exercise increases plasmatic and urinary leukotriene E4 in cyclists.

UNLABELLED: The purpose of this study was to investigate plasma and urinary levels of leukotriene (LT) and the changes in pulmonary function induced by strenuous exercise in highly trained cyclists (HT) with mild exercised-induced hypoxemia (EIH). METHOD: Nine HT and five untrained subjects (UT) performed a 30-min exercise at 78% of their VO2peak. Leukotriene E4 (LTE4) was assayed in plasma and urine. Pulmonary function tests and pulmonary diffusion capacity (DLCO) were examined before and after exercising. Ear arterialized blood gases were assessed at rest and during exercise. RESULTS: The mean drop in partial oxygen pressure was 15 mmHg in HT during exercise; and the DLCO decreased by 7.5% following exercise. No significant changes were found in forced vital capacity or forced expiratory flows. LTE4 levels increased significantly in HT following exercise: urinary LTE4 was 42.9 +/- 6.3 ng.mmol-1 creatinine at rest and 66.3 +/- 11.9 ng.mmol-1 creatinine 2 hrs after exercise, and plasma LTE4 rose from 528 +/- 91 pg.mL-1 at rest to 897 +/- 123 pg.mL-1 after exercise. By contrast, urinary LTE4 level was unchanged in the UT group. Among the HT group, there was no significant correlation between urinary LTE4 changes and PO2, air flow rates, or DLCO changes. CONCLUSION: These results suggest that strenuous exercise induces an increase of LTE4 release in highly trained cyclists with mild EIH. These changes in LTE4 levels were not related to significant impairment of lung function.

Adult↗

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Airway Resistance↗

Obliterative bronchiolitis: individual CT signs of small airways disease and functional correlation.

PURPOSE: Individual features of small airways disease depicted at computed tomography (CT) were correlated with functional indexes in patients with obliterative bronchiolitis. MATERIALS AND METHODS: Fifteen patients (all women) who fulfilled the strict criteria for diagnosis of obliterative bronchiolitis underwent thin-section CT at full inspiration and at end expiration. The CT scans were scored by two observers for extent of decreased attenuation of the lung parenchyma; end-expiration CT signs of air trapping; and bronchial dilation, wall thickening, and mucous plugging. The functional importance of each CT sign was evaluated. RESULTS: Areas of decreased attenuation were present in all patients (median score at end expiration, 61%; range, 21%-83%). Bronchial wall thickening was identified in 13 of the 15 patients. Correlations of the extent of decreased attenuation and measures of air-flow obstruction were strongest between decreased attenuation at end expiration and air flow at low lung volumes (r(s) = -.70, P < .005). This relationship remained intact after correction for the severity of bronchial wall thickening. CONCLUSION: In patients with obliterative bronchiolitis, the extent of decreased attenuation at CT was most strongly related to depression of pulmonary function tests of the small airways. Decreased attenuation is the cardinal sign for further quantitative studies of obliterative bronchiolitis.

Adult↗

Pulmonary emphysema: comparison of preoperative quantitative CT and physiologic index values with clinical outcome after lung-volume reduction surgery.

PURPOSE: To compare quantitative computed tomographic (CT) and preoperative physiologic values in emphysema with outcome after lung-volume reduction surgery. MATERIALS AND METHODS: In 46 patients, emphysema was quantified by measuring lung attenuation on preoperative CT scans. Quantitative CT and preoperative physiologic values and postoperative outcomes (1-second forced expiratory volume, PaO2, and 6-minute walk distance) were compared. RESULTS: Moderately strong correlations were found between several quantitative CT and preoperative physiologic values (magnitude of r = .29-.58, P < .05) and several quantitative CT and outcome measures (magnitude of r = .31-.47, P < .05). With stratification, postoperative outcome was better with mean lung attenuation greater than -900 HU; 75% or greater of upper lung below -900 HU (emphysema index); greater than 25% of lung below -960 HU (severe emphysema index); ratio of upper- and lower-lung emphysema indexes 1.5 or greater; volume of normally attenuated lung (-850 to -701 HU) greater than 1 L; and full width at half maximum of attenuation-frequency distribution 80 HU or less. Differences in outcome measures between groups stratified with quantitative CT values were often two- to threefold; patients with greater numbers of favorable quantitative CT values had better outcome. Correlations between preoperative physiologic measures and outcome were few. CONCLUSION: In emphysema, quantitative CT values correlate with outcome. Quantitative assessment of emphysema in candidates for lung-volume reduction surgery is potentially useful.

Adult↗

Factors influencing pulmonary and cutaneous arterial blood flow in the toad, Bufo marinus.

In the conscious, undisturbed toad, Bufo marinus, pulmonary arterial blood flow increased during periods of lung ventilation and decreased in intervening periods of pulmonary apnea. In unidirectionally ventilated, anesthetized toads, lung inflation produced by increasing the outflow resistance to pulmonary gas flow to 3 cmH2O caused a significant increase in pulmonary arterial blood flow and a significant decrease in cutaneous arterial blood flow. Changes in flow were associated with reciprocal changes in calculated vascular resistance. Mean pulmocutaneous pressure and cardiac frequency did not change significantly. Thus lung inflation (in the absence of changes in the composition of intrapulmonary gases) increased the proportion of total pulmocutaneous flow routed to the lungs and decreased the proportion directed to the skin. Unidirectional ventilation with air + 5% CO2 at constant lung volume produced a significant decrease in pulmonary arterial blood flow, an increase in calculated pulmonary arterial flow resistance, and a small increase in the flow to the cutaneous artery. Concomitant mild hypoxia potentiated the effects of pulmonary hypercapnia, although hypoxia alone was less effective than hypercapnia alone in decreasing pulmonary flow. Pulmonary arterial blood flow was decreased by infusion of acetylcholine into the pulmocutaneous artery, but epinephrine had no effect on either the pulmonary or cutaneous artery at doses below those that produced systemic effects. Atropine blocked all changes in pulmonary arterial blood flow. This and other evidence suggest that calculated arterial resistance changes are due to reflex changes in the tone of vascular smooth muscle. Intrapulmonary CO2-sensitive mechanoreceptors possess appropriate response characteristics to mediate the afferent limb of the reflex.

Acetylcholine↗

Pulmonary vascular response to increase in intracranial pressure: role of sympathetic mechanisms.

The pulmonary vascular response to intracranial hypertension was studied in anesthetized controlled ventilated dogs in which intracranial pressure (ICP) was elevated to 20 Torr below the mean arterial pressure for a 20-min period, and regulated at this level. Pulmonary vascular resistance (PVR) increased from control value of 2.7 +/- 0.30 to 8.3 +/- 0.51 Torr-l-1-min at the end of 20-min increase in ICP. The increase in PVR was associated with marked increase (P less than 0.001) in pulmonary arterial pressure from 14.4 +/- 1.3 to 35.4 +/- 4.0 Torr, small increase in left atrial pressure from 5.4 +/- 1.2 to 7.9 +/- 1.9 Torr, and no significant change in pulmonary blood flow. The increase in PVR occurred independently of changes in the arterial pressure. The increase in PVR induced by elevated ICP was correlated with increases in lung water, physiological shunt (Qs/Qt), alveolar dead space (VD), and with hypoxemia. Pretreatment with propranolol (1.5 mg-kg-1) attenuated the increase in PVR during elevation in ICP; the smaller increase in PVR was associated with a marked increase in left atrial pressure and a smaller increase in pulmonary perfusion pressure than in the control group. The propranolol-treated dogs also developed increases in lung water, Qs/Qt, VD, and hypoxemia. In contrast, pretreatment with phenoxybenzamine (1.5 mg-kg-1) inhibited the increases in pulmonary perfusion pressure and PVR induced by ICP elevation as well as the associated increases in lung water, Qs/Qt, VD, and hypoxemia. Therefore, a sustained elevation in ICP at a level below the mean arterial pressure in the intact dog evokes pulmonary vasoconstriction which is mediated by alpha-adrenergic mechanisms. The neurogenic pulmonary vasoconstriction results in the increases in lung water, Qs/Qt, VD, and in the hypoxemia.

Animals↗

Identification of functional lung unit in the dog by graded vascular embolization.

To study the dimensions of the functional gas exchange unit, spherical polystyrene beads (diam 50-500 micrometers) were injected intravenously into 12 normal anesthetized paralyzed dogs (15-24 kg wt). We argued that beads small enough to lodge within gas exchange units would not give rise to a population of high ventilation-perfusion ratio (VA/Q) areas, whereas embolization of larger vessels supplying these units would. Each dog received only one bead size in cumulative 0.25-g doses up to a maximum of 2.25 g. Multiple inert gas elimination data were obtained after each dose to monitor the development of high VA/Q regions. Injection of 50- and 100-micrometers beads never gave rise to high VA/Q regions, whereas 150-, 250-, and 500-micrometers beads consistently induced a high VA/Q mode comprising up to 45% of the ventilation. Histological examination of lungs from five additional dogs injected with small (approximately 0.5 g) doses revealed that beads rarely formed clusters and appeared in vessels of their own diameter in over 90% of instances. By the above criterion, the functional gas exchange unit in these lungs is that volume of tissue subtended by 150- micrometers-diam arteries (vessels associated with respiratory bronchioles).

Animals↗

Augmented diffusion in the airways can support pulmonary gas exchange.

Bohn et al. (J Appl. Physiol.: Respirat. Environ. Exercise Physiol, 48: 710-716, 1980) reported that paralyzed beagle dogs maintained normal gas exchange for 6 h or more when small tidal volumes at high breathing rates were maintained at the airway opening (15 ml tidal volume at 15 breaths/s). These tidal volumes were 25% of dead space and thereby were too small to permit convective gas exchange with pulmonary air spaces. I have used a semiempirical analysis to show that augmented diffusion in the central airways, akin to Taylor's turbulent dispersion (Proc. R. Soc. Ser. A 223: 446-468, 1954) combined with molecular diffusion in the periphery of the lung, can account for most if not all of the observed gas transport during small tidal volume, high-frequency ventilation. Ventilation efficiency (alveolar ventilation/minute ventilation) is approximately 2-5% and is insensitive to the combination of frequency and tidal volume giving rise to the minute ventilation.

Airway Resistance↗

Influence of increased alveolar PCO2 on thoracic gas volume measurements.

We examined the possibility that cyclic gas exchange between alveolar space and the surrounding tissue, induced by alveolar pressure variations, could interfere with plethysmographic measurements of thoracic gas volume (TGV). A model study suggested that TGV could be overestimated by up to 100 ml and that the phenomenon could account for some of its previously reported negative frequency dependence (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 739-747, 1982). As the error would be mainly due to CO2 exchange and be proportional to its partial pressure (PCO2), we studied in nine normal subjects the influence of increasing alveolar PCO2 from 30 to 50 Torr on TGV measurements at panting frequencies (f) of 0.5 and 2-2.5 Hz. Contrary to model predictions, CO2 tended to decrease TGV estimates at low frequency and to increase them at high frequency. As a consequence, frequency dependence of TGV (delta TGV/delta f) was less at high than at low PCO2 (-39 +/- 32 vs. -84 +/- 49 ml x Hz-1, P less than 0.001). The data are not satisfactorily explained but suggest that gas exchange is not an important factor in TGV measurements.

Adult↗