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Results for “Pulmonary Emphysema”

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PubMed2000

Disruption of the klotho gene causes pulmonary emphysema in mice. Defect in maintenance of pulmonary integrity during postnatal life.

Homozygous mutant klotho (KL(-/-)) mice exhibit multiple phenotypes resembling human aging. In the present study, we focused on examining the pathology of the lungs of klotho mice and found that it closely resembled pulmonary emphysema in humans both histologically and functionally. Histology of the lung of KL(-/-) mice was indistinguishable from those of wild-type littermates up to 2 wk of age. The first histologic changes appeared at 4 wk of age, showing enlargement of the air spaces accompanied by destruction of the alveolar walls, and progressed gradually with age. In addition to these changes, we observed calcium deposits in type I collagen fibers in alveolar septa and degeneration of type II pneumocytes in 8- to 10-wk-old KL(-/-) mice. Pulmonary function tests revealed prolonged expiration time in KL(-/-) mice, which is comparable with the pathophysiology of pulmonary emphysema. The expression level of messenger RNA for type IV collagen, surfactant protein-A and mitochondrial beta-adenosine triphosphatase was significantly increased in KL(-/-) mice, which may represent a compensatory response to alveolar destruction. Additionally, the heterozygous mutant klotho mice also developed pulmonary emphysema late in life, around 120 wk of age. These findings indicate that klotho gene expression is essential to maintaining pulmonary integrity during postnatal life. The klotho mutant mouse is a useful laboratory animal model for examining the relationship between aging and pulmonary emphysema.

Aging↗
PubMed1985

Weights of the body and cardiac ventricles in pulmonary emphysema.

We analysed statistically the association of emphysema, determined on inflation fixed specimens, with the weights of the body and heart, and of the cardiac ventricles, weighed separately, in 170 male and 86 female adult autopsies. The cases were grouped according to the cause of death into cardiovascular, cancer and other deaths. In men the body weight was inversely proportional to the severity of emphysema, but no association existed between the body weight and the cause of death. In male cardiovascular deaths the total heart weight, total ventricular weight and the weight of the left ventricle with the septum were also inversely proportional to the severity of emphysema while this was not true in the other deaths. In male cardiovascular deaths a decrease, and in the other deaths an increase, of the weight of the free wall of the right ventricle was associated with an increasing severity of emphysema. In all male deaths, however, the left to right ratio decreased with an increasing severity of emphysema. Thus, pulmonary emphysema is associated both with a general atrophy, including the myocardium, and a mainly relative right ventricular hypertrophy. An absolute right ventricular hypertrophy, however, seems to accompany emphysema only in the absence of other major cardiovascular diseases.

Adult↗
PubMedDate not supplied

Assessment of lung volumes in pulmonary emphysema using multidetector helical CT: comparison with pulmonary function tests.

The purpose of this study is to evaluate the usefulness of multidetector helical CT (MDCT) with three-dimensional (3D) postprocessing for assessing the lung volume at inspiration and expiration of the pulmonary emphysema and for comparing it with pulmonary function tests. Percentage lung volume at the threshold of -930, -900, -810, -790, and -770 at expiration showed good correlation with FEV1, FEV1/FVC, and DLCO/Va. Excellent correlation was observed between percentage lung volume at the threshold of -900 and FEV1/FVC. CT densitometry at expiration showed better correlation than that at inspiration with pulmonary function tests. MDCT with 3D technique is useful for assessing the severity of pulmonary emphysema.

Adult↗
PubMed1997

Retinoic acid treatment abrogates elastase-induced pulmonary emphysema in rats.

Pulmonary emphysema is a common disease in which destruction of the lung's gas-exchange structures (alveoli) leads to inadequate oxygenation, disability and frequently death; lung transplantation provides its only remediation. Because treatment of normal rats with all-trans-retinoic acid increases the number of alveoli, we tested whether a similar effect would occur in rats with emphysema. Elastase was instilled into rat lungs, producing changes characteristic of human and experimental emphysema: increased lung volume reflecting a loss of lung elastic recoil, larger but fewer alveoli and diminished volume-corrected alveolar surface area due to destruction of alveolar walls. Treatment with all-trans-retinoic acid reversed these changes providing nonsurgical remediation of emphysema and suggesting the possibility of a similar effect in humans.

Animals↗
PubMed1995

[Minimally invasive surgery of large bullous pulmonary emphysema].

An enormous pulmonary cyst (phi approx. 20 cm) in a 72-year-old male patient with large bullous pulmonary emphysema caused compression of the right lung and the mediastinum with consecutive, O2-dependent dyspnoea at rest. The symptoms did not improve under conservative therapy of an accompanying COPD. Thus, in spite of two heart attacks in the previous history, an operation with bullectomy was indicated. A thoracotomy had to be avoided because of the very high cardiac risk. In the present case, a minimally invasive procedure enabled the complete cyst resection with a smooth postoperative course and an excellent functional therapeutic result.

Aged↗
PubMed1997

[Prevalence and specific features of pulmonary emphysema in patients with pulmonary tuberculosis].

The prevalence and specific features of emphysema of the lung were studied in patients with pulmonary tuberculosis. The temporal pattern of the process and secondary obstructive genesis were established. It was stated that there was a redistribution of the existing emphysematous changes into the unaffected parts of the lung along with the higher scope of the chronic tuberculosis process.

Adolescent↗
PubMed2006

Modulators of cigarette smoke-induced pulmonary emphysema in A/J mice.

Mice develop pulmonary emphysema after chronic exposure to cigarette smoke (CS). In this study, the influence of gender, exposure duration, and concentration of CS on emphysema, pulmonary function, inflammation, markers of toxicity, and matrix metalloproteinase (MMP) activity was examined in A/J mice. Mice were exposed to CS at either 100 or 250 mg total particulate material/m(3) (CS-100 or CS-250, respectively) for 10, 16, or 22 weeks. Evidence of emphysema was first seen in female mice after 10 weeks of exposure to CS-250, while male mice did not develop emphysema until 16 weeks. Female mice exposed to CS-100 did not have emphysema until 16 weeks, suggesting that disease development depends on the concentration and duration of exposure. Airflow obstruction and increased pulmonary compliance were observed in mice exposed to CS-250 for 22 weeks. Decreased elasticity was likely the major contributor to airflow obstruction because substantial remodeling of the conducting airways, beyond mild mucous cell hyperplasia, was lacking. Exposure to CS increased the number of macrophages, neutrophils, lymphocytes (B cells and activated CD4- and CD8-positive T cells), and activity of MMP-2 and -9 in the bronchoalveolar lavage fluid (BALF). Treatment with antioxidants N-acetylcysteine or epigallocatechin gallate (EGCG) did not decrease emphysema severity, but EGCG slightly decreased BALF inflammatory cell numbers and lactate dehydrogenase activity. Inflammation and emphysema persisted after a 17-week recovery period following exposure to CS-250 for 22 weeks. The similarities of this model to the human disease make it promising for studying disease pathogenesis and assessing new therapeutic interventions.

Animals↗
PubMed1996

[Effects of pulmonary rehabilitation on vital capacity in patients with chronic pulmonary emphysema].

To evaluate the effects of pulmonary rehabilitation on pulmonary function, 15 patients with chronic pulmonary emphysema underwent pulmonary rehabilitation for six weeks as inpatients. Pulmonary rehabilitation consisted of relaxation techniques, breathing retraining, thoracic massage, physical exercise, and walking. In 8 of the 15 patients vital capacity increased by more than 200 ml (over 10%), and in 7 of the 15 patients the load of maximal exercise increased by more than 5 watts (over 10%). Increases in vital capacity were not associated with increases in maximal exercise load. The percent change in vital capacity associated with pulmonary rehabilitation correlated significantly with the percent change in tidal volume and the percent change in expiratory minute ventilation at the maximal load. The percent change in tidal volume at the maximal load correlated significantly with the percent change in maximum oxygen uptake. We attribute the increase in vital capacity to an improvement in thoracic cage movement. These findings suggest that pulmonary rehabilitation can increase vital capacity in some patients with chronic pulmonary emphysema, and that such an increase is not directly connected to increases in exercise capacity.

Aged↗
PubMed2003

[Quantitative study of 99mTc-technegas SPECT for ventilatory impairment in pulmonary emphysema--regional distribution: correlation of SPECT with pulmonary function test].

99mTc-Technegas scintigraphy is used for evaluation of abnormality of ventilation in pulmonary emphysema. Although the abnormality of ventilation distribution is very easy to find, there is not an objective index. The evaluation is subjective and different by each radiologist. It was also difficult to compare each cases and the clinical course in the same case. The present study for quantitative evaluation has proved that excellent correlations is obtained between the mean voxel values of the lung and stage classification. Furthermore, a correlation is observed between the mean and FEV1.0%. These deta indicate that quantitative analysis of SPECT seem to be useful to classify the clinical stage and compare the each cases. And respiratory function decreases as much as chronic pulmonary emphysema exists in the lower lung field.

Forced Expiratory Volume↗
PubMed1997

Assessment of the severity of pulmonary emphysema by computed tomography.

Pulmonary emphysema is defined as an abnormal enlargement of alveolar spaces distal to the terminal bronchioles, with alveolar wall disruption and without obvious fibrosis. Clinico-functional evaluation and chest radiographic diagnosis are not highly accurate in detecting emphysema and in establishing the extent of the process of alveolar destruction. Several computed tomography (CT) techniques are now available for detection and quantitative assessment of emphysema. The results appear to correlate significantly better than chest radiography with functional impairment and pathological score. Many options have been proposed by different authors regarding CT technique. The choice, however, is essentially between inspiratory high resolution CT (HRCT) with a visual scoring system, and automated quantitative evaluation by means of a "density mask" (DM) program. This paper presents the state of the art on CT quantification of pulmonary emphysema and briefly discusses the technical options and parameters to be used, together with the problems to be solved.

Humans↗