Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pulmonary effects of endotoxin-induced, repetitive, intravascular leukocyte sequestration were studied in dogs and were compared to the effects of intratracheal papain. Lung specimens from 7 animals receiving 20 to 23 weekly injections were histologically and physiologically similar to those from 10 control animals. Dogs receiving 50 injections of endotoxin during 17 wk developed histologic evidence of emphysema as seen on whole lung sections, a significant increase in mean linear intercept, and loss of elasticity at high lung volumes. The group of animals given intratracheal papain also developed histologic evidence of emphysema, with increased mean linear intercepts and loss of lung elasticity. However, the effects on lung elasticity were much greater in the papain group. Endotoxin-induced, repetitive leukocyte sequestration in the lungs results in mild emphysema; however, similar changes in alveolar size appear to cause less effect on the pressure-volume loop than does papain-induced emphysema.
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PMID:Emphysema associated with intravascular leukocyte sequestration. Comparison with papain-induced emphysema. 700 78

Inhalation of papain by dogs produced morphological changes corresponding to a centrolobular emphysema. The papain inhalation also induced a purulent catarrhal bronchitis. However, the functional changes seen in chronic obstructive bronchitis were not observed. During papain inhalation an increased sensitivity of the bronchial systems develops corresponding to a tremendous increase in bronchospasm in response to Acetylcholine aerosol. The parenchymal lung tissue in dogs is more vulnerable in developing emphysema after papain exposure than is teh bronchial system in developing a chronic obstructive airway disease.
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PMID:[Proteolytic lung emphysema and obstructive airway disease (author's transl)]. 701 38

The authors formed lung emphysema in white rats under experimental conditions by intratracheal application of various concentrations of papaine at different intervals. In the performed experiment the most suitable dose for formation of emphysema was two fold administration of 2 milligrams of papaine. The following indices were observed in the experimental and control animals: body weight, weight coefficient of the internal organs, indices of lipid and nucleinic metabolism in homogenates of lung as well as histomorphologic examination of lung.
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PMID:[Creation of experimental emphysema by the intratracheal administration of papain]. 725 20

To correlate lung structure and function in an animal model of emphysema, 17 dog lungs were treated with intrabronchial instillation of papain (range of concentration 0.5-5%); the contralateral lungs served as controls. The lungs were inflated to the volume at a transpulmonary pressure (PL) of 25 cmH2O (V25), and static pressure-volume and maximal expiratory flow-volume curves were obtained. Eight pairs of lungs were processed for histology at a PL of 5 cmH2O, and eight pairs of lungs were processed at a PL of 25 cmH2O. Significant loss of elastic recoil was found in the papain-treated lungs, between 30 and 90% predicted V25 (P less than 0.02). However, there was no correlation between the mean linear intercept corrected to predicted lung volume (indicative of alveolar destruction) and loss of elastic recoil. There was a significant reduction of maximal flow (Vmax) between 20 and 90% predicted V25. However, the reduction in Vmax was commensurate with the reduction of elastic recoil, since there was no significant change in resistance of the upstream segment between 30 and 70% predicted V25. Airway morphometry demonstrated no significant differences in small airway dimensions between control and emphysema-treated lungs. In both control and papain-treated lungs, small airway dimensions changed relatively more than lung volume a PL of 25 and 5 cmH2O.
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PMID:Correlation between lung structure and function in a canine model of emphysema. 726 39

Experimental lesions of emphysema were produced in SPF rats after laryngotracheal injection of papain and coal dust. The infrastructural changes were investigated a different intervals. The lesions observed are progressive, characterized by atrophy and ruptures of the interalveolar septa, and the disappearance of pneumocytes II. Passage through the septa of mineral particles is enhanced and total dust clearance seems to be increased. The results are discussed in the light of alveolar clearance studies using Fe-59 and surface tension measurements on pulmonary washings.
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PMID:Experimental study of pulmonary emphysema in rats exposed to coal dust and papain: effects on the infrastructure and the cell dynamics. 735 17

These studies show that very soon after exposure of canine lungs to crude papain mixed with a marker (India ink), the alveolar surface-active lining was both morphologically and functionally altered, and alveolar macrophages were destroyed in significant numbers. These changes occurred before other identifiable major alterations. The morphologic changes were characterized by replacement of the normal alveolar surface lining by an amorphous material adhering to the alveolar surfaces and penetrating the pores of Kohn, which were significantly enlarged. Type II epithelial cells and alveolar macrophages were increased in number, with a significant proportion of the latter observed to be disintegrating. Polymorphonuclear leukocytes were also noted in increased numbers, but this was also observed in control lungs (instilled only with saline plus India ink). Functionally the alveolar surface lining as studied in lung extracts showed an abnormal stability index after either in vivo or in vitro exposure to crude papain. These findings suggest that the early effects of this exogenous protease on the lung are interrelated, alveolar surface lining injury appearing to set the stage for accelerated macrophage lysis, with the probable release of phagocytosed exogenous protease as well as intracellular endogenous proteases. These events may represent early steps in the pathogenesis of experimental papain-induced pulmonary emphysema.
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PMID:Early ultrastructural changes in papain-induced experimental emphysema. 735 91

Adult rats were exposed to an aerosol of 10% papain for 8 h twice in a 2-wk interval. The control rats were exposed to isotonic saline in the same manner. Three weeks after the final exposure rats were divided into four groups: emphysema-fed, emphysema-starved, control-fed, and control-starved. Starved animals received one-third of their measured daily food consumption and water ad libitum for 6 wk. Final body weight, dry and wet weights of lungs and postfixation lung volume (VL) were significantly lower in starved rats. Dry-to-wet weight ratios were not significantly different among the groups, but VL/body weight was significantly higher in starved animals. Elastic recoil pressure of lung tissue determined in saline-filled lungs decreased and chord compliance over mid- and high-volume ranges increased significantly in starved animals both in control and emphysema groups. Mean linear intercept of air spaces was greater and internal surface area was smaller in starved rats in each group. Therefore, it appears that starvation aggravates the preexisting emphysematous processes in rat lungs.
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PMID:Influence of starvation on enzyme-induced emphysema. 736 14

Of the twenty-three employees at a pharmaceutical plant manufacturing a new product containing papain, twelve had respiratory symptoms of cough, wheezing, dyspnoea, or chest paint. Most were studied with in-depth interviews by a doctor, extensive pulmonary function tests, and immunoserological tests for IgE and precipitating antibodies specific for papain, as well as total IgE antibodies to common natural allergens. There were significant correlates (all P values < 0.05) between the presence of specific IgE antibodies to papain and decreases of FEV1, FEF75--85, TLC, RV, and response to bronchodilators as percentage change from baseline for all spirographic flow rates. Atopic workers developed pulmonary symptoms and antipapain antibodies significantly sooner after papain exposure than did the others. Duration of exposure had no effect on symptomatology, pulmonary function, or immunological response. However, those judged to have the greatest amount of dust exposure per work-day had significantly more pulmonary symptoms (P < 0.005). Papain produced lung diseases by acting as an inhalant allergen rather than a proteolytic enzyme. Papain is a potent sensitizer in humans for the production of respiratory disease. The pulmonary reactions, based on physiological data, seem to involve small airways, alveolar, and interstitial lung tissue in an inflammatory rather than destructive manner, and thus resemble bronchitis and interstitial lung disease rather than pulmonary emphysema or typical bronchial asthma.
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PMID:Pulmonary disease in workers exposed to papain: clinico-physiological and immunological studies. 746 Feb 65

The aim of the study was to evaluate the protease and antiprotease activity in the fluid obtained from the culture of cells isolated from the lungs of animals with experimental emphysema. An attempt was made to correlate the results of biochemical examinations with adherence degree and ultrastructural changes of the surface of BAL-isolated cells. The experiment was carried out on male Wistar rats, of 180-220 g b.w. Two i.p. injections of BCG-vaccine (4 x 10(8) microorganisms) on the 1st and 14th day were applied as macrophage mobilizing and activating agent. Papain (2 mg/l ml/100 g b.w.) was given once i.t. on the 21st day. The animals were sacrificed on the 28th day of the experiment. We found a correlation between the increase in the cell adherence and ultrastructural changes (in SEM), suggesting an increased activity of the cells isolated from BCG-treated rats. In the culture medium of cells isolated from the rats which were given BCG or papain and BCG+papain we observed an increased base protease activity and decreased Cathepsin D activity comparing with the control group. Increased antitrypsin activity in the BCG and BCG+papain-treated rats and decreased antitrypsin activity in papain-treated rats only was observed, too. There was no obvious difference in the levels of the antiplasmin and antichymotrypsin activities between the groups. The present results indicate that activated pulmonary macrophages are one of the sources of the protease-antiprotease intraalveolar imbalance. However, an increased production of proteolytic enzymes may not be the only factor responsible for the progression of lung emphysema in BCG-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of morphological and biochemical changes of BAL-isolated cells in experimental lung emphysema. 749 38

The deposition and dispersion of inhaled aerosol boluses were investigated as markers of lung injury in three dogs before and after emphysema was induced by papain exposure. After the experiments, lung damage was assessed histologically. Four unexposed dogs were used as controls. Effective air space diameter (EAD) was determined from aerosol deposition during a 5-s breath hold. Nonuniform ventilation was assessed from the spreading of the expired bolus, quantified as a coefficient of dispersion (CD), and from expired bolus skewness (SK). Experiments were done with a range of bolus penetrations and ventilatory flow rates. After papain exposure, EAD measured with the most penetrating boluses increased an average of 89% (P < 0.0001); CD and SK measured with boluses of medium penetration and a flow rate of 0.5 l/s increased an average of 24% (P < 0.02) and 98% (P < 0.002), respectively. The effects of lung injury on CD and SK increased with flow rate. Lung injury was confirmed by changes in lung mechanics and by histology. EAD measured with deeply penetrating boluses correlated significantly with the mean chord length measured morphometrically (P < 0.05). No correlation was found with more shallow boluses. The results indicate that EAD, CD, and SK are sensitive markers of lung injury in experimental emphysema and that EAD is a specific marker of increased air space size.
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PMID:Aerosol deposition and dispersion characterize lung injury in a canine model of emphysema. 761 74


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