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PubMed1977

A comparative study of experimental and spontaneous emphysema.

Normal lung architecture of the rat, mouse, hamster, horse, and human was compared to that of emphysematous lungs from the same species by utilizing a light microscope and a scanning electron microscope (SEM). The results obtained by SEM examination of normal and emphysematous lungs corresponded to those obtained with the light microscope. However, the SEM provided a view of alveoli and airway morphology not obtainable with the light microscope. Because of the variability in pore size and number of pores per alveolus, a pore-to-alveolus ratio was determined with the SEM on the normal lungs of the above species plus the rabbit, dog, guinea pig, and rhesus monkey. Depending on the extent of other pathways for collateral ventilation, differences in number of pores per alveolus may affect a species' susceptibility to a given mechanism in the genesis of spontaneous or induced emphysema. The small number of pores per alveolus in the rat, mouse, rabbit, and hamster suggests that they would not be responsible for emphysematous changes. Pores do appear to be involved in human and horse emphysema.

Aged↗
PubMed1987

Augmentation of elastase-induced emphysema by cigarette smoke: effects of reducing tar and nicotine content.

The effects of reducing the tar and nicotine concentration of cigarette smoke were examined in a rat model of smoke-augmented, porcine pancreatic elastase- (PPE-) induced, pulmonary emphysema. Sixty-eight female Long-Evans rats were divided approximately evenly into seven groups: control, PPE, PPE plus sham smoke, high-tar/nicotine cigarette smoke (2R1; 38.8 mg total particulate matter and 2.2 mg nicotine per cigarette), low-tar/nicotine cigarette smoke (1R4F; 10.8 mg total particulate matter and 0.8 mg nicotine per cigarette), PPE + 2R1, and PPE + 1R4F. Three days after intratracheal administration of PPE (400 IU/kg), animals in the smoke-treated groups were exposed to 8-10 puffs of cigarette smoke daily, 7 d/wk for 12 wk. Sham-treated animals received room air in place of cigarette smoke. At the conclusion of the exposures, pulmonary function tests were performed under general anesthesia. Cigarette-smoke exposure alone did not produce significant changes in pulmonary function. Elastase-treated groups demonstrated significant increases in total lung capacity, functional residual capacity, and dynamic and static compliance, as well as significant decreases in carbon monoxide (CO) diffusing capacity and CO diffusion coefficient. Morphometric measurements of mean linear intercept demonstrated a loss of alveolar fine structure with enlargement of distal airspaces in PPE-treated rats. Exposure to either 2R1 or 1R4F cigarette smoke significantly enhanced many of the emphysematous changes produced by PPE, but there were no significant differences between the effects of the two smokes. These data indicate that reducing the tar and nicotine concentration of cigarette smoke does not lessen its ability to augment PPE-induced pulmonary emphysema in the rat.

Animals↗
PubMed2004

N-acetylcysteine treatment protects against VEGF-receptor blockade-related emphysema.

Administration of the VEGF receptor blocker SU5416 to rats causes alveolar septal cell apoptosis and emphysema; both can be prevented by a superoxide dismutase mimetic. Here we show that SU5416 induces the expression of heme oxygenase-1 in the lung tissue and that administration of antioxidant N-acetyl-l-cysteine protects alveolar septal cells against apoptosis, as demonstrated by caspase-3 lung immunohistochemistry, and against emphysema.

Acetylcysteine↗
PubMed2004

Severe, early-onset emphysema with normal alphal-antitrypsin levels in nonsmokers: a clinical dilemma.

Approximately 85% of all cases of chronic obstructive pulmonary disease are attributed to cigarette smoking. The only other established risk factor for the development of chronic obstructive pulmonary disease that is of comparable importance is the deficiency of alpha1-antitrypsin, a rare genetic defect that is present in less than 1% of all cases. Other risk factors are not well characterized in the literature. This article describes one patient without a significant smoking history and with a normal alphaa-antitrypsin level who developed severe early-onset emphysema and gives a brief discussion about other genetic and environmental risk factors for the development of emphysema.

Adult↗
PubMed2005

Adenovirus-mediated transfer and overexpression of heme oxygenase 1 cDNA in lungs attenuates elastase-induced pulmonary emphysema in mice.

Heme oxygenase 1 (HO-1) is an inducible enzyme that catalyzes heme to generate bilirubin, ferritin, and carbon monoxide. Because enhanced expression of HO-1 provides an anti-inflammatory effect and confers cytoprotection, we examined whether HO-1 overexpression induced by inoculation of mice with an adenovirus encoding HO-1 (Ad.HO-1) in the lung would prevent pulmonary emphysema induced by porcine pancreatic elastase (PPE). Pretreatment with Ad.HO-1, which upregulated production of HO-1 in the lung, attenuated the PPE-induced increase of neutrophils in bronchoalveolar lavage fluid (BALF) and enlargement of alveoli. It also reduced PPE-induced elevated levels of tumor necrosis factor alpha, interleukin (IL)-6, and keratinocyte-derived chemokine, and increased the level of anti-inflammatory cytokine IL-10 in BALF. These results suggest that Ad.HO-1-induced HO-1 overexpression suppressed PPE-induced emphysema by attenuating neutrophilic inflammation via modulating cytokine and chemokine profiles in mouse lungs.

Adenoviridae↗
PubMed2003

Response of whole-body protein and urea turnover to exercise differs between patients with chronic obstructive pulmonary disease with and without emphysema.

BACKGROUND: Exercise is known to improve physical capacity and muscle mass in patients with chronic obstructive pulmonary disease (COPD). However, recent evidence suggests that exercise may also negatively influence metabolism in COPD. OBJECTIVE: The objective was to investigate whether exercise influences whole-body protein metabolism differently in COPD patients and control subjects and to elucidate the effect of the specific underlying lung disease. DESIGN: Whole-body protein synthesis and breakdown and urea synthesis were measured by using stable-isotope methods in 14 male patients with severe COPD (forced expiratory volume in 1 s: 37 +/- 12% of predicted) and in 8 male control subjects during and after 20 min of exercise. Subjects were normal weight [body mass index (in kg/m2) of COPD patients and control subjects: 25.8 +/- 3.9 and 25.7 +/- 4.4, respectively]. The COPD group was selected to include patients with (Emph+, n = 7) and without (Emph-, n = 7) emphysema. Absolute workload was 35 +/- 5 W, corresponding to 17 +/- 2%, 33 +/- 9%, and 52 +/- 14% of the maximal obtained workload in the control, Emph-, and Emph+ groups. RESULTS: Exercise induced a 9% increase in protein synthesis and breakdown in the Emph- and control groups, which normalized postexercise. In the Emph+ group, protein turnover did not change significantly during exercise but decreased postexercise (+/- 10%). Exercise did not change net protein breakdown (protein breakdown - synthesis) or urea synthesis, except in the Emph+ group, which showed a 14% reduction in urea synthesis postexercise (P < 0.05). CONCLUSION: Low-intensity exercise suppresses whole-body protein and urea turnover in COPD patients with emphysema and needs to be considered when maximal anabolism is targeted through a combination of exercise and nutrition.

Aged↗
PubMed2005

The singer's breath: implications for treatment of persons with emphysema.

This study investigated the effects of group singing instruction on the physical health and general wellness of senior citizens with emphysema. Subjects (n = 7) participated in 6 weeks of group vocal instruction, which emphasized breath management techniques. Dependent measures reflected physical health, functional outcomes, and quality of life. No significant differences were found on measures of physical health (FEV1, inspiratory threshold, distance walked, and The DUKE physical health subscale). Measures of functional outcomes each showed a significant change across time. Results of the ANOVAs for breath management (extent of counting) and breath support (intensity of speech) were significant (p < .038 & p < .000 respectively). Descriptive analyses showed a clear and dramatic shift in breathing mode from clavicular to diaphragmatic breathing that was maintained 2 weeks after the treatment period. Quality of life measures (subjective scales and The Duke Health Profile) yielded mixed results. Findings of this study suggest that vocal instruction, inclusive of breathing exercises, may help to improve the quality of life for senior citizens with emphysema. Subjects in this study responded positively to the instruction and further investigation of the treatment method is warranted.

Aged↗
PubMed1995

Case report: congenital absence of the left pulmonary artery accompanied by ipsilateral emphysema and adenocarcinoma.

Unilateral absence of the left pulmonary artery is a rare congenital anomaly that may remain unrecognized until adulthood, in which case it may lead to inappropriate diagnosis and management. The authors describe a case in which a patient came to their institution with dyspnea and a chest roentgenogram showing a prominent right pulmonary artery, right aortic arch, and a left lung mass accompanied by ipsilateral volume loss. Although the initial evaluation suggested a differential diagnosis that included thromboembolic pulmonary disease and vascular compression by tumor, further workup revealed unilateral absence of the left pulmonary artery accompanied by left lung hypoplasia, and interestingly, ipsilateral emphysema and adenocarcinoma. The embryologic factors responsible for this abnormality and how it may potentially affect the development of emphysema and adenocarcinoma are discussed.

Adenocarcinoma↗
PubMed1995

Placental transmogrification of the lung, a histologic variant of giant bullous emphysema. Clinicopathological study of three further cases.

Placental transmogrification of the lung was described by Chesney in 1978 as an unusual cystic lesion involving a single pulmonary lobe (3). We studied three additional cases with identical clinical and pathologic features. The patients were a 33-year-old woman and men aged 24 and 27 years. Each patient was first seen with respiratory distress; one had repeated pneumothoraces. Radiographically, an enlarging cystic lesion was present in a lower (two) or middle (one) lobe. The lesion had been present for 10 years in one patient. In two patients, mediastinal shift was noted. Lobectomy was curative in all instances. Grossly there was a uni- or paucilocular cyst lined by papillary structures. Microscopically, the papillae contained proliferating blood vessels, lymphoid nodules, smooth muscle, and fat. Sclerotic foci obliterated the vessels in some areas. The growth pattern and topography resembled those of placental villi. Systematic review of the histologic features in other lungs with marked emphysema revealed a spectrum of similar changes and suggested that the lesion in our patients may be a complication of bulla formation and is most likely the clinico-pathologic analog of the "vanishing lung" syndrome (idiopathic giant bullous emphysema).

Adult↗
PubMedDate not supplied

Breathing out into water during subtotal immersion: a therapy for chronic pulmonary emphysema.

OBJECTIVE: To determine the importance of a breathing out into water exercise during subtotal immersion for emphysematous patients. DESIGN: Results of a respiratory function test and arterial blood gas analysis were examined to compare the programs of breathing exercise with and without the breathing out into water exercise. The breathing exercises in a pool filled with 38 degrees C water were performed 30 min/day, 5 days/wk, for 2 mo in 17 patients with stable chronic emphysema. Patients were randomly assigned to breathing exercise programs including subtotal water immersion with the nose and mouth either immersed (9 patients) or out of the water (8 patients) during exhalation. RESULTS: The ratio of %forced expired volume in 1 sec to forced vital capacity and %forced vital capacity at rest were significantly increased in the program with the breathing out into water exercise, but they did not change in the program without the breathing out into water exercise. A significant increase in peak flow was observed in the former program, although it did not change in the latter program. The maximal expiratory flow at 25% did not change in either program. Pao2 was significantly increased and Paco2 was significantly decreased in the former program, although a trend for a decrease in Paco2 was observed in the latter program. CONCLUSIONS: These results suggest that the breathing out into water exercise enhances the effects of a breathing exercise during immersion and is useful in rehabilitation for chronic pulmonary emphysema.

Aged↗
PubMed1995

Orbital emphysema following remote skull trauma.

In an unusual case of orbital emphysema following nose blowing, a reliable patient history and examination demonstrated no direct trauma to the orbit. Blunt posterior skull trauma was sustained several hours before the development of the orbital emphysema. A "seismic" transmittal of force to the orbital walls is postulated.

Craniocerebral Trauma↗
PubMed1987

Radiographic appearance of the chest in emphysema.

The essential point of this analysis is that, although arterial deficiency was shown to be virtually useless as a diagnostic criterion for emphysema, it does not follow that use of other validated radiographic criteria for diagnosing and excluding emphysema, using conventional films, should be abandoned. Interested readers can find further detailed information in reference 1.

Humans↗
PubMed2004

Optimization and standardization of lung densitometry in the assessment of pulmonary emphysema.

Currently, lung densitometry for the assessment of pulmonary emphysema has been fully validated against pathology, pulmonary function, and health status, and it is therefore being applied in pharmacotherapeutic trials. Nevertheless, its application for the early detection of emphysema has not yet been introduced in daily clinical practice. The main reason for this is the fact that it is not yet regarded a fully optimized and standardized technique. In this work, an overview is given on the current status of different standardization aspects that play an important role in this, ie, image acquisition, choice of densitometric parameter and image processing. To address these issues, solutions have been sought from the literature and from original data from previous studies. Standardization and optimization of lung densitometry has reached a more advanced stage than has been reported so far. If normal values will become available, this technique will be feasible for clinical practice. As a result, standardization for the detection and assessment of other density-related lung diseases can be achieved in a shorter period of time.

Absorptiometry, Photon↗
PubMedDate not supplied

Spirometric-gated computed tomography quantitative evaluation of lung emphysema in chronic obstructive pulmonary disease: a comparison of 3 techniques.

OBJECTIVE: To compare the quantitative assessment of pulmonary emphysema with spirometric-gated computed tomography (gated CT) using 3 different acquisition techniques and to determine if low-current spiral CT could be used effectively to quantitate emphysema. METHODS: Eleven patients with chronic obstructive pulmonary disease (COPD) underwent gated CT and pulmonary function tests (PFTs). Spiral whole-lung 10-mm collimation acquisitions at standard (146 mAs) and low (43 mAs) current and sequential 3-slice 1-mm collimation high-resolution computed tomography (HRCT) acquisitions at standard current were obtained at 90% of the patient's vital capacity. The mean lung density (MLD) and the pixel index (PI) derived from the 3 data sets were compared using one-way analysis of variance and correlated with PFTs using linear regression. Moreover, the radiation dose associated with each technique was measured. RESULTS: The MLDs were not significantly different. The PIs calculated from the standard- and low-current spiral acquisitions were similar, and both were significantly different from that of HRCT. The MLDs correlated with the PFTs in standard-current spiral and HRCT but not in low-current spiral acquisitions, whereas the PIs correlated with the PFTs in all 3 techniques. High-resolution computed tomography implied the lowest dose (0.08 mSv) compared with low-current (1.2 mSv) and standard-current (4 mSv) spiral techniques. CONCLUSIONS: Low- and standard-dose spiral CT provides similar lung density data in COPD. The combination of low-dose whole-lung spiral CT and 3-slice HRCT represents the best compromise between the amount of information provided and radiation exposure to the patient and could be substituted for standard-dose spiral CT for quantitative evaluation of COPD.

Aged↗
PubMedDate not supplied

Morphological progression of emphysema on thin-section CT: Analysis of longitudinal change in the number and size of low-attenuation clusters.

OBJECTIVES: To evaluate morphological changes in the number and size of low-attenuation clusters on computed tomography (CT) in patients with emphysema. MATERIALS AND METHODS: In 27 patients who had follow-up CT scans for 6 months or greater, initial 27 scans and follow-up 39 scans were analyzed. The number per slice (LAN/s) and mean size (LAS) of low-attenuation clusters less than -950 HU, and total low-attenuation area below -950 HU per slice (LAA-950/s) were calculated. RESULTS: LAS and LAA-950/s were significantly increased over time. No significant correlation was found between LAN/s and follow-up period. LAS increased in 37 of 39 (95%) follow-up scans, whereas LAN/s decreased in 17 of 39 (44%) follow-up scans. CONCLUSIONS: On the morphological progression of emphysema, the mean size of low-attenuation clusters was significantly increased during the follow-up period, whereas no significant correlation was found between the number of low-attenuation clusters and follow-up period.

Aged↗
PubMed1986

The biochemical pathogenesis of chronic obstructive pulmonary diseases: protease-antiprotease imbalance in emphysema and diseases of the airways.

Emphysema is believed to result from destruction of elastic fibers due to an imbalance between proteases and their inhibitors in the lung. The imbalance can arise from a primary failure of secretion of the inhibitors, as occurs in hereditary alpha-1-protease inhibitor deficiency, or as the result of complex interactions of environmental agents with the lung. Environmental agents may produce their effects by stimulating degradation of elastic fibers by neutrophils and macrophages, damaging protease inhibitors by oxidative or proteolytic mechanisms or by impairing the biosynthetic repair of damage to the connective tissue. Protease excess has also been consistently observed in purulent sputum. Since experimentally administered proteases stimulate secretion of mucus and damage mucociliary clearance, protease-antiprotease imbalance might be involved in the pathogenesis of bronchitis and bronchiectasis as well as emphysema. Because the protease inhibitors of bronchial mucus are distinct from those of the acinar units, and no hereditary deficiencies are known, there is no direct proof of this hypothesis in man.

Animals↗
PubMed1993

Precocious emphysema in intravenous drug abusers.

It is becoming increasingly clear that obstructive airway disease and early emphysema occur in some drug addicts who intravenously abuse drugs intended for oral use. We report four patients with such a history who had clinical, pathophysiologic, and radiologic evidence of severe obstructive airway disease with hyperinflation. Three patients had bullae. All had radiologic changes of intravenous talc granulomatosis. One patient had moderately severe emphysema at autopsy. The pathogenesis of this disease is uncertain but may involve synergism with cigarette smoke, direct toxic effects of the drug, or induced intravascular leukocyte sequestration causing proteolytic pulmonary injury.

Adult↗