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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The herbicide paraquat induces irreversible progressive pulmonary fibrosis in human beings and animals. The mechanisms of the fibrosis are still unresolved. There is histological and ultrastructural evidence that an early destructive phase followed by a proliferative phase occurs in the lungs post paraquat-exposure. In this study, lungs obtained from a dog 7 days following intravenous administration of paraquat (12 mg paraquat dichloride per kg bodyweight) are compared with lungs obtained from a normal dog. Examination included gross post mortem inspection, histology, transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Comparison of the TEM of the paraquat affected canine lung with the normal showed: alveolar collapse; detachment of alveolar epithelial cells from the basement membrane; alteration of the type II alveolar cell morphology; infiltration of granulocytes and erythrocytes into both the interstitium and alveolar air spaces; and fibroblasts associated with collagen fibrils. The SEM of the paraquat-exposed canine lung, reported here for the first time, demonstrated irregular, alveolar walls with type I alveolar epithelial cell detachment, and erythrocyte and alveolar macrophage infiltration. These findings suggest that the detachment of alveolar epithelial cells and the alveolar macrophage play a significant role in paraquat-induced pulmonary fibrosis.
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PMID:Ultrastructure of canine lung during the proliferative phase of paraquat toxicity. 334 60

A single intrapulmonary injection of 3.8% trisodium citrate and acid-citrate-dextrose (ACD) into rabbits results in extensive degeneration and necrosis of alveolar pneumocytes, including the type II pneumocyte, and of bronchiolar or bronchial epithelial cells. Subsequently, the alveoli and alveolar ducts collapse, and the septa and ductal walls adhere to each other, accompanied by the proliferation of interstitial fibroblasts. These fibroblasts produce fibrous connective tissue which is followed by pulmonary fibrosis in 1 week. Epithelial regeneration, especially that resulting from the proliferation of immature type II pneumocytes, occurs around the periphery of the fibrous lesions. The synthesis and release of large amounts of surfactant materials by the proliferated type II pneumocytes may induce the surfactant materials to reopen the air spaces of the collapsed and adhesive alveoli. By 4 weeks those fibrous areas in the pathological lungs become smaller and/or appear normal. These results suggest that this is a useful experimental animal model for pulmonary fibrosis, and that epithelial cells, especially type II pneumocytes, are associated with both the induction of and the recovery from the disorder; in the early stage, interference by reepithelization resulting from type II pneumocyte proliferation may elicit the proliferation of fibroblasts, and in later stages, reepithelization and surfactant synthesis by newly proliferated type II pneumocytes may permit the reopening of collapsed and adhesive air spaces.
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PMID:Experimental pulmonary fibrosis induced by trisodium citrate and acid-citrate-dextrose. 397 21

Sprague-Dawley rats were exposed for 6 h daily to 0.8 ppm of ozone and 14.4 ppm of nitrogen dioxide. Approximately 7 to 10 wk after the initiation of exposure, animals began to demonstrate respiratory insufficiency and severe weight loss. About half of the rats died between Days 55 and 78 of exposure; no overt ill effects were observed in animals exposed to filtered air, to ozone alone, or to nitrogen dioxide. Biochemical findings in animals exposed to ozone and nitrogen dioxide included increased lung content of DNA, protein, collagen, and elastin, which was about 300% higher than the control values. The collagen-specific crosslink hydroxy-pyridinium, a biomarker for mature collagen in the lung, was decreased by about 40%. These results are consistent with extensive breakdown and remodeling of the lung parenchyma and its associated vasculature. Histopathologic evaluation showed severe fibrosis, alveolar collapse, honeycombing, macrophage and mast cell accumulation, vascular smooth muscle hypertrophy, and other indications of severe progressive interstitial pulmonary fibrosis and end-stage lung disease. This unique animal model of progressive pulmonary fibrosis resembles the final stages of human idiopathic pulmonary fibrosis and should facilitate studying underlying mechanisms and potential therapy of progressive pulmonary fibrosis.
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PMID:A new model of progressive pulmonary fibrosis in rats. 834 14

1. Cell proliferative activity of atypical bronchioalveolar epithelia in lung fibrosis cases treated with bleomycin (BLM) or radiation was investigated by studying the histochemistry of the argyrophil nucleolar organiser regions (AgNORs) and proliferating cell nuclear antigen (PCNA). 2. Five and 14 autopsy cases of individuals who died of pulmonary fibrosis, caused by BLM treatment and irradiation respectively, were compared with (i) six control subjects who proved to have no apparent fibrosis of the lung at autopsy and (ii) four lung squamous cell carcinoma cases. 3. Histopathologically, both the BLM-treated and irradiated cases showed extensive collapse of the lung caused by severe fibrosis, although proliferative epithelial lesions such as atypical bronchioloalveolar hyperplasia and squamous metaplasia were more prominent in the former. 4. The mean AgNOR numbers in both atypical hyperplasias and metaplasias, of either BLM or irradiation cases, were significantly higher than in control bronchioalveolar epithelial areas, whereas they were lower than in the lung cancers. Data for PCNA-labelling indices were in time with those for AgNORs. 5. The results indicate that atypical hyperplastic lesions in the bronchioloalveoli arising during the fibrosing process as induced by BLM, and by irradiation, are highly proliferative.
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PMID:Cell proliferation in lung fibrosis-associated hyperplastic lesions. 857 79

We present a comparative histopathological study of both acute and chronic human adenovirus pneumonia, with reference to the cellular and extracellular matrix components. Seventeen lungs from autopsied patients whose ages ranged from 2 to 60 months were studied. Adenovirus types 1, 2, 3, 5, and 7 were isolated from 15 patients with acute lung disease, and types 2 and 7 were isolated from the other two patients with chronic pulmonary illness. The results indicated the occurrence of two basic patterns of adenovirus interstitial pneumonia (1) classic pattern (acute), characterized by necrosis and degeneration and many type II pneumocytes with intranuclear inclusion bodies, which were positive for adenovirus DNA by in situ hybridization, and (2) proliferative or proliferative-productive pattern (chronic), which presented with diffuse pulmonary fibrosis and the interstitial proliferation of fibroblast-like cells, compatible with myofibroblasts (positive for vimentin and alpha smooth muscle actin), and increase in collagen types I and III, elastic fibers, and proteoglycans. Alveolar collapse appears to be an important pathogenetic mechanism in the development of this pattern.
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PMID:Acute and chronic human adenovirus pneumonia: cellular and extracellular matrix components. 902 50

Non malignant asbestos diseases are dominated numerically by pleural plaques. This form of circumscribed fibrosis of the parietal pleural is generally asymptomatic and its potential for evolution is weak. More rarely diffuse pleural fibrosis results from disease of the visceral pleura with a secondary fusion of the two pleural layers. Usually it follows a pleural effusion which resolves spontaneously. Its functional effects are sometimes important. The generalised practice of computerized tomographic scanning as a work up for asbestos related disease has revealed the frequent association of this diffuse pleural fibrosis with a particular form of peripheral pulmonary collapse called round atelectasis. Asbestosis or pulmonary fibrosis induced by the inhalation of asbestos has become rarer due to the improvement in working conditions in the asbestos industry. It develops following heavy exposure. The frequency of bronchopulmonary cancer is increased when asbestosis exists although it is not currently possible to say if the two disorders are independent and each is only conditioned by exposure to asbestos or if the two diseases are inextricably linked by the same physiopathological process.
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PMID:[Non-malignant asbestos-related diseases]. 980 58

Non malignant asbestos diseases are dominated numerically by pleural plaques. This form of circumscribed fibrosis of the parietal pleural is generally asymptomatic and its potential for evolution is weak. More rarely diffuse pleural fibrosis results from disease of the visceral pleura with a secondary fusion of the two pleural layers. Usually it follows a pleural effusion which resolves spontaneously. Its functional effects are sometimes important. The generalised practice of computerized tomographic scanning as a work up for asbestos related disease has revealed the frequent association of this diffuse pleural fibrosis with a particular form of peripheral pulmonary collapse called round atelectasis. Asbestosis or pulmonary fibrosis induced by the inhalation of asbestos has become rarer due to the improvement in working conditions in the asbestos industry. It develops following heavy exposure. The frequency of bronchopulmonary cancer is increased when asbestosis exists although it is not currently possible to say if the two disorders are independent and each is only conditioned by exposure to asbestos or if the two diseases are inextricably linked by the same physiopathological process.
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PMID:[Nonmalignant asbestos-related diseases]. 1002 50

Physical examination of the pulmonary system includes inspection, auscultation, percussion, and palpation. By integrating these findings, it is often possible to diagnose and differentiate pulmonary edema, pleural effusion, pneumothorax, pulmonary fibrosis, and tracheal collapse. The veterinarian can use the physical examination optimally by initially performing examinations with those who are experienced with the methods and with an understanding of the relatively simple laws of physiology and physics governing transmission of sounds from the patient's lung.
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PMID:Physical examination of the pulmonary system. 1122 76

Paraquat poisoning is characterized by multiorgan failure and pulmonary fibrosis with respiratory failure. Multiorgan failure with circulatory collapse is a major cause of early death within 3 days of paraquat ingestion. Recent studies suggested that continuous venovenous hemofiltration (CVVH) had a role in the treatment of multiorgan failure by promoting hemodynamic stability. We therefore evaluated the effect of prophylactic CVVH in 80 patients with paraquat poisoning (August 1996 to February 1999). The amount ingested was 2.1 +/- 1.0 mouthfuls (as 20% concentrate). All patients were treated with hemoperfusion (HP; duration, 6.4 +/- 3.0 hours) within 24 hours of ingestion and then randomly assigned to the HP-alone or HP-CVVH group. Forty-four patients underwent HP only, and 36 patients underwent CVVH (duration, 57.4 +/- 31.3 hours; ultrafiltration volume, 40.2 +/- 4.8 L/d) after HP. Although time to death after ingestion was significantly longer in the HP-CVVH than HP group (5.0 +/- 5.0 versus 2.5 +/- 2.1 days; P < 0.05), there was no difference in mortality rates between the two groups (66.7% versus 63.6%; P = 0.82). In the HP group, early circulatory collapse was a major cause of death compared with the HP-CVVH group, in which late respiratory failure was a major cause of death. In conclusion, prophylactic CVVH after HP prevented early death caused by circulatory collapse and prolonged survival time. However, it could not prevent late death caused by respiratory failure and did not provide a survival benefit in acute paraquat poisoning.
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PMID:Failure of continuous venovenous hemofiltration to prevent death in paraquat poisoning. 1177 2

Congenital tracheobronchomegaly or Mounier-Kuhn Syndrome is a rare disorder of controversial etiology. It is characterized by an abnormal enlargement of the trachea and primary bronchi, because of atrophy or absence of their elastic fibers and smooth muscles. Such alterations lead to the collapse of the respiratory tract during forced exhalation, making expectoration by coughing of little use. Subjects with this disorder are, therefore, predisposed to the development of phlogistic bronchopulmonary pathologies such as bronchitis, emphysema, bronchiectasis and pulmonary fibrosis. The present work reports the case of a 65-year-old man suffering from asymptomatic congenital tracheobronchomegaly which was unknown until preoperative testing was performed (standard chest x-ray, tracheobronchoscopy) following a diagnosis of squamous cell carcinoma of the larynx. The patient underwent total laryngectomy and bilateral neck dissection without any intra- and postoperative complication. This is the first case reported in the literature of an association between laryngeal carcinoma and Mounier-Kuhn Syndrome, although a cause-effect relationship between the two pathologies cannot be advanced at this time. This paper also reports how the patient was managed in terms of anesthesiology and surgical technique, both conditioned by the marked tendency for anteroposterior tracheal wall collapse and its high reactivity to mechanical insults.
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PMID:[Laryngeal carcinoma associated with congenital tracheobronchomegaly (Mounier-Kuhn syndrome): a case report]. 1223 10


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