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PubMed1995

Excessive neutrophil elastase in bronchoalveolar lavage fluid in subclinical emphysema.

In an attempt to further evaluate the role of neutrophil elastase (NE) in the development of emphysema, we examined the immunologic quantity of NE bound to alpha 1-protease inhibitor (PI), the NE inhibitory activity, and the molecular pattern of alpha 1-PI in unconcentrated bronchoalveolar lavage fluid (BALF) supernatant from 36 community-based older volunteers. They were classified into three groups: 10 current smokers with low attenuation areas (LAAs) on the lung computed tomography (CT) scans who were considered to have subclinical emphysema, 13 current smokers who had a comparable smoking history but no LAA, and 13 noncurrent smokers without LAA. The concentration of NE-alpha 1-PI complex was significantly increased in the subjects with subclinical emphysema when compared not only with the noncurrent smokers (0.52 +/- 0.10 versus 0.21 +/- 0.03 SEM micrograms/mg albumin, p < 0.01) but also with the LAA(-) current smokers (0.52 +/- 0.10 versus 0.23 +/- 0.07 SEM micrograms/mg albumin, p < 0.01). NE inhibitory activity measured by a spectrophotometric method using methoxysuccinyl-alanyl-alanyl-prolyl-valyl-paranitroanilide did not show any significant difference between the two groups of current smokers. There was no difference in the pattern or density of native and proteolysed alpha 1-PI bands between the three groups by Western blotting. We conclude that NE-alpha 1-PI complex in BALF is a factor that may differentiate smokers who are potentially developing emphysema from those who are not.

Aged↗
PubMed1997

The relations between expiratory chest CT using helical CT and pulmonary function tests in emphysema.

Chest computed tomography (CT) and pulmonary function tests are usually used for the evaluation of emphysema. We performed the present study to evaluate more accurately the relationship between the degree of morphological change and the functional abnormality in emphysema. We used a helical CT apparatus to obtain the CT images both at full inspiration and full expiration. We classed the degree of emphysema into 5 grades (0-4) by visual observation on CT image obtained at the two levels, upper and lower fields, on each side. We assigned each of these grades a visual score. We also calculated the average ratio of CT numbers of each of the lung fields at full expiration to that at full inspiration for each level. We designated this the E/I ratio. We then examined the relationship between the findings acquired by each of these two methods and pulmonary function test results. The visual score showed correlations with FEV1(% predicted) (-0.592, p < 0.0001), RV/TLC(%)(0.425, p < 0.025), and DL(CO)/VA(% predicted)(-0.538, p < 0.0001). The E/I ratio showed correlations with FEV1(% predicted) (-0.620, p < 0.0001), RV/TLC(%)(0.661, p < 0.0001), and DL(CO)/VA(% predicted) (-0.299, p < 0.05). Compared with the E/I ratio, the visual score showed much higher correlation with DL(CO)/VA(% predicted), but the E/I ratio showed stronger correlation with RV/TLC(%) than did the visual score. The visual score may reflect the degree of emphysema, whereas the E/I ratio reflects the air trapping. These findings suggest that the helical CT is useful in the evaluation of emphysematous changes and that the E/I ratio reflects the air trapping.

Aged↗
PubMed1998

Long-term risk of emphysema in patients with farmer's lung and matched control farmers.

We evaluated the long-term outcome of farmer's lung (FL) patients and matched control farmers using high-resolution computed tomography (HRCT). The study population consisted of 88 FL patients and 83 control farmers, matched by age, sex, and smoking habits. The mean time after the first diagnosed episode of FL was 14 yr. The great majority, 82%, of the studied subjects were nonsmokers. Clinical studies included HRCT, spirometry, and pulmonary diffusing capacity. Emphysema was found significantly more often (23%) in FL patients than in control farmers (7%) (p = 0.006). The presence of emphysema was 18% in nonsmoking and 44% in smoking FL patients, the respective values being 4% and 20% in control farmers. Patients with recurrent attacks of FL tended to have emphysema more often (p = 0. 08) than patients who had experienced only a single attack. Fibrosis was observed in 17% of the FL patients and in 10% of the control farmers (p = 0.2). Miliary changes were found in 12% of the FL patients compared with 4% of the control farmers (p = 0.07). Both emphysematous and fibrotic but not miliary changes correlated significantly with impaired pulmonary function. In conclusion, farmer's lung disease seems to be associated with an increased risk of developing emphysema.

Age Factors↗
PubMed1998

Pseudophysiologic emphysema resulting from severe small-airways disease.

Loss of lung elastic recoil causing hyperinflation with increased TLC and decreased diffusing capacity and expiratory airflow are physiologic hallmarks of emphysema. We studied lung mechanics in 10 patients (seven men and three women) aged 69 +/- 9 yr (mean +/- SD) who had fixed, severe expiratory airflow limitation with a mean FEV1 = 0.73 +/- 0.1 L (mean +/- SD) (32 +/- 7% predicted) and lung computed tomographic picture grade score <= 20, indicating no or trivial emphysema. Three patients died, in whom whole-lung emphysema scores were 15 each and small airways were abnormal. Marked hyperinflation was present in all 10 patients studied, with TLC 7.3 +/- 1.1 L (140 +/- 12% predicted); FRC 5.6 +/- 0.8 L (177 +/- 30% predicted); and RV 5.2 +/- 0.8 L (242 +/- 28% predicted). Diffusing capacity of carbon monoxide (DLCO was reduced, at 12 +/- 6 ml/min/mm Hg (61 +/- 29% predicted). The pressure-volume curves of the lung were markedly abnormal. Pst(L) at TLC was 11.6 +/- 1.4 cm H2O. Transdiaphragmatic pressure (Pdi) in five patients was 66 +/- 13 cm H2O. These results indicate that severe small-airways disease with no or trivial emphysema may cause a spurious reduction in diffusing capacity as well as severe loss of lung elastic recoil resulting in marked hyperinflation, increased TLC, and decreased Pdi and expiratory airflow.

Aged↗
PubMed1999

Cellular and connective tissue changes in alveolar septal walls in emphysema.

Emphysema is commonly defined as enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls, but without obvious fibrosis. Morphometric techniques were used to correlate changes in components of the alveolar septa surrounding enlarged airspaces in human emphysema with the mean linear intercept (Lm) of those airspaces. Alveolar and capillary surface density decreased with increased Lm, but the ratio of these surface densities to each other remained close to normal for mild to moderate increases in Lm. This suggests that the decreased gas exchange observed in emphysema is initiated by a total loss of septa and not by selective pathological changes of the microvasculature. Increases in septal wall thickness directly correlated with increases in Lm. For the mild to moderate emphysema lesions included in this study, an increase of 100% in Lm correlated with a 130% increase in the relative volume of the alveolar septal interstitium. Significant increases occurred in both elastin (0.14 to 0.56 microm(3)/microm(2) basement membrane [BM]) and collagen (0.49 to 1. 63 microm(3)/microm(2) BM). The increase in elastin and collagen raises the possibility of a remodeling process in the connective matrix in alveolar walls. Whether or not the new connective tissue represents a disordered, nonfunctional regional response needs to be determined.

Aged↗
PubMed2000

Altered glutamate metabolism is associated with reduced muscle glutathione levels in patients with emphysema.

Chronic obstructive pulmonary disease (COPD) is often characterized by an impaired skeletal muscle energy metabolism, which is at least partly related to chronic hypoxia and a reduced diffusing capacity. We have found that muscle glutamate (Glu), which is negatively influenced by these conditions, was reduced in patients with severe COPD. The aim of this study was to investigate whether the reduced intracellular Glu level in patients with emphysema is associated with an increased muscle glycolytic metabolism. Since Glu is an important substrate in the synthesis of glutamine (Gln) and glutathione (GSH), the influence of Glu status on muscle GSH and Gln was also examined. In 13 patients with emphysema and 25 control patients, arterial blood and biopsies from the vastus lateralis muscle were obtained. Expressed as a percentage of the control values, the patients with emphysema had reduced values for muscle Glu (64 +/- 12%; p < 0.001), GSH (76 +/- 23%; p < 0.01), and Gln (93 +/- 5%; p < 0.01), and higher values for lactate (p < 0.01) and pyruvate (p < 0.05). No differences were found in plasma values. Muscle Glu was highly associated with GSH (R(2) = 0.61; p < 0.001), but not with Gln. This study illustrates that reduced Glu levels in skeletal muscle of patients with emphysema are possibly related to an enhanced glycolytic activity and associated with decreased GSH levels.

Biomarkers↗
PubMed2001

Roles of mechanical forces and collagen failure in the development of elastase-induced emphysema.

Emphysema causes a permanent destruction of alveolar walls leading to airspace enlargement, loss of elastic recoil, decrease in surface area for gas exchange, lung hyperexpansion, and increased work of breathing. The most accepted hypothesis of how emphysema develops is based on an imbalance of protease and antiprotease activity leading to the degradation of elastin within the fiber network of the extracellular matrix. Here we report novel roles for mechanical forces and collagen during the remodeling of lung tissue in a rat model of elastase-induced emphysema. We have developed a technique to measure the stress-strain properties of tissue sections while simultaneously visualizing the deformation of the immunofluorescently labeled elastin-collagen network. We found that in the elastase treated tissue significant remodeling leads to thickened elastin and collagen fibers and during stretching, the newly deposited elastin and collagen fibers undergo substantially larger distortions than in normal tissue. We also found that the threshold for mechanical failure of collagen, which provides mechanical stability to the normal lung, is reduced. Our results indicate that mechanical forces during breathing are capable of causing failure of the remodeled extracellular matrix at loci of stress concentrations and so contribute to the progression of emphysema.

Analysis of Variance↗
PubMed2001

Amplification of inflammation in emphysema and its association with latent adenoviral infection.

This study examines the hypothesis that the cigarette smoke-induced inflammatory process is amplified in severe emphysema and explores the association of this response with latent adenoviral infection. Lung tissue from patients with similar smoking histories and either no (n = 7), mild (n = 7), or severe emphysema (n = 7) was obtained by lung resection. Numbers of polymorphonuclear cells (PMN), macrophages, B cells, CD4, CD8 lymphocytes, and eosinophils present in tissue and airspaces and of epithelial cells expressing adenoviral E1A protein were determined using quantitative techniques. Severe emphysema was associated with an absolute increase in the total number of inflammatory cells in the lung tissue and airspaces. The computed tomography (CT) determined extent of lung destruction was related to the number of cells/m(2) surface area by R(2) values that ranged from 0.858 (CD8 cells) to 0.483 (B cells) in the tissue and 0.630 (CD4 cells) to 0.198 (B cells) in the airspaces. These changes were associated with a 5- to 40-fold increase in the number of alveolar epithelial cells expressing adenoviral E1A protein in mild and severe disease, respectively. We conclude that cigarette smoke-induced lung inflammation is amplified in severe emphysema and that latent expression of the adenoviral E1A protein expressed by alveolar epithelial cells influenced this amplification process.

Adenoviridae Infections↗
PubMed2002

A pilot study of all-trans-retinoic acid for the treatment of human emphysema.

Emphysema results from progressive destruction of alveolar septae and was considered irreversible until all-trans-retinoic acid (ATRA) was shown to reverse anatomic and physiologic signs of emphysema in a rat model. To evaluate the feasibility of ATRA as a clinical therapy, 20 patients with severe emphysema were enrolled into a randomized, double-blind, placebo-controlled pilot study. Participants included 16 male and 4 female former smokers, two with alpha(1)-antitrypsin deficiency. Patients were treated with either 3 mo of ATRA (50 mg/m(2)/d) or 3 mo of placebo, followed by a 3-mo crossover phase. Plasma drug levels were followed and outcome measures included serial pulmonary function tests, blood gases, lung compliance, computed tomography (CT) imaging, and quality of life questionnaires. In general, treatment was well tolerated and associated with only mild side effects including skin changes, transient headache, hyperlipidemia, transaminites, and musculoskeletal pains. Plasma drug levels varied considerably between subjects and decreased significantly over time in 35% of the participants. Physiologic and CT measurements did not change appreciably in response to therapy. We conclude that ATRA is well tolerated in patients with emphysema, and trials evaluating higher doses, longer treatment, or different dosing schedules are feasible.

Aged↗
PubMed1987

High resolution computed tomography of inflation-fixed lungs. Pathologic-radiologic correlation of centrilobular emphysema.

Centrilobular emphysema (CLE) is a disease defined pathologically. Assessment of the accuracy of high resolution computed tomography (CT) in the diagnosis of centrilobular emphysema has been hampered by a lack of pathologic correlation. We applied high resolution computed tomography to 20 postmortem lung specimens fixed by a method that allows for direct one-to-one pathologic-radiologic correlation. The degree of centrilobular emphysema was assessed radiologically on a visual grading system based on nonperipheral low-attenuation areas. The lungs were then sectioned along the plane of the CT image, and the degree of centrilobular emphysema was graded pathologically by scoring against a panel of standards. A significant correlation (r = 0.91, p less than 0.005) was found between the pathologic grade and the in vitro CT score.

Histological Techniques↗
PubMed1988

CT measurements of lung density in life can quantitate distal airspace enlargement--an essential defining feature of human emphysema.

We used a computerized microscopic image analysis system to directly measure the surface area of distal air spaces in methacrylate-embedded blocks randomly selected from inflation-fixed lobes that were resected from 45 patients as treatment of their peripheral lung tumors. In 28 of these patients, a preoperative computer tomography (CT) scan, at 6 and 10 cm below the sternal notch, was used to generate frequency histograms of CT numbers (measured as EMI units), a measure of lung density, in pixels from the lung or lobe that was subsequently resected. A similar CT number histogram was also derived from the lateral two fifths of the area of lobe/lung that was to be resected. The EMI unit that defined the lowest fifth percentile of this latter histogram correlated (n = 28, r = -0.77, p less than 0.001) with the mean value of the surface area of the walls of distal airspaces per unit lung volume (AWUV) in the five 1 mm x 1 mm microscopic fields with the lowest AWUV values, out of the 20 to 35 such fields examined in each patient. In the 34 of the 45 patients in whom we also measured volume-corrected diffusing capacity (DLCO/VA), this also correlated (n = 34, r = 0.84, p less than 0.001) with this value of AWUV, which measures the surface area of airspaces distal to the terminal bronchioles--reflecting an increase in airspace size, a defining characteristic of emphysema. However, a low DLCO/VA is nonspecific, whereas an abnormally low regional lung density is more likely to be specific for emphysema. In addition, highlighting those pixels of the CT display with low CT numbers (i.e., EMI units -500 [air] to -450, where zero = water) can locate areas of macroscopic emphysema, as shown by subsequent pathologic examination. Thus the quantitative CT scan can diagnose, quantitate, and locate mild to moderate emphysema, in humans, in life, noninvasively.

Aged↗
PubMed1989

Unilateral lung transplantation in end-stage pulmonary emphysema.

Patients with end-stage pulmonary emphysema are usually proposed for either heart-lung or double-lung transplantation. The single-lung transplantation is reversed for patients with pulmonary fibrosis. Patients with emphysema are thought to be unsuitable for single-lung transplantation because of the ventilation-perfusion imbalance that is supposed to occur, the ventilation being preferentially distributed to the native lung when the perfusion is distributed to the transplanted lung. We now report a preliminary success with single-lung transplantation in two consecutive patients with end-stage pulmonary emphysema. Despite the persistence after transplantation of an obstructive syndrome, the clinical status was good, the blood gases were markedly improved, and ventilation-perfusion imbalance did not occur on lung scans. After discharge from the hospital, the patients could return to an almost normal life. Thus, our data support the feasibility of single-lung transplantation in patients with end-stage pulmonary emphysema, and we consider that single-lung transplantation could be the optimal form of lung transplantation in these patients.

Humans↗
PubMed1990

The antielastase screen of the lower respiratory tract of alpha 1-proteinase inhibitor-sufficient patients with emphysema or pneumothorax.

The present study was aimed at testing whether alpha 1-proteinase inhibitor-sufficient patients with lung emphysema or idiopathic spontaneous pneumothorax have an impaired antielastase protection at the lung alveolar level. We have collected bronchoalveolar lavage fluids (BALF) from 20 PIMM emphysematous patients (44 +/- 12 yr), 24 patients with pneumothorax but no radiologic evidence of emphysema (30 +/- 11 yr), 32 healthy subjects (27 +/- 6 yr), and 56 patients with sarcoidosis (30 +/- 11 yr). The BALF were assayed for immunoreactive albumin, alpha 1-proteinase inhibitor (alpha 1PI), leukocyte elastase-alpha 1PI complex (LE-alpha 1PI), and mucus proteinase inhibitor (MPI) as well as for porcine pancreatic elastase inhibitory capacity, a measure of active alpha 1PI. The healthy subjects and the patients with emphysema or pneumothorax had comparable levels of total and active alpha 1PI and total MPI. In contrast, the levels of LE-alpha 1PI complex were elevenfold higher in patients with emphysema than in normal subjects (p = 0.021) and tended to increase with the severity of the disease because they were negatively correlated with FEV1/FVC% (r = -0.55; 0.05 less than p less than 0.1). They did not vary with age in a population of patients with sarcoidosis (r = 0.03), suggesting that their eleven-fold increase in emphysematous patients is not related to the age of these subjects. Patients with pneumothorax had levels of LE-alpha 1PI complex that did not significantly differ from those of normal subjects (p = 0.24).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of nitrendipine and hypoxia on pulmonary vascular resistance in experimental emphysema.

We evaluated the hemodynamic effects of nitrendipine, a dihydropyridine Ca2+ channel blocker, and hypoxia in intact dogs with emphysema produced by treatments with aerosolized papain. We also determined the effects of emphysema, chronic Ca2+ channel blocker treatment, and acute hypoxia on the distribution of vascular resistance in isolated left lower lobes. Pulmonary vascular resistance was increased (4 +/- 1 mm Hg/L/min) in the animals studied 6 months after receiving 4 weekly treatments with papain compared with control animals (2.6 +/- 0.6 mm Hg/L/min, p less than 0.05), and this effect of emphysema was blunted with chronic nitrendipine, 3 mg/kg twice a day (3.1 +/- 0.9 mm Hg/L/min). Both at baseline and at 6 months, hypoxia-induced increases in pulmonary vascular resistance were abolished by nitrendipine. The total pulmonary pressure gradient (delta Pt) was partitioned into pressure gradients across arterial (delta Pa), middle (delta Pm), and venous (delta Pv) vessels by occlusions performed during normoxia (PIO2 = 200 mm Hg) and hypoxia (PIO2 = 30 mm Hg). Papain-treated animals had elevated delta Pt compared with that in control animals because of an increased delta Pv (9.7 +/- 1.1 mm Hg versus 5.2 +/- 0.4 mm Hg in control animals, p less than 0.05). In contrast, only delta Pm was increased with papain + nitrendipine (2.6 +/- 1.0 mm Hg versus 0.2 +/- 0.3 mm Hg in control animals, p less than 0.05). An increase in the downstream pressure gradient was also observed when lobes from animals with emphysema were studied under conditions of reverse perfusion. Hypoxic responses were similar in the control and papain groups, with increases in delta Pa and delta Pm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Covalently linking a peptidyl carbamate elastase inhibitor to a hydrophilic polymer increases its effectiveness in preventing emphysema and secretory cell metaplasia in the hamster.

A peptidyl carbamate, p-nitrophenyl N-(succinyl-L-alanyl-L-alanyl-L-prolyl-methyl)-N-isopropylcarbamate++ + (PCI) was tested for its ability to inhibit the elastolytic activity of human neutrophil elastase (HNE) and to prevent HNE-induced emphysema and secretory cell metaplasia in the hamster. In vitro, 50% of the elastolytic activity of 10 micrograms of HNE was inhibited by 0.9 micrograms of PCI, a molar ratio of PCI to HNE of 4.5. Bronchoalveolar lavage of hamsters receiving PCI intratracheally showed a rapid decrease in HNE inhibitory activity (4 min for 50% decrease), suggesting rapid clearance, binding, or inactivation of the PCI. Instillation of 300 micrograms of HNE combined with 100, 500, or 3,000 micrograms PCI, a 16-, 83-, and 503-fold molar excess of PCI, respectively (molar ratios of 17, 84, and 504), suppressed HNE-induced lung hemorrhage, but it did not moderate HNE-induced emphysema despite the large molar excess of inhibitor. When PCI was covalently bound to a linear hydrophilic polymer of alpha,beta-poly[N(2-hydroxyethyl)-D,L-aspartamide], producing a polymer-bound carbamate inhibitor (PPCI) of HNE, the time for a 50% decrease of PPCI functional activity from the hamster lung lavage was 421 min. Instillation of 100 micrograms of PPCI 1 h before instillation of 300 micrograms HNE resulted in significant amelioration of emphysema; 900 micrograms of PPCI was required to obtain amelioration of bronchial secretory cell metaplasia. The larger dose of PPCI also provided significant amelioration of emphysema when the interval between PPCI and HNE administration was 8 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Inhibition of lipopolysaccharide-induced pulmonary emphysema by intratracheally instilled recombinant secretory leukocyte proteinase inhibitor.

Experiments were performed to test whether recombinant secretory leukocyte proteinase inhibitor (rSLPI) was able to prevent the development of lipopolysaccharide (LPS)-mediated pulmonary emphysema, hemorrhage, and secretory cell metaplasia (SCM) in hamsters. Several groups of eight animals were intratracheally treated for four weeks, twice a week with 0.5 mg Escherichia coli LPS or with saline. In the first experiment, an additional group of eight hamsters was treated with 0.5 mg LPS mixed with 0.5 mg rSLPI, and the animals received another instillation of 0.5 mg rSLPI 7 h later. In the second experiment, 0.5 mg LPS, mixed with 1 mg rSLPI, was given while additional instillations of 1 mg rSLPI were performed 7 h and 31 h after the first dosage. In the third experiment, 0.5 mg LPS, mixed with 0.5, 1.5, or 3.0 mg rSLPI, was given while additional instillations of 0.5, 1.5, and 3.0 mg rSLPI, respectively, were performed 24 h and 48 h after the first dosage. Hamster lungs were examined for emphysema, hemorrhage, and SCM. In all three series of experiments, we observed a significant inhibition of LPS-mediated emphysema by rSLPI. This inhibition tended to be dose related. Inconclusive results were obtained on the inhibition of LPS-mediated hemorrhage. The development of LPS-mediated SCM was not affected by rSLPI. The LPS-mediated polymorphonuclear leukocyte (PMN) influx did not change when administrations of rSLPI were given additionally. We conclude that rSLPI is able to diminish significantly the development of LPS-mediated pulmonary emphysema in hamsters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Inactivation of alpha 1-proteinase inhibitor by alveolar inflammatory cells from smoking patients with or without emphysema.

The aim of this study was to evaluate the ability of alveolar inflammatory cells recovered by bronchoalveolar lavage from the lower respiratory tract of 17 smoking patients with or without emphysema to inactivate alpha 1-proteinase inhibitor (alpha 1-Pl). The presence of emphysema was determined and quantified using CT scan and was evidenced in 8 patients (Group 1), whereas 9 patients exhibited a normal CT scan (Group 2). Patients with emphysema had lower values of FEV1, DLCO, and resting PO2 and higher values of RV/TLC ratio than patients without emphysema. BAL analysis showed a higher percentage of neutrophils and of myeloperoxidase (MPO) in BAL fluid in Group 1 than in Group 2. Alveolar inflammatory cells stimulated or not with phorbol myristate acetate (PMA) were incubated for 45 min with purified alpha 1-Pl, and the results were expressed as a percentage of inactivation of alpha 1-Pl as evaluated by its inhibitory activity against porcine pancreatic elastase or human neutrophil elastase. In Group 2, unstimulated alveolar inflammatory cells inactivated only 3.3 +/- 0.7% alpha 1-Pl and stimulated cells inactivated only 5.4 +/- 1.1% alpha 1-Pl. In marked contrast, in Group 1, a significant loss of the antielastase function of alpha 1-Pl was observed (p < 0.001) when alpha 1-Pl was incubated with unstimulated cells (24.2 +/- 8.9%) or stimulated cells (35 +/- 8.9%) from Group 1. The addition of catalase to the cell suspension was associated with a significant decrease in the inactivation of alpha 1-Pl (from 35 +/- 8.9 to 10.2 +/- 1.2%, Group 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchoalveolar Lavage Fluid↗
PubMed1976

Mechanisms of maximal expiratory flow limitation in clinically unsuspected emphysema and obstruction of the peripheral airways.

We studied the determinants of maximal expiratory flow in 7 patients in whom surgical lung specimens showed evidence of mild emphysema or obstruction of the peripheral airways. All the patients showed frequency dependence of dynamic lung compliance and low maximal expiratory flow. Lung elastic recoil pressures were reduced at all lung volumes in 4 of 5 patients with emphysema but were normal in 2 patients with obstruction of the peripheral airways. Maximal flow-static recoil curves showed a high intercept in the pressure axis when the slope between 50 per cent and 30 per cent of vital capacity was extrapolated to zero flow (transmural pressure in the flow-limiting segment) in all patients. The slope of these curve represents the conductance of the segment that extends from the alveoli to the flow-limiting segment and includes the latter. Conductance of this segment was higher than normal in 4 patients with emphysema and borderline low in one, and low in one patient with obstruction of the peripheral airways and borderline low in the other. Increased transmural pressure in the flow-limiting segment was interpreted as being due to peripheral location of collapsible flow-limiting segment and, in part, limiting maximal expiratory flow. The results also suggested that flow limitation in emphysema may occur without physiologic evidence of increased resistance of peripheral airways when, in fact, bronchiolitis is present on histologic examination.

Adult↗