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PubMed2003

[An experimental study on airway inflammation and remodeling in a rat model of chronic bronchitis and emphysema].

OBJECTIVE: To study the pathological features of airway inflammation and remodeling in rats with chronic bronchitis (CB) and emphysema and to evaluate the protective and therapeutic effects of erythromycin (EM). METHODS: Forty-three Wistar rats were assigned to eight groups: normal control group (A group, n = 5), normal saline solution group (P group, n = 5), CB group (L group, n = 6), CB and emphysema group (S group, n = 6), low-dose EM-treatment group (E(1) group, n = 5), high-dose EM-treatment group (E(2) group, n = 6), low-dose EM-prevention group (E(10) group, n = 5) and high-dose EM-prevention group (E(20) group, n = 5). The rat model of CB and emphysema was established by intratracheal instillation of lipopolysaccharide (LPS) and daily exposure to cigarette smog. After four weeks, total and differential cell counts in bronchoalveolar lavage fluid (BALF) were observed, and the pathomorphological changes in the lung were analyzed. The thickness of the smooth muscles and collagen in the bronchial wall were measured. Expression and localization of transforming growth factor beta(1) (TGF-beta(1)) were observed in the bronchi and lung tissues by immunohistochemistry. The levels of hyaluronic acid (HA) and procollagen type III (PCIII) in the serum and BALF were determined by the radioimmunoassay (RIA). RESULTS: (1) Compared with A group [(0.9 +/- 0.7) x 10(5)/ml], absolute neutrophil count in BALF from S group [(17.1 +/- 10.8) x 10(5)/ml] were significantly higher (P < 0.01). (2) Both the pathologic scores obtained from the S group (329 +/- 114) and P group (67 +/- 25), and the thickness of smooth muscles and collagen from S group [(9.6 +/- 2.6)%] and A group [(6.1 +/- 1.8)%] were statistically different (P < 0.01, P < 0.05, respectively). Expression of TGF-beta(1) in the lung of S group was significantly higher than that in A group. (3) The levels of HA [(152.5 +/- 36.3) micro g/ml] and PCIII [(40 +/- 8) micro g/ml] in serum and the levels of HA [(94 +/- 35) micro g/ml] and PCIII [(39 +/- 7) micro g/ml] in BALF in S group were higher than those in A group (P < 0.01). (4) After treatment with 100 mg/kg EM, absolute neutrophil count in BALF, the pathologic scores, the thickness of smooth muscles and collagen in the bronchi, the levels of PCIII and HA in serum and the levels of PCIII and HA in BALF were reduced to (2.1 +/- 1.4) x 10(5)/ml, 187 +/- 61, (6.0 +/- 2.3)%, (9.69 +/- 5.61) micro g/ml, (63.0 +/- 11.6) micro g/ml, (16 +/- 6) micro g/ml, (52 +/- 12) micro g/ml, respectively. Statistical analysis revealed that there were significant differences as compared to those of group S (P < 0.05). CONCLUSIONS: Many inflammatory cells especially neutrophils and alveolar macrophages might play an important role in the airway inflammation of CB and emphysema. Thickening of smooth muscles and collagen in the bronchi and the excessive depositions of extracellular matrix (ECM) constitute the fundamental pathological characteristic of airway remodeling in CB and emphysema. EM may prevent airway inflammation and remodeling to some degree.

Animals↗
PubMed2005

[A case of emphysema suggesting cystic lung disease in computer tomography].

Pulmonary emphysema is anatomically defined as abnormal persistent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls, without evident fibrosis. High-resolution computer tomography (HRCT) imaging is a valuable tool for diagnosis of this disease. The presence of minute cysts distributed evenly through all lung zones is rarely observed in pulmonary emphysema. In such cases, emphysema should be differentiated from other cystic lung diseases. We present a case of a 45-year-old women admitted to our Department with dyspnoea on exertion. Physical examination revealed no abnormalities. A chest radiograph showed diffused interstitial lesions in both lungs; HRCT revealed multiple oval-shaped cysts equally dispersed in all lung areas. The pulmonary function tests revealed increased lung volumes (total lung capacity 114.6% predicted, residual volume 200.6% of predicted), while both vital capacity and FEV1 were decreased (73.6% and 54.0% of predicted volumes, respectively). Diffused lung capacity was normal. Trans-bronchial biopsy was non contributory. Histiological examination of lung tissue obtained by videothoraco-scopy (VTS) was diagnostic for bullous emphysema. The patient had prescribed ipratropium bromide and teophyline. Differential diagnosis, apart from pulmonary emphysema, should take into consideration lymphangioleiomyomatosis, histiocytosis and sarcoidosis.

Diagnosis, Differential↗
PubMed1991

[Comparison of acute bronchodilator response between cases of diffuse panbronchiolitis and pulmonary emphysema].

Diffuse panbronchiolitis (DPB) is a disease characterized clinically by chronic airflow limitation, therefore patients with DPB are frequently treated with bronchodilators. However, there have been no reports on bronchodilator effects in patients with DPB. Because bronchodilator effects can be influenced by low baseline level of pulmonary function, we evaluated acute responses to inhaled metaproterenol (10 mg) in 31 patients with DPB and in 40 patients with pulmonary emphysema. Patients of both groups were clinically diagnosed, and, in addition, by usage of high-resolution computed tomography. All the subjects in both groups had a post-bronchodilator FEV1/FVC less than 0.7. There was no difference in baseline FEV1 between either group; FEV1 was 1.24 +/- 0.64 l (47.1 +/- 17.8% pred) in DPB vs. 1.24 +/- 0.64 l (51.0 +/- 19.0% pred) in pulmonary emphysema. Two indices, post FEV1/pre FEV1 and post FEV1-pre FEV1/predicted FEV1, were used for the judgement of bronchodilator response. Post FEV1/pre FEV1 was 110.3 +/- 9.3% in DPB and 119.9 +/- 17.1% in pulmonary emphysema. Post FEV1-pre FEV1/predicted FEV1 was 4.5 +/- 4.2% in DPB and 8.6 +/- 6.2% in pulmonary emphysema. Bronchodilator responses for both indices was larger in pulmonary emphysema than in DPB (both, p less than 0.01). It has been reported that post FEV1/pre FEV1 correlates negatively to baseline FEV1 and that post FEV1-pre FEV1/predicted FEV1 is positively correlated to baseline FEV1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed2006

[Newborn emphysema attributed to medical actions (3 case report)].

Three cases of newborn emphysema were reported. Parenchymatous emphysema, interstitial emphysema and bullous emphysema were all found in the three cases. One of the three cases showed accumulation of air in interstitial tissue. The air penetrated into septa of the lung at the beginning, then it probably split the hilus pulmonis to reach mediastinum as well as subcutaneous tissues of the chest, neck, abdomen, inguinal region and scrotum. The oxygen inhalation under pressure during first-aid may be the cause of the newborn emphysema.

Autopsy↗
PubMed1991

Prevention of leucocyte elastase-induced emphysema in mice by heparin fragments.

Heparin and its derivatives inhibit human leucocyte proteinases i.e. elastase and cathepsin G, but do not inhibit porcine pancreatic elastase and Pseudomonas aeruginosa elastase. In vitro experiments, reported here, also indicate that elastin, one of the physiological substrates of human leucocyte elastase (HLE), could decrease by 30-fold the inhibitory potential of an hexadecasaccharide heparin fragment (dp 16) isolated from CY 222. Nevertheless, the inhibitory capacity of the heparin fragment still remains elevated with IC50 = 2.7 x 10(-7) M and still inhibits HLE in its free and adsorbed state to elastin. These overall data prompted us to evaluate the influence of CY 222 in HLE-induced emphysema. Emphysema was induced in mice eight weeks old, following a single instillation of 200 micrograms of HLE. CY 222 treated animals received 2.5 mg.kg-1 subcutaneously once daily, 6 days per week during 4 weeks prior to HLE instillation, and for eight weeks following HLE instillation. The heparin fragment treatment of the mice halved the mortality rate observed early following HLE instillation. After 8 weeks, surviving animals were examined for lung histological and morphometrical changes: mean linear intercept (MLI) and internal alveolar area (ISA). The CY 222 heparin fragments exerted a protective effect against HLE-induced emphysema by decreasing by 70% the MLI; these heparin fragments exerted no effect on emphysema induced by pancreatic elastase in hamsters or mice. Heparin derivatives represent a new class of physiological HLE low molecular weight inhibitors capable of preventing HLE-induced emphysema.

Animals↗
PubMedDate not supplied

Tissue-space emphysema, tissue necrosis, and infection following use of compressed air during pulp therapy: case report.

The intraoperative development of tissue-space emphysema in a child undergoing restorative treatment under general anesthesia is presented. Emphysema development seems to be concomitant with the use of compressed air around patent root canals, complicated by tissue destruction due to movement of canal irrigants/medicaments into the periapical tissues and by secondary infection. Several recommendations for the prevention of tissue-space emphysema are presented including the use of a rubber dam, judicious use of compressed air, and maintenance of canal irrigants and medicaments within the root canal. Treatment recommendations vary from palliative care with follow up in cases of facial emphysema to immediate medical attention in cases of pharyngeal or mediastinal emphysema.

Abscess↗
PubMed1991

[The CT diagnosis of emphysema and correlation with pathologic findings].

It is difficult to diagnose clinically silent or mild emphysema. The efficacy of CT scans for the diagnosis of emphysema has attracted attention and comparisons have been made between CT images and the pathological grade of emphysema in resected lungs. With a view to determine to what extent high resolution CT images are accurate concerning the diagnosis of mild emphysema, we conducted an extensive comparative study on CT scores of emphysema, based on high resolution CT, the pathology score derived from the cut surface of the lung identical in its plane with that of the CT and destructive index (DI) which is said to be instrumental in representing the degree of deterioration of alveolar walls in the same regions of the lungs. In this study, 42 patients who underwent thoracotomy and their lung specimens including a solitary nodule of considerable size have been employed. The CT scores and pathology scores depend on the picture grading system developed by Thurlbeck and coworkers for the basis of counting. The findings were such that with 1 mm collimation, the CT scores ranged between 12 and 57 with a mean +/- SD of 22.1 +/- 9.6 (n = 35) while with 5 mm collimation, the CT scores ranged between 7 and 46 with a mean +/- SD of 16.5 +/- 8.3 (n = 33). The pathology scores stood at 10 to 57 with a mean +/- SD of 23.2 +/- 9.8 (n = 42).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Evaluation of pulmonary emphysema with high resolution computed tomography and the effect of smoking].

Cigarette smoking is thought to play an important part in the development of pulmonary emphysema. The authors previously reported on the correlation of high resolution computed tomography (CT) with the pathology grade of emphysema and the destructive index of lung specimens from 42 patients undergoing thoracotomy for a solitary pulmonary nodule. High resolution CT was effective to identify the presence and grade of mild emphysema. The mean per cent predicted FEV1 was 97 per cent. There were 28 smokers and 14 nonsmokers. In this report, the correlation of smoking history with pathology score and high resolution CT was analyzed. There was significant correlation among these indices. These results further support the relationship between smoking and pulmonary emphysema. High resolution CT scan may help in the understanding of the role of cigarette smoking in the development of early pulmonary emphysema.

Adult↗
PubMed1990

Diagnosis and follow-up of emphysema.

The definition of pulmonary emphysema is based on pathological examination. Clinical diagnosis is imprecise with no relationship between the extent of emphysema and either the "pink puffer" or the "blue bloater" types. The correlations between lung function tests and the extent of anatomically defined emphysema remain poor with a wide scatter. Plain chest radiograph is unreliable for the exclusion of emphysema whereas it is of value when positive. Major advance in the in vivo diagnosis has come from computed tomography (CT). It remains to be tested however whether serial quantitative CT scans will allow follow-up of the progression of emphysema.

Forced Expiratory Volume↗
PubMed1975

[Pulmonary function in papain induced emphysema in dogs (author's tranls)].

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 artificially 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.

Airway Resistance↗
PubMed1989

[Comparison of high resolution computed tomography and pulmonary function tests in diagnosis of mild emphysema].

To assess the ability of high resolution CT scan and pulmonary function tests in detecting and grading mild emphysema, we correlated the high resolution CT scan and pulmonary function tests with the pathologic grade of emphysema and the destructive index of lung specimens from 42 patients undergoing thoracotomy for solitary pulmonary nodules. Using the high resolution CT scan, we could identify the pathologic grade of mild and moderate emphysema. By measuring diffusing capacity per unit alveolar gas volume (DLco/VA), it seemed to be possible to detect the mildest degree of alveolar destruction assessed by the destructive index, which was not detected by high resolution CT scan. The reason for these results seemed to be that we assessed the severity of emphysema by detecting the air space enlargement on high resolution CT scan images caused by the destruction of alveolar walls, which were detectable by measuring DLco/VA. We conclude that it is possible to detect mild emphysema using the combination of high resolution CT scan and pulmonary function tests.

Adult↗
PubMed1989

[A study of antielastase activity in the development of pulmonary emphysema in a family with alpha 1-antitrypsin deficiency].

The five siblings of a family with alpha 1-antitrypsin deficiency including three of Pi- and two of PiM- phenotypes, were studied for the development of pulmonary emphysema during nine years. The changes of pulmonary function showed significant decrease in FEV1.0 and V50, and increase in RV/TLC. Clinical diagnoses for each patient were assessed by pulmonary function, inhalation and perfusion lung scintigram. Two case of Pi- phenotypes were diagnosed definite pulmonary emphysema 9 years previously, in one case of Pi- emphysema was suspected and two PiM- cases were also suspected of emphysema. alpha 1-antitrypsin and elastase inhibitory capacity (EIC) were investigated in serum and bronchoalveolar lavage fluids (BALF) from four patients with alpha 1-antitrypsin deficiency, healthy non-smokers and smokers. alpha 1-Antitrypsin and EIC in BALF in patients with alpha 1-antitrypsin deficiency were markedly decreased. There were no differences between non-smokers and smokers in alpha 1-antitrypsin and EIC, but EIC in BALF showed a significant correlation with DLCO or %DLCO. These findings suggest that a deficiency of alpha 1-antitrypsin results in insufficient antielastase protection in the lower respiratory tract, and EIC in BALF may be useful for detecting early changes of emphysema.

Adult↗
PubMed1985

The role of neutrophils in the development of cadmium chloride-induced emphysema in lathyrogen-fed hamsters.

This study was designed to evaluate the role of neutrophils (PMNs) in the pathogenesis of emphysema. After administration of CdCl2 intratracheally to hamsters fed a lathyrogen, beta-amino propionitrile fumarate (BAPN), the classic lesions of emphysema developed. Administration of specific antineutrophil serum markedly reduced the PMN influx into the lungs which followed CdCl2 exposure and produced a substantial decrease in elastase and collagenase content of bronchoalveolar lavage fluid (BAL). The degree of emphysema in PMN-depleted hamsters given BAPN and CdCl2 was not different from that in hamsters given BAPN and CdCl2. Furthermore, the degree of acute lung injury following CdCl2, as determined by hydroxyproline content of BAL and by lung lipid peroxidation, was the same in PMN-depleted and non-depleted groups. Thus, PMNs were not necessary for the induction of emphysema in BAPN-CdCl2-treated hamsters. The results suggest that PMNs may not be obligate mediators of emphysema.

Aminopropionitrile↗
PubMed1988

Lower incidence of death from chronic renal disease in patients with nonlethal emphysema: a statistical study.

Pulmonary emphysema is an extraordinarily prevalent disease, especially among men, and is found in about 40% of all autopsies at this Veterans Medical Center. However, in the great majority of cases, it is an incidental finding, and the individual has died of another lesion, either pulmonary or in another organ system. These facts have permitted the authors to examine the interrelationships between presence or absence of emphysema and the cause of death in a consecutive series of 1033 autopsies. Results show that chronic renal disease is much less common as a cause of death in persons with, than in those without, emphysema. Since emphysema is closely associated with smoking, the data also show a reduction in risk of death from renal disease in smokers. These trends persist, even when individuals who have died from smoking-related diseases are eliminated from the population. Further analyses suggest that it is the presence of emphysema which is mainly responsible for this effect. A likely mechanism for it is proposed.

Emphysema↗
PubMed1988

Capillary structure in elastase-induced emphysema.

The essential component of pulmonary emphysema is destruction of alveoli. Because capillaries make up much of the alveolar wall, it has been a long-held opinion that capillary loss in this disease parallels the loss of other elements of the alveolar septum. Yet the nature of the damage to capillaries and the occurrence of microvascular remodeling are unknown. Scanning electron microscopy of vascular casts of lungs from rats given intratracheal elastase were studied for identifying capillary changes in this type of experimental emphysema. The pressure-volume curves showed a clear distinction between the elastase and saline control animals, and light microscopy showed alveolar enlargement consistent with mild emphysema. The casts of capillaries in the elastase lungs appeared to have larger alveolar baskets, and capillaries ended abruptly near areas of focally destroyed lung. The elastase animals had more nonconnecting capillary segments on the pleural surface where the emphysema was worse and folds in the capillaries were more pronounced, suggesting weakened alveolar walls. The capillary density was decreased on the pleural surface, although this decrease could have resulted from hyperinflation. No difference in capillary diameters or branching frequency occurred. It appears that in this model of emphysema, decreased elastic recoil occurs before diffuse loss of capillaries.

Animals↗
PubMedDate not supplied

Morphological aspects, classification and epidemiology of emphysema.

Emphysema is an anatomically defined disorder, which leads to chronic airflow obstruction. Airflow obstruction, however, may also result from bronchial disease. Pulmonary function tests, as applicable in population studies, do not differentiate between anatomical emphysema and other causes of airflow obstruction. Standard radiology of the thorax provides a morphological approach, but is only indicative of emphysema in advanced cases. Post mortem studies, in which emphysema was quantitated, show that age, smoking habits, sex and environment factors are important for the prevalence of pulmonary emphysema.

Humans↗
PubMed1979

Ultrastructural studies of elastase-induced experimental emphysema.

Experimental emphysema in the guinea pig was made by intracheal instillation of porcine pancreatic elastase in order to analyze the proteolytic factors related to the pathogenesis of pulmonary emphysema. Ultrastructural and morphometric studies were performed in the elastase-induced emphysema in vivo. The following results were obtained: 1) Ultrastructural studies in vivo revealed that interstitial edema and degradation of fibrous tissue already occurred 2 hours after elastase instillation. Subsequently we observed fragmentations of elastin and dissociation between elastic tissue and collagen fibers 2 days later. Apparent degradation and fragmentation of elastin was found after 7 days. 2) Morphometric studies by electron microscope on elastase-induced experimental emphysema showed significant degradation of elastin fragments. Thus, it was suggested the importance of elastolytic process on the pathogenesis of pulmonary emphysema.

Animals↗
PubMed1982

[Proteases, antiproteases and pulmonary emphysema].

A deficiency of alpha 1 antiproteases is associated with severe and early emphysema. This emphysema can be experimentally produced in animals by endotracheal instillation of elastolytic proteases. Thus it would seem that emphysema is linked to an imbalance between proteases and antiproteases at the pulmonary level. This work studies the proteases, whose role in the genesis of emphysema is highly probable in view of the data in the literature (leukocyte elastase), disputed (macrophage elastase) or transitory (microbial elastases). We contrast the main agents capable of inhibiting these proteases (alpha 1 antiprotease and bronchial inhibitors) or of changing their activity (alpha 2 macroglobulins). The relative importance of these antiproteases is discussed in the light of studies made on bronchial secretions and bronchoalveolar lavage. These irritants may influence the protease - antiprotease equilibrium and favour the development of emphysema by increasing the proteases or decreasing the antiproteases. It appears that tobacco, as well as infection and anything which sets in motion the pulmonary phagocytes favour the liberation of leucocyte elastase. These attacks inactive the alpha 1 antiproteases in addition to the bronchial inhibitor. They may be recognized by a change in elastolytic and anti-elastolytic activity observed in bronchial secretions and in bronchoalveolar lavage (which is more disputed in the latter).

Animals↗