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PubMed1989

[Pulmonary circulatory disturbance on magnified peripheral pulmonary wedge angiography in chronic pulmonary emphysema].

Magnified peripheral pulmonary wedge angiography was performed in chronic pulmonary diseases. We classified the wedge angiography into five types based on the changes of capillary background (CBG) findings. Type I (normal), Type II (CBG is scattered and pulmonary arterial branches are tortuous), Type IIIa (CBG is decreased and pulmonary arterial branches are normal), Type IIIb (CBG and pulmonary arterial branches are also decreased or disappeared), Type IV (totally convergent). Using this classification, wedge angiography was performed in 42 patients out of 66 patients with chronic pulmonary emphysema diagnosed by selective alveolo-bronchography (SAB). Each type was compared in terms of hemodynamic data, blood gases and pulmonary function. Pulmonary emphysema was classified into types II, IIIa, and IIIb. There was no relation between SAB findings and wedge angiography classification. Severe hemodynamic data cases were found in types II and IIIb. The PaO2 of type II and IIIb were significantly lower than that of type IIIa. In pulmonary function tests, the mixed impairment type of ventilation was more frequently seen in type IIIb than IIIa. There was no relationship between SAB findings (66 cases) and hemodynamic data. These results suggest that classifying wedge angiography into five types (I, II, IIIa, IIIb, IV) may be useful for evaluating severity and determining prognosis and therapeutic measures in chronic pulmonary emphysema.

Adult↗
PubMed1989

[Oscillometric differentiation of lung fibrosis and lung emphysema].

In three groups of healthy subjects and patients with pulmonary fibrosis or pulmonary emphysema, the secondary periodical oscillatory phenomena observed under conditions of normal breathing and a slow VC manoeuvre on the Siregnost FD 5 were broken down into a volume- and a flow-synchronous component, as also a third component with no correlation with either volume or flow, and which can be observed in the primary parameters Ros and psi, as also the secondary parameters Rre and phi. While both fibrotic patients and healthy subjects revealed a volume-inverse phase behaviour, patients with pulmonary emphysema revealed a volume-proportional phase behaviour. This difference in volume dependence is explained by the difference in elastic recoil in patients with fibrosis as compared with those suffering from emphysema, and the associated different influence on the filling of the lungs with air and blood.

Adult↗
PubMedDate not supplied

The pathogenesis of emphysema.

Emphysema is an increase in size of the air spaces distal to the terminal bronchioles, and can thus only be diagnosed pathologically, but new quantitative CT methods hold promise, diagnosing, quantitating and locating the lesions in man, in life, non-invasively. The protease/antiprotease theory of the pathogenesis of emphysema proposes that cigarette smoke attracts alveolar macrophages to distal terminal bronchioles, these in turn releasing neutrophil chemotactic factors which attract circulating polymorphonuclear leucocytes, to release potent proteolytic enzymes (serine protease) in addition to the alveolar macrophage protease. These enzymes, which can cleave all the macromolecules of the lung interstitium, are antagonized (at least the serine elastase) in health by alpha 1-antitrypsin, a normal constituent of lung lining fluid. However, this can be oxidized by oxidants in cigarette smoke, and oxidants released by polymorphonuclear leucocytes in microbial killing. The role of these actions, and of antioxidants (both natural and therapeutic) and antielastases are reviewed, as well as the activities of lung defence cells in this process. Despite this explosion of recent knowledge, we are still unable to answer the all important question "Why don't all smokers develop emphysema?", and further research is needed into variability in these multiple factors involved in this important new theory of the pathogenesis of this, possibly the commonest of all respiratory disorders of a chronic disabling nature.

Chemotactic Factors↗
PubMed1987

Emphysema alters the deposition pattern of inhaled particles in hamsters.

How does pulmonary emphysema affect aerosol deposition? Groups of awake hamsters with emphysema (intratracheal elastase, 0.2 mg/100 g body wt) and age-matched controls (intratracheal saline) were exposed for 30 minutes to an insoluble radioactive aerosol (0.45 mu aerodynamic diameter) at 30, 60, or 90 days after instillation. Immediately after exposure, the animals were sacrificed. The lungs were excised, dried at total lung capacity, and sliced into 1-mm thick sections. Each slice was cut into pieces, which were counted for radioactivity and weighed. Then a measure of the uniformity of deposition, the evenness index (EI), was calculated. With perfect uniformity, all EIs would be one. We found fewer particles in the emphysematous, as compared with the control, lungs at 60 or 90 days after elastase instillation. The deposited particles were distributed less uniformly throughout the emphysematous lungs than in the control lungs. In controls, the standard deviation (SD) of the EI distribution (mean 1.0) averaged 0.33 for the three times studied. In elastase animals, the SD increased to 0.48 at 30 days, and at 60 days and 90 days the distributions were no longer normally distributed. This increased heterogeneity of deposition was also manifested as a loss of the normal apex-base gradient observed in control animals, an increase in the amount of nonventilated parenchyma, enhanced airway deposition, and an altered lobar deposition pattern. Morphometric analysis showed an increase in the mean linear intercept (MLI) of emphysematous lungs as compared with control lungs. However, the author found no correlation between MLI, a measure of emphysema, and EI, a measure of deposition, quantified in the same lung pieces. It is concluded that the emphysematous lesions produced by elastase markedly alter the deposition of an inhaled submicrometric aerosol. Factors that may contribute to these changes include airway obstruction and differences in breathing pattern in emphysematous as compared with control animals.

Aerosols↗
PubMed1986

[Surgical therapy of interstitial pulmonary emphysema in a premature infant].

Pulmonary interstitial emphysema is a frequent complication in the use of respirators in newborn infants suffering from respiratory insufficiency. If it is diffuse and bilateral, treatment often is without success; occasionally, interstitial emphysema may be localized in a lobe, in which case it may persist and lead to therapeutic difficulties. We report a successful surgical approach to a unilateral pulmonary interstitial emphysema in a premature infant.

Brain Damage, Chronic↗
PubMed1985

[External respiratory function in patients with primary pulmonary emphysema etiologically related to alpha 1-antitrypsin deficiency].

To improve the diagnosis of primary lung emphysema etiologically linked with alpha-trypsin deficiency, the authors provide the results of a detailed clinico-functional study of 6 patients with an appreciable deficiency of this enzyme. According to the clinical and functional signs, all the patients were diagnosed to have a typical, pronounced lung emphysema. Therefore, the measurement of the alpha-antitrypsin content plays the crucial part in differential diagnosis of primary (hereditary determined) and secondary (obstructive) emphysema.

Adult↗
PubMedDate not supplied

Mediastinal emphysema in mountain climbers: report of two cases and review.

Two cases of mediastinal emphysema occurring in healthy individuals climbing to the summit of Mount Rainier (4,393 m.) are described. In both, the condition was probably attributable to a voluntary, forced pressure breathing technique--a modified Valsalva maneuver. The various circumstances in which mediastinal emphysema may occur are discussed, along with its possible serious complication of cardiorespiratory compromise. The means of diagnosis are presented, emphasizing that cases in which the important finding of subcutaneous emphysema is absent may be those in which the danger is greatest. Therapeutic measures that occasionally may be necessary are outlined, though the condition is usually a benign one that subsides without specific treatment.

Adult↗
PubMed1978

[Lung emphysema].

1. Elastic recoil, size of the perfused surface for gas exchange and flow resistance of the small airways influence the symptomatology and lung function of pulmonary emphysema independently of each other. 2. The loss of elastic force and surface for gas exchange are predominant in panlobular emphysema. Ventilation-perfusion disturbances due to increased airway resistance during inspiration and expiration predominate in chronic obstructive bronchitis with centrilobular emphysema. 3. In the presence of identical values for vital capacity and FEV1.0, arterial blood gas studies during rest and exercise provide the most reliable information on gas exchange surface and ventilation-perfusion disorders.

Airway Obstruction↗
PubMed1983

Pathophysiology of emphysema.

The pathophysiology of emphysema is best explained on the basis of decreased pulmonary elastic recoil. At any pleural pressure, the lung volume is higher than normal. Additionally, the altered relation between pleural and alveolar pressure facilitates expiratory dynamic compression of airways. Such compression limits airflow during forced expiration and, in severe instances, during tidal expiration. Another factor contributing to airflow limitation is disease of the airways, both large and small. In general, patients with relatively pure emphysema maintain blood gases in or near the normal range until very late in their course. PaO2 is maintained because of the preserved matching of ventilation and perfusion as alveolar walls are destroyed. PaCO2 is maintained because the ventilatory response to CO2 is not usually impaired. It is not clear why patients who are categorized clinically as "chronic bronchitics" are more likely to respond to an increased flow-resistive work of breathing by hypoventilating. Physical findings in emphysema are not specific. Radiologic changes are insensitive and are of less value than physiologic measurements.

Humans↗
PubMed1983

Surgical management of emphysema.

The history of surgery for the treatment of emphysema and its complications is long and complex and, with improved understanding of the pathophysiology, most procedures have been discarded. Present clear indications for surgery are mainly large or increasing bullae that result in compression of apparently good lung tissue, and complications of bullous emphysema such as pneumothorax and infection. With localized giant bullae the results of local resection can be as dramatic as the effects of pleural drainage for tension pneumothorax. Lobectomy should not be undertaken until bullae have been removed locally and application of positive pressure has failed to reveal any expandable lung tissue--a rare situation. Resection of small bullae generally has no effect on lung function. The indications for resection of large bullae in the presence of diffuse emphysema require careful individual study. In such cases even a small increment of function may be of great clinical benefit, and there is evidence that longevity can be increased. Finally, two-stage local drainage of tension bullae may be indicated in those rare cases in which open thoracotomy cannot be considered for other reasons.

Adult↗
PubMed1983

[The proteolytic etiopathogenesis of pulmonary emphysema].

Laennec and later workers attributed the aetiopathogenesis of emphysema to mechanical causes. This view has been superseded by the current proteolytic theory. It is now believed that the destruction of the pulmonary parenchyma in emphysema occurs when the homeostatic equilibrium between cellular proteases (polymorphonucleates and macrophages) and serum antiproteases (primarily alpha-1-antitrypsin) which protects the respiratory ways, is disturbed. This imbalance not only produces idiopathic emphysema due to alpha-1-antitrypsin but also post-bronchitic forms due to increased protease release.

Humans↗
PubMed1984

Overview of the pathology of pulmonary emphysema in the human.

While the anatomic definition of emphysema has been adopted for more than 20 years, the precise application of the definition to the lung is not established. This article examines the application of the definition, pointing out that emphysema may differ from normal in a quantitative rather than a qualitative way. Then the author reviews the functional abnormalities that are associated with emphysema and speculates why airflow obstruction and abnormal gas exchange are associated with it.

Animals↗
PubMed1984

Site predilection of airway inflammation by emphysema type.

To elucidate interrelations of airway inflammation and emphysema, bronchi from subjects with severe panlobular and centrilobular disease and normal lungs were compared. This disclosed an intense infiltration with chronic inflammatory cells, mucous gland hypertrophy, and thickening of bronchi, primarily in association with emphysema having a panlobular configuration. These changes complement a generalized thickening and inflammation of nonrespiratory bronchioles previously observed in these cases. We conclude that the panlobular pattern may be a close function of inflammatory thickening of the conductive airways to respective lungs and lung parts, but centrilobular emphysema is not reliant on these changes. The precursory defect for the centrilobular lesion instead has been shown to be a more peripherally oriented respiratory bronchiolitis around the centers of lobules.

Aged↗
PubMed1984

A comparison of starvation and elastase models of emphysema in the rat.

Starvation and elastase-induced changes in rat lung structure, biochemistry, and function were compared as models of human pulmonary emphysema. Ten-week-old male rats were instilled intratracheally with either porcine pancreatic elastase in saline (E) or with saline alone. A group of the saline-instilled rats were fed one third of their normal food intake until a 45% loss of body weight occurred (S). The remaining saline-instilled rats served as control animals (C). Post-treatment evaluations included in vivo respiratory function, lung histopathologic and morphometric analyses, lung tissue proteinolytic activity, and lung collagen. The E rats had in vivo respiratory function changes more similar to human emphysema than those of S rats. All lung volume subdivisions were decreased in S rats and increased in E rats. The volume-pressure curve of S rats was shifted to the right of the C curve, whereas that of E rats was shifted to the left. Forced expiratory flow rates of E rats were decreased at all lung volumes, but those of S rats were not. Both E and S rats had larger terminal air spaces and less alveolar surface area than did C rats. The S rats had more collagen per gram lung and higher proteinolytic activity than did C or E rats. These results show that, although starvation induces some changes characteristic of human emphysema, elastase-treatment provides a model more similar to the human disease.

Animals↗
PubMed1984

Pulmonary arterial hypertension and emphysema.

Pulmonary artery pressures were estimated by an indirect method using echocardiography (Boyd et al. 1980), in a group of patients with chronic airflow obstruction, in order to investigate the degree of pulmonary hypertension in patients with emphysema. We found a positive correlation between the estimated pulmonary artery end diastolic pressure (PAEDP) and the radiological emphysema score (r = 0.58, P less than 0.005), and between the estimated PAEDP and the transfer constant for carbon monoxide (KCO) (r = 0.66, P less than 0.002). There was no correlation between the PAEDP and the arterial partial pressure of oxygen (PaO2) before exercise, between the PAEDP and the change in oxygen partial pressure after exercise, or between the KCO and the PaO2. It is suggested that emphysema does predispose to pulmonary arterial hypertension and that the relationship is probably secondary to vessel destruction rather than hypoxia.

Aged↗
PubMed1982

[A case report of an aged patient with erythroleukemia coexistent with pulmonary emphysema, responding well to AAAP therapy].

A case of erythroleukemia coexistent with pulmonary emphysema is reported. A 67-year-old male was admitted to our hospital in May 1981, with a few year history of cough, sputum and fatigue. He had already been diagnosed as having pulmonary emphysema and moderate anemia. On physical examination, except for pallor, no other findings were remarkable. The initial hematological examination showed hemoglobin, 9.6 g/dl, red cell count, 251 x 10(4)/microliters, platelet count, 7.3 x 10(4)/microliters, white cell count, 2600/microliters with neither myeloblasts nor erythroblasts. A sternal marrow aspiration revealed 21% myeloblasts and 40% erythroblasts including 7.5% megaloblastoids. Periodic Acid Schiff staining was strongly positive for a part of erythroblasts. A chest X-P finding was typical for pulmonary emphysema. Pulmonary function was moderately damaged. He was started on chemotherapy with AAAP (ACNU 50 mg/d i.v. drip over 4 hr x 4d, adriamycin 20 mg/d i.v. push x 4d, Methotrexate 20 mg i.v. push x 4d). The first course of AAAP brought him a complete remission with both disappearance of myeloblasts and erythroid precursors with megaloblastoid nuclei in the marrow and the normalization of white cell count and platelet count in the blood. He was discharged in September 1981 after completion of a consolidation chemotherapy with AAAP. Since then, he received two courses of AAAP as an intensification chemotherapy and has been in complete remission for more than 13 months. His pulmonary function has not been affected and no myocardial damage has been seen throughout AAAP therapy. Thus, AAAP therapy seems to be an excellent chemotherapy even for an aged patient with erythroleukemia.

Aged↗