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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative and morphological analyses (in SEM) of blood platelets collected from the left and right ventricles of the rat heart in the course of experimental lung emphysema were done. Platelet aggregation index was estimated, too. Emphysema was induced by a single intratracheal instillation of papain solution in a dose of 20 mg/kg b.w/1 ml PBS. The animals were sacrificed after 2 and 24 hours and 7, 14, 28 days later. Within 24 hours of the experiment a slight decrease was observed in the number of platelets in the blood collected from the left ventricle compared to the right one as well as to control animals. Also a reduction in platelet aggregation coefficient value was noted. However, in the later period of emphysema progression (after 7th day), a statistically significant increase was found in the number of blood platelets in the left ventricle. A relation was noted between quantitative changes of blood platelets and emphysema progression evaluated morphometrically. The ultrastructural examinations in SEM suggest the occurrence of platelet satellitosis in animals intratracheally injected with papain solution. The present results indicate the possibility of a significant contribution of blood platelets to the pathogenesis of experimental lung emphysema.
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PMID:Blood platelets in experimental lung emphysema. Comparative analysis of the number and aggregation abilities of platelets in left and right ventricular blood of the heart. 769 33

Glycosaminoglycans are constituents of proteoglycans, which are integral components of lung connective tissue. Glycosaminoglycans not only provide structural support to organs, but also influence extracellular matrix assembly, cell adhesion, and cell proliferation. Changes in the metabolism of glycosaminoglycans have been noted in several pulmonary diseases, for example, pulmonary fibrosis and emphysema. We studied quantitative and qualitative changes of glycosaminoglycans in the lungs of rats exposed to a range of ozone levels (0, 0.12, 0.5, 1.0 parts per million) for 20 months. Glycosaminoglycans were isolated from dry-defatted lung tissues through successive digestions by pronase, papain, and 2 M sodium hydroxide. The glycosaminoglycans then were fractionated into individual components using high-performance liquid chromatography. The concentration of total glycosaminoglycans in the tissues varied from 1.5 to 4.2 micrograms of uronate/mg of dry-defatted tissue. Although wide variations in total glycosaminoglycan concentrations exist among individual animals within each exposure group, regression analyses of data indicate a monotonic and statistically significant decrease of total glycosaminoglycans after ozone exposure (p = 0.02). Among individual glycosaminoglycans, hyaluronan, chondroitin 4-sulfate, and chondroitin 6-sulfate levels decreased significantly (p < 0.001, p < 0.05, and p < 0.01, respectively) in animals exposed to ozone when compared with control animals. Heparan sulfate concentration exhibited a significant (p < 0.05) trend toward increase with increasing doses of ozone, but the difference in heparan sulfate concentration between ozone-exposed animals and control animals was not significant. Gel filtration studies of glycosaminoglycans in pooled samples indicated that the molecular size of hyaluronan in animals exposed to ozone was lower than it was in control animals. We noted differences in heparan sulfate's chemical properties and affinity to antithrombin III in ozone-exposed animals and control animals. Although these studies do not provide the mechanism responsible for the observed changes in the lung glycosaminoglycans in ozone-exposed animals, the observations indicate that inhalation of ozone for 20 months affects normal cellular metabolism of proteoglycans, which may contribute to the functional impairment of the lung.
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PMID:Consequences of prolonged inhalation of ozone on F344/N rats: collaborative studies. Part III: Effects on complex carbohydrates of lung connective tissue. 781 21

The effect of chronic right ventricular (RV) pressure overload on left ventricular (LV) systolic function in chronic obstructive lung disease is unclear. To examine LV systolic performance in pulmonary emphysema, a chronic canine model was developed in which pulmonary artery pressure could be elevated to a level found in human disease. Severe emphysema was produced by the repeated instillations of the enzyme papain into the lung. Sonomicrometry was used to assess LV dimensions along the septal-lateral, apex-base, and anterior-posterior orthogonal axes of the LV. With the animal conscious, measurements of LV systolic function were obtained over a wide range of LV circumferential end-ejection stresses at baseline and after 1 yr of emphysema (post-1-yr study). In the emphysema group (n = 5), the results showed that at the post-1-yr study, measurements of LV ejection fraction, mean velocity of circumferential shortening, and rate of anterior-posterior dimensional shortening were reduced compared with those obtained at the baseline study. In the emphysema group, end-systolic volume was increased for a given end-systolic pressure or stress at the post-1-yr study compared with baseline values, while fractional shortening measured along the three axes was decreased. There were no similar changes in systolic parameters in control groups. We conclude that chronic RV pressure overload may cause an impairment in LV systolic performance in chronic emphysema.
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PMID:Left ventricular systolic performance is depressed in chronic pulmonary emphysema in dogs. 804 89

A study was made of ultrastructural changes in alveolar epithelial cells after a single intratracheal papain injection. The experiment was carried out on male Wistar rats, of 180-220 g body weight. The animals were sacrificed after 1, 7, 14 and 28 days that followed proteolytic enzyme administration. The study revealed that the development of emphysematous changes in the rat lungs was accompanied by alterations in the epithelium of alveoli. In early stages of emphysema (up to 1 week), destructing changes dominated within the epithelial cells. Similar changes were observed in the endothelium of adjacent blood vessels. In later periods an increased number of type II pneumocytes were seen and focal accumulation of elastic and collagenic fibres was noticed in alveolar septa. Correlation was found between changes in the number of type II cells and their ultrastructure as well as between alveolar epithelium damage and alveolar septal interstitium alterations.
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PMID:Alveolar epithelial cells in experimental lung emphysema. Ultrastructural analysis of cells in situ in TEM. 805 30

Ultrastructural changes in alveolar epithelial cells and free alveolar cells after a single intratracheal papain injection were studied. The experiment was carried out on male Wistar rats, of 180-220 g body weight. The animals were sacrificed 1, 7, 14 and 28 days following proteolytic enzyme administration. The study revealed that the development of emphysematous changes in the rat lungs was accompanied by alterations in the epithelium of alveoli. In early stages of emphysema (up to 1 week) destructive changes predominated in the epithelial cells. In later periods an increased number of type II pneumocytes were seen and focal accumulation of elastic and collagenic fibres was noticed in alveolar septa. Correlation was found between changes in ultrastructure and number of type II cells, alveolar macrophages and neutrophils and alterations in the interstitium of alveolar septa.
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PMID:Ultrastructural analysis of the type II epithelial cells and free alveolar cells in experimental lung emphysema. 817 20

Total and differential counts of cells isolated from the lungs of Wistar rats with experimental emphysema were performed. Emphysema was induced by a single intratracheal dose of papain solution (20 mg/kg b.w.). Rats were sacrificed 1, 7, 14 and 28 days later. Cells were isolated from the lungs through multiple bronchoalveolar lavage. An attempt to identify type II pneumocytes was undertaken. Our observations suggest that none of the methods applied for identification of type II pneumocytes are completely specific. At the same time they stain type II cells and subpopulations of alveolar macrophages heavily loaded with phagocytized surfactant elements. However those methods are simple and enable an approximate evaluation of damage and regeneration processes in the extracellular alveolar lining layer and epithelium.
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PMID:Alveolar epithelial cells in experimental lung emphysema. Analysis of methods for type II pneumocyte identification among cells isolated from the respiratory tract of rats. 819 74

We studied dogs with unilateral papain-induced emphysema to answer two questions: (1) Do emphysema lung-apposed hemidiaphragm (DiE) and normal lung-apposed hemidiaphragm (DiN) have equal capacities for lowering lung surface pressure? and (2) Are side-to-side differences in intrathoracic pressure the result of unequal force outputs by DiE and DiN or are they caused by differences in their mechanical efficiency as pressure generators? After the airways of the emphysematous and normal lungs were intubated with a dual lumen endotracheal tube, both phrenic nerves were maximally stimulated at rates between 1 and 50 Hz and the changes in airway occlusion pressure (delta PaoE,N) and diaphragm length (sonomicrometry) were recorded. In all animals, delta PaoN exceeded delta PaoE. Differences in pressure ranged from 1.2 +/- 0.6 cm H2O during a twitch to 6.0 +/- 2.9 cm H2O during a 50-Hz tetanus. Midcostal bundles of DiE shortened less than corresponding bundles of DiN, but both reached the same active length relative to their optimal lengths, which were measured in vitro. There was no significant difference in fiber type distribution, fiber cross-sectional area, or maximal isometric tetanic tensions among midcostal regions of DiE and DiN. We conclude that unilateral hyperinflation impairs the mechanical efficiency of the apposing hemidiaphragm as a pressure generator.
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PMID:Diaphragm mechanics in dogs with unilateral emphysema. 847 3

Aim of the present study was to evaluate cathepsin D, base protease, antiplasmin, antitrypsin and antichymotrypsin activities and protein content in the 24h culture medium of the alveolar macrophages (AM) deriving from the rats treated BCG-vaccine and from rats with papain-induced emphysema. In the culture medium of cells isolated from the rats which were given BCG or papain and BCG+papain we observed an increase of base protease activity and a decrease of cathepsin D activity comparing with control group. Increased antitrypsin activity in BCG and BCG+papain-treated rats and decreased antitrypsin activity in papain-treated rats were observed. There were not significant differences in antiplasmin and antichymotrypsin activities between examined groups. The obtained results indicate that activated pulmonary macrophages are one of the sources of the protease-antiprotease intraalveolar imbalance. However, increased production of proteolytic enzymes may not be the only factor responsible for the progression of lung emphysema in BCG-treated rats.
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PMID:The effect of activated alveolar macrophages on experimental lung emphysema development. I. Protease and antiprotease activities in the culture medium of alveolar macrophages. 883 14

The cell-cell interaction between fibroblasts and alveolar macrophages was examined using a co-culture system. Alveolar macrophages (AM) were harvested from the bronchoalveolar lavages (BAL) of rats with papain induced lung emphysema. The BCG-vaccine was applied as a macrophage mobilizing and activating agent. The morphological examinations carried out in scanning electron microscope (SEM) as well as the evaluation of the uptake of 3H-thymidine did not show any significant differences between respective co-cultures of fibroblasts and AM isolated both from the lungs of control and experimental animals (treated with BCG or papain, and BCG+papain). However, significant growth were noted in 3H-thymidine uptake between fibroblast cultures done with or without cells isolated from the lungs. The results obtained suggest that AM can promote fibroblast proliferation during the progression of experimental lung emphysema.
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PMID:The effect of activated alveolar macrophages on experimental lung emphysema development. II. The study of fibroblast and alveolar macrophage co-culture. 883 15

Morphological (in light and transmission electron microscope) as well as morphometrical analysis of the lungs was performed on experimental, papain-induced lung emphysema. Development of emphysematous changes was studied seven days after a single intratracheal instillation of papain solution. The effect of alveolar macrophages (AM) activation by BCG-vaccine on changes in pulmonary tissue was analyzed. In the rats given BCG the number of AM increased and demonstrated enhanced activity. Increase in reticulin fibre density in places of AM cumulation, particularly in BCG+papain-treated rats was observed. The lungs of animals treated with BCG+papain showed enhancing of emphysema comparing with the papain-treated rats. Development of emphysematous changes, especially in BCG+papain-treated rats coexisted with cumulation of activated alveolar macrophages and collagen fibres as well as type II alveolar epithelial cells proliferation. Our data support the inflammatory-repair hypothesis of emphysema pathogenesis and indicate that AM regulate collagen production in the lung. Type II alveolar epithelial cells seem be important in lung injury and repair.
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PMID:The effect of activated alveolar macrophages on experimental lung emphysema development. III. Morphological analysis of the lung tissue and alveolar macrophages in situ. 883 16


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