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At least 19 recordsLinked to original sources
PubMed1976

The scanning electron microscopy of elastase-induced emphysema. A comparison with emphysema in man.

Emphysema was produced in hamsters by a single intratracheal injection of 25 units of porcine pancreatic elastase. The lungs were examined by scanning electron microscopy at intervals from 24 hours to 1 year after the injection, and the appearance was compared to examples of human emphysema. Within 24 hours of injection, the alveolar ducts were dilated and air spaces were of more variable size than normal. Fibrin strands, erythrocytes and phagocytic cells were present in air spaces. By a week the hemorrhage and exudate had resolved, but adnormal air spaces continued to enlarge over the period of study. The abnormal airspaces formed by progressive dilation of alveolar ducts with shortening and occasionally effacement of interalveolar septa. Interalveolar pores were occasionally enlarged but only focally increased in number. The appearance of single examples of human congenital lobar emphysema and panlobular emphysema resembled the animal model. Abnormal air spaces were formed by dilated alveolar ducts with retraction of interalveolar septa. In contrast, in some cases of centrolobular emphysema marked fenestration of alveolar septa occurred and large air spaces were often traversed by threadlike strands of tissue remnants of some preexisting alveolar walls. The results suggest that there are at least two morphogenetic processes leading to emphysema. One is the coalescence of fenestrations leading to destruction of alveolar walls, and the other is a gradual remodeling of lung structure by mechanisms still to be defined.

Adult↗
PubMed1977

[Pulmonary emphysema. Changes in the pulmonary function of experimentally induced emphysema].

By intratracheal injection of the protease papain to experimental animals parenchymal changes in the lung can be induced, that resemble human emphysema. Papain (dosage 26 to 112 mg, 1 to 4 injections) was given intratracheally to 8 bastard dogs (weighing from 12.5 to 20 kg) during light general anesthesia. Pulmonary function was assessed in weekly intervals and related to morphologic changes in the lung. Static compliance of the lung and FRC measured during respiratory arrest were increased after papain, bronchial resistance, measured while artifically ventilated at constant pressure was also increased. Changes of static lung compliance and FRC were seen after the first administration of papain, but further increased with time of observation and after multiple doses of papain. Increase of resistance was not found before 5 weeks. At quiet breathing resistance was not increased at all. No significant changes were found of arterial pO2 and pCO2, pH, standard and actual bicarbonate, diffusion capacity for O2, tidal volume, minute ventilation and ventilatory rate. Morphological findings confirmed the changes described by others. Pulmonary function appears to be pathological at a time when morphology still seems to be normal. The question is discussed to what extent the model of experimental emphysema induced by proteolytic enzymes can contribute to the understanding of human pulmonary emphysema. Lung function in the course of experimental emphysema is compared with function in different clinical types of emphysema.

Acid-Base Equilibrium↗
PubMed1978

Protease-induced experimental emphysema: the relationship between elastolytic activity and emphysema induction.

Induction of experimental emphysema by protease was performed with several proteases both in vivo and in vitro to compare the ability of inducing emphysematous change and their elastolytic activity. The following results were obtained. 1) Only elastase and papain have emphysema inducing capacity. Emphysematous changes induced by elastase in vitro were dose dependent. But papain has no genuine elastolytic activity. Nature of the emphysema-inducing capacity of papain remains obscure. 2) Advantages of using the isolated lung for experiment were discussed, especially for the small dose required for enzyme-instillation. Moreover, there is no interferencey by endogeneous enzyme or protease-inhibitors. 3) Guinea pig is useful for the experiemnt of emphysema-induction both in vivo and in vitro. Minimal requirement of elastase is 50 microgram in vitro and 250 microgram for in vivo experiment.

Animals↗
PubMed1978

Radiographic appearance of the chest in emphysema.

Accuracy of the radiologic diagnosis of emphysema was assessed in 696 patients from whose lungs paper-mounted whole-lung sections had been made. Emphysema was diagnosed radiographically primarily on the basis of arterial deficiency. In addition, lung length, lung width, size of the retrosternal space, heart size, and diaphragm position were recorded from the chest films. Recognition of emphysema was poor when radiographs of inadequate quality were included (anteroposterior films or films from patients with acute or chronic lung disease). When these films were excluded, only occasional radiographs from patients without emphysema or with mild emphysema were thought to have emphysema radiologically. Of the patients with moderately severe and severe emphysema, 41% were diagnosed as having emphysema, as were two-thirds of those with the most severe grade of emphysema. For a given grade of emphysema, the radiologic diagnosis of emphysema was made more frequently when patients had severe chronic airflow obstruction. Emphysema was usually most severe in the zones of the lung in which emphysema was radiologically apparent. Centrilobular emphysema was usually present when emphysema was diagnosed radiologically in the upper zones of the lung, and panacinar emphysema was usually present when emphysema was diagnosed in the lower zones. Lung length and the size of the retrosternal space increased, the level of the diaphragm lowered, heart size decreased, and lung width was unchanged as emphysema became more severe. Lung length and diaphragm level were the most discriminating measurements, followed by size of the retrosternal space. No combination of radiologic variables was found that recognized emphysema better than the subjective diagnosis of emphysema based on arterial deficiency. Radiologic lung dimensions are related to stature; for given stature these measurements are larger in men and women.

Diagnostic Errors↗
PubMed1991

Emphysema type in relation to silica dust exposure in South African gold miners.

The relationship between silica dust exposure in gold mines and the type of emphysema was studied in a group of 1,553 white gold miners who had undergone autopsy examination between 1974 and 1987. Of particular interest was the contrast between centriacinar and panacinar emphysema as they relate to silica exposure and the presence of silicosis. Subjects with significant emphysema, that is, with an emphysema score of 30% or more, were classified as having predominantly panacinar or predominantly centriacinar emphysema, and compared to those without emphysema (emphysema score less than or equal to 10%). Of those who had significant emphysema (greater than or equal to 30%), 24% had predominantly panacinar, 43% predominantly centriacinar, and 33% were classified as mixed. The odds ratios (OR) for the association between each emphysema type and dust exposure (one unit of the cumulative dust index) were found to be statistically significant and of equal magnitude [1.019, with a 95% confidence interval (CI) of 1.005 to 1.033 for panacinar and 1.019 with a 95% CI of 1.007 to 1.031 for centriacinar emphysema]. In 163 nonsmokers insignificant panacinar emphysema was more common than centriacinar emphysema. The results indicate that a miner with 20 yr in high-dust occupations has a 3.5 (1.7;6.6) times higher odds of having a significant degree of emphysema at autopsy than a miner not in a dusty occupation. This is likely to be true of smoking miners only because there were only four nonsmokers with an emphysema score between 30 and 40%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Microscopic and macroscopic measurements of emphysema: relation to carbon monoxide gas transfer.

BACKGROUND: Studies of the relation between the severity of structural change in emphysema and physiological abnormality have been based on macroscopic assessments, which have not been truly quantitative or sensitive enough to detect early changes. With a highly reproducible method for measuring emphysema using histological sections and a semiautomatic image analysis system, this quantitative assessment of emphysema was compared with a semiquantitative macroscopic assessment of emphysema and measurements of carbon monoxide gas transfer. METHODS: Microscopic and macroscopic measurements of emphysema on 44 thoracotomy specimens were compared; only two were from non-smokers. Airspace wall surface area per unit volume was measured microscopically with an automatic image analyser and expressed as both the mean airspace wall surface area per unit volume and the mean value of the five fields with the lowest values. Macroscopic emphysema was measured directly on a tracing of the midsagittal slice using a digitising tablet attached to a microcomputer and expressed as a percentage of the total area of lung. In cases with centriacinar emphysema the number of discrete lesions was counted. RESULTS: The area of macroscopic emphysema ranged from 0 to 78% of the total area of lung examined, but most patients had less than 1% involvement so that the distribution was highly skewed. Both mean airspace wall surface area per unit volume and the mean of five fields with the lowest airspace wall surface area per unit volume were normally distributed, with mean airspace areas ranging from 8.8 to 25.4 mm2/mm3 (mean 18.1 mm2/mm3). In lobes with centriacinar emphysema the number of discrete lesions correlated with airspace wall surface area per unit volume and with preoperative carbon monoxide transfer factor (TLCO) per unit lung volume. However, other measurements of macroscopic emphysema did not correlate with loss of alveolar wall surface area, and there was considerable overlap between subjects with no or minimal macroscopic emphysema and those with more severe disease. TLCO correlated with both mean airspace wall surface area per unit volume and the mean of five fields with the lowest airspace wall surface area per unit volume but not with the severity of macroscopic emphysema. CONCLUSION: If emphysema is to be quantified it must be measured microscopically; macroscopic measurements do not, in general, reflect the microscopic loss of airspace wall.

Aged↗
PubMed1976

Lung surface area in various morphologic forms of human emphysema.

The relation between lung surface area and the extent and morphologic type of emphysema was examined at autopsy in 69 men. It was found to be conceptually preferable to express the area as internal surface area per unit lung volume (specific surface area) rather than to use the more conventional, inversely related, mean linear intercept for comparison with other morphometric data. In the whole group, fixed inflated lung volume generally increased with increasing per cent involvement of lung parenchyma by emphysema, and total internal surface area decreased, but those changes were not so regular as the decline in specific surface area with increasing per cent emphysema (r=-0.574). Lungs with no emphysema had a significantly higher specific surface area than did lungs with very little emphysema (1 to 9 per cent), suggesting noticeable effects on the physical properties of lung by minimal degrees of this disease at high levels of inflation. The way in which specific surface area decreased with increasing percentage of emphysema was not noticeably different among patients with centrilobular, panlobular, or mixed forms of emphysema, although lungs with only centrilobular emphysema were much more common and had a significantly lower mean percentage of emphysema than did those with only panlobular emphysema; the prevalence and mean percentage of emphysema of the mixed group were intermediate. These observations, coupled with the association of older mean age with increasing percentage of emphysema, were interpreted as support for the concept that many examples of panlobular emphysema are derived from confluence of extensive centrilobular emphysematous lesions.

Adult↗
PubMedDate not supplied

Alpha 1-proteinase inhibitor and mucus proteinase inhibitor in human lung emphysema.

The role of the antiproteases alpha 1-proteinase inhibitor (alpha 1PI) and mucus proteinase inhibitor (MPI) in human lung emphysema was investigated by measuring their amount and functional activity against trypsin, leukocyte elastase, and pancreatic elastase in the bronchoalveolar lavage fluid (BALF). In addition, leukocyte elastase was quantified in the lavage samples by measuring the concentration of the elastase-alpha 1PI-complex. The study population consisted of 38 patients (5 nonsmokers, 8 former smokers, 25 smokers) with acquired emphysema (i.e., emphysema which is not caused by alpha 1PI deficiency), and 44 individuals (16 nonsmokers, 8 former smokers, 20 smokers) without emphysema. No differences were found between patients with and without emphysema in the activities of alpha 1PI and MPI, or in the concentration of alpha 1PI. The concentration of MPI was significantly higher in the BALF of patients with emphysema than in that of patients without emphysema (p = 0.025). A significantly higher concentration of elastase-alpha 1PI complex was found in patients with emphysema than in those without emphysema (p = 0.041). This finding could reflect the higher proteinase burden to which patients with emphysema are exposed. The increase of MPI in lavage fluid of patients with emphysema seems to be the result of increased production in emphysematous lungs. However, it remains unclear why patients develop emphysema while showing an increased content of MPI.

Bronchoalveolar Lavage Fluid↗
PubMed2025

Proteomic discovery analysis of quantitatively assessed emphysema in the general population. The MESA Lung Study.

BACKGROUND: Pulmonary emphysema occurs frequently in older adults, often without airflow limitation. Its presence predicts symptoms, respiratory hospitalizations and deaths, and all-cause mortality. Proteomics may provide further insights into emphysema pathogenesis and inform therapeutic targets. OBJECTIVE: We performed a proteomic discovery analysis of percent emphysema on computed tomography (CT) in a population-based, multiethnic sample from the Multi-Ethnic Study of Atherosclerosis (MESA) Lung Study. Replication was performed in two chronic obstructive pulmonary disease (COPD)-based studies, the SubPopulations and InteRmediate Outcome Measures in COPD Study (SPIROMICS) and the Genetic Epidemiology of COPD (COPDGene) Study. METHODS: MESA recruited participants from the general population in 2000-02. The MESA Lung Study performed full-lung CT scans in 2010-12. Percent emphysema was defined as the percentage of lung voxels&#x2009;<&#x2009;-950 Hounsfield units. Over 7,200 plasma aptamers were measured via SomaScan. Cross-sectional linear and least absolute shrinkage and selection operator (LASSO) regression models were adjusted for demographics, anthropometrics, smoking, renal function, and scanner parameters. Statistical significance was defined as a false discovery rate p-value&#x2009;<&#x2009;0.05. Gene Ontology (GO)/Reactome enrichment analyses were performed. LASSO-selected proteins' predictive performance was evaluated. RESULTS: Among 2,504 participants in the MESA Lung Study, mean age was 69.4&#xa0;years, 1,291 had ever smoked, and median percent emphysema-like lung was 1.4%. In total, 1,234 aptamers were significantly associated with percent emphysema in the MESA Lung Study, and 35 replicated in the SPIROMICS and COPDGene Studies. Novel associations included protein family with sequence similarity (FAM) 177A1, syntenin-2, ubiquitin carboxyl-terminal hydrolase 25, and uncharacterized protein C20orf173. Previously identified emphysema-associated proteins included soluble advanced glycosylation end product-specific receptor (sRAGE), protein S100-A12, high mobility group protein B1, and roundabout homolog 2. Enrichment analyses identified 40 GO biological processes, including chemokine production and regulation and cell-cell adhesion and regulation, and two Reactome pathways, including RAGE signaling. In tenfold cross-validation, novel proteins were largely retained by LASSO (R2&#x2009;=&#x2009;5.4%), improved overall model performance (R2&#x2009;=&#x2009;24.8%), and uniquely explained greater variance in percent emphysema. CONCLUSIONS: This analysis in a general population sample identified novel and previously characterized proteins whose functional roles were validated by GO/Reactome enriched pathways, offering new insights into emphysema pathophysiology and therapeutics.

Humans↗
PubMed1992

Regional distribution of emphysema: correlation of high-resolution CT with pulmonary function tests in unselected smokers.

High-resolution computed tomography (CT) was correlated with pulmonary function tests in the evaluation of regional emphysema in 59 smokers. The lung was divided into upper (above the carina tracheae) and lower (below the carina tracheae) zones, and the degree of emphysema was graded with a subjective and an objective measurement. Functional emphysema was defined as a diffusion capacity less than 75% of predicted and forced expiratory volume in 1 second less than 80% of predicted. Three of 15 (20%) subjects with functional emphysema had no subjective evidence of emphysema at high-resolution CT, and 10 of 25 (40%) with emphysema at high-resolution CT had no functional abnormalities consistent with emphysema. Even though the upper lung zones were more severely affected by emphysema, the degree of emphysema in the lower zones had a stronger correlation with pulmonary function abnormalities. The upper lung zones are a relatively silent region where extensive destruction may occur before functional abnormalities become known.

Aged↗
PubMed1977

"Acquired" lobar emphysema: a complication of respiratory distress in premature infants.

Ten premature infants with respiratory distress developed a type of pulmonary lobar emphysema that is clinically and histologically distinct from interstitial or congenital lobar emphysema. In eight patients emphysema was noted in the right lower lobe, while in two the left upper lobe was affected. Five infants exhibited nonresolution of the emphysema and an inability to be weaned from ventilator support. Lung scans in these five infants showed absent or markedly decreased perfusion of the involved lobe. Lobectomy was necessary. Postoperatively, their respiratory status improved and they were successfully weaned from the ventilator. Five premature infants with identical radiographic emphysematous changes had normal lung scans. These infants did not require lobectomy and were also successfully weaned from the ventilator. Radiographic changes of lobar emphysema in these five infants completely resolved. Pathologic changes in the excised lobes were characteristic of bronchopulmonary dysplasia and obstructive intraalveolar emphysema. The long-term effects of positive pressure ventilation, oxygen, and suctioning techniques directed toward the right lower lobe may play an important role in the etiology of "acquired" lobar emphysema.

Female↗
PubMed1978

Diaphragm and body weight in emphysema.

The weight of the diaphragm has been investigated in 103 male patients and 81 female patients, and the relationship between body weight and emphysema has been assessed in 662 male and 431 female patients. Diaphragm weight is related to body weight in both male (r = + 0.76) and female patients (r = +0.77) and is relatively larger in the former. Dissecting the diaphragm free of fat or freeze drying it does not appreciably improve the relationship between body weight and diaphragm weight. Diaphragm weight is better related to body weight than body length and is diminished in emphysema. Patients with emphysema weigh less. This is apparent with only moderate grades of emphysema, and there is no further loss of body weight as emphysema in the lung becomes more severe. The loss of diaphragm weight not only reflects the loss of body weight that occurs in emphysema, but the diaphragm is also less in weight than predicted from body weight. The diaphragm also appears abnormal on gross inspection in some patients with emphysema. Heart weight and diaphragm weight are related, probably because both are related to body weight.

Airway Obstruction↗
PubMed1991

In vitro release of neutrophil elastase, myeloperoxidase and beta-glucuronidase in patients with emphysema and healthy subjects.

Evidence is accumulating that cigarette smoking plays an important role in the protease-antiprotease imbalance in alpha 1-antitrypsin-sufficient emphysema. Since most smokers, however, do not develop emphysema, it has to be presumed that other factors in addition to smoking contribute to the origin of the imbalance. The major source of proteases is the polymorphonuclear leucocyte (PMN). We tested the hypothesis that an abnormality in the releasability of PMN might predispose for the development of emphysema. Therefore, the release of elastase, myeloperoxidase, and beta-glucuronidase from PMN was investigated in patients with emphysema and healthy controls, matched for sex, age, and smoking habits. PMN were isolated from peripheral blood and stimulated with calcium-ionophore A23187, formyl-methionyl-leucyl-phenylalanine (FMLP), and serum-treated zymosan (STZ). Total enzyme content of PMN was measured after cell lysis with Triton X-100. Total elastase, myeloperoxidase, and beta-glucuronidase content of PMN were not significantly different in healthy subjects and patients with emphysema. In vitro release of elastase and myeloperoxidase from both stimulated and unstimulated PMN was not significantly different in healthy subjects and emphysematous patients. Moreover, no differences were found between smoking and ex-smoking individuals. Beta-glucuronidase release tended to be lower in patients with emphysema than in healthy controls. We conclude that an abnormality in the releasability of peripheral PMN is unlikely to be a pathogenetic factor in emphysema.

Glucuronidase↗