Alterations In Lung Tissue Research Articles

Desferrioxamine treatment reduces histological evidence of lung damage in rats after acute nitrogen dioxide (NO2) intoxication.

1. In previous studies a rat inhalation model was developed to investigate the efficacy of treatment in acute NO2 intoxication. 2. Desferrioxamine was administered intravenously to study its effect on histological alterations in lung tissue in rats after acute NO2 exposure. 3. Twenty four hours after exposure to 175 ppm NO2 for 10 minutes the lung injury observed by light microscopy in the desferrioxamine treated rats was less pronounced than in the saline treated rats. 4. Desferrioxamine appeared to provide more protection with a dose of 100 mg kg-1 24 h-1 than with 200 mg kg-1 24 h-1.

Radiobiologic and pathologic characteristics of the irradiated lung and roentgenographic aspects.

Experimental radiobiologic factors help to better understand and interpret the development of radiographic alterations in lung tissues due to radiant treatments. In this paper the authors summarize the radiologic factors and technical bases about radiotherapy of the lung. The conventional radiologic iconography has been examined in a large series of patients (n = 2151) with iatrogenic pulmonary lesions determined by various types of antineoplastic radiant treatments at the Istituto Nazionale Tumori of Milan. A radiologic control and a long follow-up is essential to assess the successive phases of postactinic lesions due to "passive" irradiation therapy for any type of non-endothoracic tumor as well as those due to "necessary" lung radiotherapy for endothoracic neoplasms. A strict relation has been found between the aspects in conventional radiologic iconography and the corresponding lesions in the irradiated lung.

Ultrastructure of Hamster and Rat Lungs After Chronic Inhalation Exposure to Cadmium Compounds

Chronic inhalation exposure to aerosolized CdCl2 increases the incidence of lung tumors in rats. For the present study small numbers of rats and hamsters were derived from the experimental groups of a longterm inhalation study with CdCl2, CdSO4, CdO and CdS. The goal of our LM, SEM and TEM investigations was to collect detailed observations on fibrotic, hyperplastic, and preneoplastic alterations of lung tissue occurring during this experiment.Immediately after sacrifice, the lungs of the animals were fixed by intratracheal instillation of Karnovsky fixative. Tissue samples were collected from the right middle lobe of the lung. For TEM the samples were postfixed with OSO4 and routine embedded in Epon. For SEM the tissue was CPD dried, mounted on Al-stubs and sputtered with Au.Exposure to all Cd compounds caused a significant increase in tumor incidence in rats but not in hamsters. In both species a multifocal alveolar bronchiolization and a generalized thickening of the alveolar septa were observed.

Are there Characteristic Alterations of Lung Tissue Associated with Crohn's Disease?

Two male patients aged 12 and 31 years suffered from Crohn's disease for more than six years and were treated with Cortison for more than four years. Surgical excision of parts of the terminal ileum was performed in both patients. They suffered from pulmonary symptoms as dyspnoea, shortness of breath and ventilation disturbances two years after operation. Wedge biopsies of the lungs revealed the following histomorphological findings: 1. Granulomatous interstitial lymphocyte infiltrates 2. Acute alveolitis with severe dysplasia of pneumocytes 3. Moderate interstitial fibrosis. Immunohistology performed in one case showed predominantly lambda chains expressed by lymphocytes associated with IgA and IgM. IgG was missing, furthermore kappa chains could not be detected. Macrophages contained endogenous lectins (sugar receptors) for fucose, maltose, and N-acetyl-D-glucosamine (glcNAc). No receptors specific for mannose, lactose, and heparin could be found. Pneumocytes did not bind the neoglycoproteins but were found to express HLA-DR receptors detectable by the monoclonal antibody LN 3 in dysplastic pneumocytes only. The histomorphological and immunohistochemical findings suggest that the analyzed alterations of lung tissue are related to the underlying disease of enteritis regionalis.

Talc deposition and effects after 20 days of repeated inhalation exposure of rats and mice to talc

The relationship between the inhalation exposure concentration of talc and the resulting lung burdens and histologic lesions was studied using groups of 20 F344/Crl rats and 20 B6C3F mice (10 male and 10 female) exposed to one of three concentrations of asbestos-free talc for 6 hr/day, 5 days/week for 4 weeks. Controls were exposed to filtered air using the same schedule. The pulmonary retention of talc and the development of pulmonary pathology were evaluated. The mass median aerodynamic diameter (MMAD) of the talc aerosol was 3.0 microns with a geometric standard deviation (sigma g) of 1.9. The mean exposure concentrations for rats were 0, 2.3, 4.3, and 17 mg talc/m3. Lung burdens in rats averaged 0, 0.07, 0.17, and 0.72 mg talc/g lung after the 20-day inhalation exposure; thus, the amount retained in the lung per unit of exposure concentration increased with increasing concentration. Mean exposure concentrations for the mice were 0, 2.2, 5.7, and 20.4 mg of talc/m3, which resulted in lung burdens of 0, 0.10, 0.29, and 1.0 mg talc/g lung; thus, the relationship between exposure concentration and the amount retained in the lung was approximately constant. Lung burdens from this study were used to project lung burdens that would result from longer exposures of rodents and man. No clinical signs were observed in the rats or mice prior to sacrifice 24 hr after the last exposure day. Histologic alterations in lung tissue consisted of only a modest, diffuse increase of talc-containing, free macrophages within alveolar spaces in both rat and mouse groups exposed to the highest level of talc for 20 days. A model simulating chronic talc inhalation exposure of rats and mice predicted lung burdens of 2-3 mg talc/g lung (wet wt) if animals were exposed to 17 mg talc/m3 for 2 years, and deposition and clearance of talc were unchanged by continued exposure. A potential limitation in this modeling is that if clearance of talc is delayed by continued exposure, the accumulated talc lung burdens would be higher than those projected by the simulation model. Humans exposed to aerosols of respirable talc are projected to accumulate much higher lung burdens than would occur in rodents exposed to the same aerosol, because humans have a higher estimated deposition fraction and slower estimated clearance of the deposited talc dust. Equilibrium lung burdens of greater than or equal to 2 mg talc/g lung were predicted for human exposures at or near the TLV for talc.

Approaches to prevention of asbestos-induced lung disease using polyethylene glycol (PEG)-conjugated catalase

Asbestos-associated damage to cells of the respiratory tract in vitro can be prevented by the simultaneous addition of scavengers of active oxygen species to cultures. To determine if administration of scavenger enzymes to animals and humans is a plausible approach to the prevention of asbestos-induced lung disease, osmotic pumps were filled with various concentrations of PEG-coupled catalase and implanted subcutaneously into Fischer 344 rats over a 28-day period. At 3, 14, and 28 days after implantation of the pumps, the animals were evaluated for levels of catalase in serum and lung. In addition, lung tissue and lavage fluids were examined at 28 days for biochemical and morphologic indications of cell injury, inflammation, and fibrotic lung disease. At all time points examined, the administration of PEG-catalase caused a dosage-dependent increase in serum levels of catalase. The levels of lung catalase were evaluated at 28 days but not at earlier time periods. In comparison to control rats, the amounts of enzymes (lactic dehydrogenase, alkaline phosphatase), protein, and cells in lavage fluids from treated animals were unaltered. Moreover, the lungs showed no evidence of inflammation or fibrotic disease as determined by differential cell counts in lavage and measurement of hydroxyproline. These studies suggest that administration of PEG-catalase does not cause injury or other alterations in lung tissue and can be pursued as a feasible approach to prevention of asbestosis.

Lung changes after beryllium inhalation: ultrastructural and morphometric study.

Monkeys and dogs were exposed to an environmenl contaminated with beryllium oxide calcinated at 1,400 C. Two years after exposure the lung tissue was investigated fey electron microscopy, using morphometric methods. In both experimental animals and controls, unidentified particles were found inside lysosomes occurring in histiocytes, endothelium, and macrophages. No neoplastic or granulematous pulmonary lesions were observed in any of the beryllium-exposed animals. The mean thickness of the air-blood barrier was not changed in the test animals. Vacuolated interstitial cells, interpreted as degranulated mast cells, were frequently found in both control and test dogs. The beryllium compound investigated did not cause pathological alterations in lung tissue two years after exposure, although it was still deposited in the lung, as demonstrated by spectrographic analysis.

Biological effects of urban air pollution. II. Chronic exposure of guinea pigs.

Rodents exposed to the ambient atmosphere of Los Angeles throughout their lives have been studied in comparison with animals maintained in smog-filtered atmospheres. In aging inbred mice of certain strains, there was an increased incidence of pulmonary adenoma. In one strain mortality of males (but not females) during the first year of life was increased. Severe smog episodes caused lung tissue alterations at the ultrastructural level, especially in mice older than 15 months. Severe episodes produced transient increases in pulmonary resistance in old guinea pigs but no demonstrable chronic or cumulative effects on this parameter. In guinea pigs sensitized by prior stress treatment, urinary excretion of 17-ketogenic steroids was enhanced by ambient atmosphere exposure. After two or three years of exposure, rabbits exhibited reduced activity of glutamic oxalacetic transaminase in blood serum.