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PubMed2005

In vivo assessment of emphysema in mice by high resolution X-ray microtomography.

High resolution X-ray microtomography (micro-CT) was used for the detection of emphysema in live mice. Emphysema was induced in C57BL/6 J mice by intratracheal instillation of different amounts of porcine pancreatic elastase. This emphysema could be clearly detected by micro-CT seven weeks post-treatment: analysis of the whole data set of virtual cross-sections showed the presence of a dose-dependent level of emphysema.

Animals↗
PubMed1975

Emphysema in Papua New Guinea--a pathological study.

The authors examined 47 lungs obtained at post mortem in Papua New Gunea. These were inflated with formalin, fixed under pressure, sliced and examined for emphysema using a "point-counting" method. There was no emphysema before the age of 30 years. The pathological types encountered were similar to those in the United Kingdom. In patients over 50 years of age there appeared to be little difference between the amount of emphysema present in Paua New Guinea and in the United Kingdom. Enviromental air pollution seemed to be relatively unimportant in the pathogenesis. Repeated lower respiratory tract infections may be more important. Emphysema appeared to be more prevalent in lowland than highland dwellers. The findings of this pathological study supported the clinical and epidemiological studies carried out concurrently, but independently by others.

Adolescent↗
PubMed2006

Subcutaneous emphysema after dental treatment: a case report.

Subcutaneous emphysema is the condition in which air or other gases penetrate the skin and submucosa causing soft-tissue distention. This type of emphysema may be traumatic, iatrogenic or may occur spontaneously. This report describes the youngest case of subcutaneous emphysema related to dental treatment that has been documented to date. In addition to the patient's age, the case is of interest because subcutaneous emphysema is a rare complication of dental therapy.

Anesthesia, Dental↗
PubMed2006

Autologous transplantation of adipose tissue-derived stromal cells ameliorates pulmonary emphysema.

Adipose tissue is a useful tool for management of most complex cardiothoracic problems, including the reinforcement of damaged lungs, and adipose tissue-derived stromal cells (ASCs) have been suggested to secrete hepatocyte growth factor (HGF), a multipotent regenerative factor that contributes to the repair process after lung injury. The goal of this study was to demonstrate the therapeutic impact of autologous transplantation of ASCs through HGF supplementation for the enhancement of alveolar repair in a rat model of emphysema. ASCs were isolated from inguinal subcutaneous fat pads and characterized by flow cytometry. Cultured ASC were found to secrete significantly larger amounts of HGF (15 112 +/- 1628 pg per 10(6) cells) than other angiogenic factors. Transplantation of ASCs into elastase-treated emphysema models induced a significant increase in endogenous HGF expression in lung tissues with a small amount of increase in other organs, with the high levels lasting for up to 4 weeks after transplantation. Further, alveolar and vascular regeneration were significantly enhanced via inhibition of alveolar cell apoptosis, enhancement of epithelial cell proliferation and promotion of angiogenesis in pulmonary vasculature, leading to restoration of pulmonary function affected by emphysema. These data suggest that autologous ASC cell therapy may have a therapeutic potential for pulmonary emphysema, through inducing HGF expression selectively in injured lung tissues.

Adipose Tissue↗
PubMed1985

A necropsy study of Pi phenotypes, emphysema, and smoking.

Pi phenotypes, determined post mortem by isoelectric focusing and immunofixation, emphysema, assessed from inflation fixed specimens and smoking history were correlated in 186 hospital necropsies. It was possible to determine Pi phenotype in 98.4% of the specimens. Phenotype M occurred in 87.5%, MZ in a 8.1%, MS in 2.1% and FM in 0.5%. An expected association was found between smoking and emphysema but not between the Pi phenotypes and emphysema. Thus, while smoking is a major aetiological factor, the Pi MZ heterozygous state does not seem to predispose to structural emphysema. However, the small number of cases did not allow an estimation of the risk of smoking in Pi MZ heterozygous persons compared to those with the normal Pi phenotype.

Adult↗
PubMed1998

Lung morphometry by unbiased methods in emphysema: bronchial and blood vessel volume, alveolar surface area and capillary length.

We have estimated lung volume, bronchial volume, vessel volume, alveolar surface area and capillary length in patients who died of lung failure due to emphysema and chronic obstructive pulmonary disease (COPD) and in patients with no clinical signs of respiratory disease. Unbiased morphometric methods were applied to the right lung. The patients with emphysema had equal lung volumes and bronchial and vessel volumes compared to the control group. The alveolar surface area and surface density were significantly decreased to about 67%, of control values. The capillary length and length density were significantly decreased to about 68% of control values. The proportional decreases in alveolar surface area and capillary length suggest that compensatory capillary proliferation has not occurred. These unbiased morphometric studies of emphysema have yielded results in end-stage emphysema that are comparable to those previously reported using biased methods. However, the unbiased methods may provide new insights when applied to earlier stages of the disease.

Aged↗
PubMed1995

[Pathogenic bacteria isolated from the sputum of the patients with pulmonary emphysema].

Isolated pathogenic bacteria from sputum of the patients with pulmonary emphysema who were admitted in our hospital from 1984 to 1994 were examined to elucidate the relationship between isolated bacteria from sputum and pulmonary functions including vital capacity (VC), forced expiratory volume (FEV1.0), PaO2 and PaCO2. VC of the patients from whom MSSA (methicillin-sensitive Staphylococcus aureus) or Enterococcus faecalis (E. faecalis) were isolated was significantly lower than that of the patients from whom Streptococcus pneumoniae (S. pneumoniae), Branhamella catarrhalis (B. catarrhalis) or Haemophilus influenza (H. influenza) were isolated. FEV1.0 had a similar tendency as VC in terms of isolated organisms from the patients with emphysema. Similarly, PO2 of the patients from whom MSSA or E. cloacae were isolated was significantly lower than that of the patients from whom S. pneumoniae, B. catarrhalis or H. influenzae were isolated, and PCO2 of the patients from whom S. pneumoniae, B. catarrhalis or H. influenza were isolated. There was also impaired respiratory function in the patients from whom MSSA, Escherichia coli (E. coli), Pseudomonas aeruginosa (P. aeruginosa), Xanthomonas maltophilia (X. maltophilia) or Enterobacter cloacae (E. cloacae) were isolated, compared with those in the patients from whom S. pneumonia, B. catarrhalis or H. influenzae were isolated. These results suggest that isolated pathogenic bacteria are shifted from S. pneumoniae, B. catarrhalis or H. influenza to MSSA, E. coli, P. aeruginosa, X. maltophilia or E. cloacae in the course of impairment of respiratory function in pulmonary emphysema. The treatment and prophylaxis for acute exacerbation in pulmonary emphysema should be based on these results.

Bacteria↗
PubMed1971

Pulmonary emphysema and alpha 1-antitrypsin deficiency.

Of 72 patients with radiological evidence of pulmonary emphysema, emphysema occurred either alone or in association with bronchitis in 61, and 8 of these (13%) were found to have alpha(1)-antitrypsin deficiency. The main features of this condition are: exertional dyspnoea of relatively early onset (generally between 30 and 45 years of age), severely impaired FEV(1) and T(L)CO, and radiological emphysema predominantly affecting the lower zones of the lungs. It is probable that any patient with all the above abnormalities has alpha(1)-antitrypsin deficiency. There is evidence to suggest that cigarette smoking may hasten the onset of this type of emphysema.

Adult↗
PubMed1970

Emphysema in coal workers' pneumoconiosis.

A correlation survey has been carried out between the pathological, physiological, and radiological findings pertaining to emphysema in 247 deceased coal miners and ex-miners, most of whom had been diagnosed as suffering from coal workers' pneumoconiosis during life. The pathological findings, which included large lung sections and detailed histology in every case, were compared with similar findings in a contrast non-mining population matched for age and sex.The results indicated that emphysema was much more common among the coal miners, both with simple and with complicated pneumoconiosis, than among the contrast group. In addition the extent of the emphysema as measured by a recognized "counting" method carried out on paper-mounted lung sections was remarkably closely related to ventilatory impairment as evidenced by the forced expiratory volume in one second.Extensive emphysema was more commonly found in those pneumoconiosis cases, both simple and complicated, showing the finer punctiform type of radiological change than in cases showing the larger micronodular and nodular opacities.

Adult↗
PubMed1989

Bronchial gland duct ectasia in fatal bronchial asthma: association with interstitial emphysema.

To determine the incidence of bronchial gland duct ectasia in fatal asthma and its association with interstitial emphysema, the histological features of 72 patients in whom death was considered to be due to asthma, and 72 matched control subjects in whom sudden death was not attributed to asthma, were reviewed. In all cases and controls, sections of two or more blocks of lung tissue stained with haematoxylin and eosin were obtained at necropsy. Bronchial gland duct ectasia was diagnosed if there was more than one abnormally dilated epithelial lined protrusion from a bronchus, extending through the smooth muscle layer. A histological diagnosis of asthma was made if four of the five following criteria were present: mucus plugging, basement membrane thickening, epithelial shedding, submucosal eosinophil leucocyte infiltration and smooth muscle hypertrophy. A histological diagnosis of asthma was made in 53 of 72 clinical cases of fatal asthma and in five of 72 control subjects. Interstitial emphysema was present in 10 clinical cases of fatal asthma, all of whom had bronchial gland duct ectasia and a histological diagnosis of asthma. Interstitial emphysema was not observed in control subjects. It is concluded that bronchial gland duct ectasia is a common histological feature of severe asthma, and that interstitial emphysema may be consequent on rupture of these dilated gland ducts.

Asthma↗
PubMed1980

Maximum volumes in excised human lungs: effects of age, emphysema, and formalin inflation.

The volume of air at a transpulmonary pressure (PL) of 25 cmH2O was measured in 28 emphysema-free and 39 emphysematous excised adult lungs and in the lungs of 53 infants and children. In the adult emphysema-free lungs, this volume (V25) was significantly correlated with body length in males but, corrected for body length, not significantly correlated with age in either males or females. V25 was on the average 20 per cent larger than predicted TLC in non-emphysematous lungs in vivo. The lungs were also inflated and fixed with formalin at a constant PL of 25 cm H2O and their volume measured (VL). Marked and variable underinflation compared to V25 occurred in the adult lungs and VL minus lung weight averaged 75% of V25 and 91% of predicted TLC. In infants and children, the ratio of VL minus lung weight to V25 averaged 1.08 with a range of 0.58 to 1.84. The larger the lungs, the smaller the ratio, suggesting that fixation played a role in producing the small VL. In the emphysematous lungs, a significant correlation between the degree of emphysema and V25 was found. However, a statistically significant increase in V25 only occurred when the emphysema grade was greater than 5.

Adolescent↗
PubMed1993

Automated in vivo quantification of emphysema.

A computer program to automatically determine lung volume and percentage of emphysema from computed tomographic (CT) chest sections was developed. To test it, the authors reviewed scans obtained in 89 patients. Any computer errors in identification of normal or emphysematous lungs were corrected manually by tracing the boundaries of the lungs or eliminating areas of nonemphysematous lung with a roller ball. The corrected values were compared with the uncorrected values. In 33 patients from the study group, lung volumes and the percentage of emphysema were calculated by using a currently available "voxel highlighting" program. Successful computerized analysis of entire lungs was performed in 1 minute, compared to more than 1 hour for manual analysis. Correlation was high (r = .99) between results obtained manually and those obtained with the computer. Although the difference between uncorrected and corrected values of the percentage of emphysema was statistically significant, this converted to a correction of only 0.1%. The computer program allowed quick, accurate, and reproducible quantification of emphysema.

Adult↗
PubMed1994

Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor.

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.

Animals↗
PubMed1999

Effects of depletion of neutrophils or macrophages on development of cigarette smoke-induced emphysema.

The aim of this study was to ascertain the putative roles of neutrophils or macrophages in the pathogenesis of cigarette smoking-induced emphysema on the basis of effects of anti-neutrophil (anti-PMN) antibody or anti-monocyte/macrophage (anti-MoMac) antibody on the development of emphysema in cigarette smoke-exposed rats. Rats were treated with rabbit anti-PMN or anti-MoMac antibody and exposed 7 days/wk for 2 mo to cigarette smoke inhalation; rats treated with nonimmunized rabbit IgG (control antibody) and exposed to cigarette smoke or normal room air served as controls. Antibody treatments began 24 h before the start of smoke or air exposure and was continued with 1 treatment/wk. Total and differential cell counts in bronchoalveolar lavage fluid and collagenase-dissociated lung and determinations of the elastinolytic activity of lung neutrophils or macrophages in [(3)H]elastin-coated wells indicated specific suppression of neutrophil accumulation and neutrophil-related elastinolytic burden in the lungs of the anti-PMN antibody-treated smoke-exposed rats, in contrast to specific suppression of macrophage accumulation and macrophage-related elastinolytic burden in the lungs of the anti-MoMac antibody-treated smoke-exposed rats. Cigarette smoke exposure-induced lung elastin breakdown (quantitated by immunologic assay of levels of elastin-derived peptides and desmosine in lavage fluid) and emphysema in the lungs (based on morphometric analysis of alveolar mean linear intercepts and alveolar tissue density in fixed lungs) were not prevented in the lungs of anti-PMN antibody-treated smoke-exposed rats but was clearly prevented in lungs of the anti-MoMac antibody-treated smoke-exposed rats. These findings implicate macrophages rather than neutrophils as the critical pathogenic factor in cigarette smoke-induced emphysema.

Animals↗
PubMed1975

Elastic behavior of postmortem human lungs: effects of aging and mild emphysema.

The elastic behavior of postmortem human lungs has been studied in an effort to differentiate the effects of normal aging from those of mild emphysema. Static pressure-volume (P-V) curves were measured in 50 lungs obtained from men 15-85 yr of age, including 12 lungs with mild-to-moderate emphysema. The emphysema was quantitatively assessed by gross and microscopic methods. The P-V relationship in all lungs is accurately described by the empirically fitted equation, P = alpha1ea2v. This expression is useful because the two parameters separate the effects of elastic behavior (alpha1) from size (alpha2) on the P-V curve. There is a close negative correlation (R = -0.94) Between age and alpha1 in normal lungs but no significant age dependence of alpha2. Further decreases in alpha1 are found in most emphysematous lungs. Alpha1 is more than 2 SEE below the age-predicted mean in five of nine lungs with minimal emphysema (1-10% by point count) and more than 5 SEE below the mean in the three more severely affected lungs. There is a close correlation (R = +0.90) between alpha1 and the alveolar surface-to-volume ratio in both normal and emphysematous lungs.

Adolescent↗
PubMed2006

In vivo lung morphometry with hyperpolarized 3He diffusion MRI in canines with induced emphysema: disease progression and comparison with computed tomography.

Despite a long history of development, diagnostic tools for in vivo regional assessment of lungs in patients with pulmonary emphysema are not yet readily available. Recently, a new imaging technique, in vivo lung morphometry, was introduced by our group. This technique is based on MRI measurements of diffusion of hyperpolarized (3)He gas in lung air spaces and provides quantitative in vivo tomographic information on lung microstructure at the level of the acinar airways. Compared with standard diffusivity measurements that strongly depend on pulse sequence parameters (mainly diffusion time), our approach evaluates a "hard number," the average acinar airway radius. For healthy dogs, we find here a mean acinar airway radius of approximately 0.3 mm compared with 0.36 mm in healthy humans. The purpose of the present study is the application of this technique for quantification of emphysema progression in dogs with experimentally induced disease. The diffusivity measurements and resulting acinar airway geometrical characteristics were correlated with the local lung density and local lung-specific air volume calculated from quantitative computed tomography data obtained on the same dogs. The results establish an important association between the two modalities. The observed sensitivity of our method to emphysema progression suggests that this technique has potential for the diagnosis of emphysema and tracking of disease progression or improvement via a pharmaceutical intervention.

Animals↗
PubMedDate not supplied

Respiratory impedance following bronchoscopic or surgical lung volume reduction for emphysema.

BACKGROUND: Bronchoscopic methods for achieving lung volume reduction (BLVR) are presently undergoing clinical trials, and will soon be clinically available. Understanding the differential effects of surgical volume reduction therapy (LVRS) and BLVR on lung and chest wall physiology will assist physicians in selecting an optimal approach for patients. OBJECTIVES: Determine whether LVRS adversely affects lung or chest wall physiology at 3-month follow-up relative to BLVR in an experimental model of sheep emphysema. METHODS: Twelve mixed-breed sheep were treated with papain to produce experimental emphysema, and were divided into control, LVRS, and BLVR treatment groups. Lung and chest wall impedance was measured at 0, 5, and 10 cm H2O positive end-expiratory pressure at baseline and 3-month follow-up. RESULTS: Emphysema was associated with increased airway resistance, decreased lung tissue resistance and elastance, and increased chest wall tissue resistance. Following treatment, equivalent increases in lung elastance occurred in the LVRS and BLVR groups compared to controls. LVRS did not adversely affect chest wall impedance despite causing extensive pleural scarring. CONCLUSIONS: (1) Experimental emphysema following prolonged papain exposure progresses after cessation of treatment. (2) BLVR and LVRS produced equivalent lung and chest wall impedance responses at 3-month follow-up. (3) LVRS did not adversely affect chest wall impedance despite being associated with extensive pleural scarring.

Animals↗
PubMed1993

Oxidants from neutrophil myeloperoxidase do not enhance elastase-induced emphysema in the hamster.

Alpha-1-protease inhibitor is susceptible to oxidative impairment by the neutrophil myeloperoxidase (MPO) system. The purpose of this study was to assess the effect of the MPO oxidant system on elastase-induced emphysema in the hamster. Intratracheal instillation of 200 micrograms of human neutrophil elastase (HNE) induced a significant secretory cell metaplasia (SCM) and airspace enlargement [23% increase in mean linear intercept (MLI) as compared with control values]. Instillation of MPO system components [0.6 international units (U) of MPO, 5.5 U of glucose oxidase and glucose (0.02 M)] along with 200 micrograms HNE failed to enhance the severity of the SCM or emphysema induced by HNE alone. A second experiment was carried out using 50 micrograms of porcine pancreatic elastase (PPE) to induce emphysema. PPE produced a significant 45% increase in MLI, but the MPO system combined with PPE failed to enhance the emphysema induced by PPE alone. The MPO system alone had no measurable effect on airspace size or SCM. In vitro studies showed that PPE was partially inactivated by the MPO system; a 56% loss of elastolytic activity occurred during a 6-min incubation of PPE with the MPO system. This may explain why the MPO system did not exacerbate PPE-induced injury, but it does not explain the lack of enhancement for HNE. A 6-minute incubation of HNE with the MPO system resulted in a nonsignificant 10% decrease of elastolytic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗