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

The main purpose of our experimental series was to induce, in experimental animals, diffuse pulmonary fibrosis resembling that in human lungs. In the lungs of guinea-pigs injected with a soluble immune complex and continuously exposed to a 40-60 per cent oxygen-rich atmosphere, diffuse pulmonary fibrosis occurred in many cases in the course of 2 to 3 months after the injection. After the 100th experimental day, multiple foci of pulmonary adenomatosis occurred. The morphology was similar to that of Jaagsiekte. Electron microscopic observations revealed that these hyperplastic cells originated from type II pneumoncytes.
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PMID:Histopathological studies on experimentally induced pulmonary adenomatosis in guinea-pig lungs. 17 37

A case of fatal pulmonary fibrosis and atypical epithelial proliferation (AEP) in a patient with multiple myeloma treated with melphalan is presented. Review of 10 other autopsied patients with myeloma treated with melphalan but no thoracic radiation, other cytotoxic agents, or highdose oxygen therapy revealed one other patient who died with extensive pulmonary fibrosis and AEP. Four other patients with AEP not associated with pneumonitis or fibrosis were also found, while no such changes were found in 11 autopsy controls or 11 patients with myeloma who did not receive cytotoxic agents. Melphalan should be added to the growing list of agents capable of causing severe fibrotic pulmonary reactions.
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PMID:Pulmonary histopathologic changes associated with melphalan therapy. 35 22

Dyspnea is the medical term for the patient's or subject's complaint of shortness of breath. It encompasses the respiratory discomfort experienced in many different diease states as well as the shortness of breath felt by a normal subject during or after strenuous exercise. Several parameters which have been shown to correlate with the onset or severity of dyspnea are described, including reduced vital capacity, the ratio of minute ventilation to vital capacity, reduced breathing reserve, the work of breathing, and the oxygen cost of breathing. Attempts at quantitation of dyspnea have usually consisted of measuring physiological parameters associated with the sensation, such as the "dyspneic index". The direct measurement of respiratory sensations using modern psycho-physical methods is at an early stage of development. Since the observation that the existence of dyspnea is often unrelated to any disturbance of arterial blood gas composition, it has been generally held that the mechanism of dyspnea is primarily neurophysiological. The neural pathways may conceptually be divided into those which transmit the "dyspnea message" from the respiratory apparatus to integrating centers in the brain, and those concerned with subsequently bringing the sensation to the level of consciousness. It seems likely that there is no single sensing mechanism and neural pathway which will be able to explain dyspnea in the diverse populations of patients and subjects who experience unpleasant respiratory sensations. Three theories concerning mechanisms of dyspnea are briefly described: "length-tension inappropriateness", vagal afferent activity especially from the J-receptors, and the recent concept of diaphragmatic fatigue. Some specific characteristics of the shortness of breath experienced in certain disease states are described, including chronic bronchitis and emphysema, bronchial asthma, pulmonary fibrosis and congestive heart disease.
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PMID:Dyspnea. 50 81

Pulmonary precapillary hypertension present only during exercise is the first stage of corpulmonale. Examination of the reaction of central haemodynamics to exercise is the only way to detect it. In a model situation like unilateral pulmonary artery occlusion (UPAO) in healthy subjects, an increase in pulmonary artery pressure (Ppa) during exercise is a linear function of restriction of the pulmonary vascular bed and blood flow increase. Central haemodynamics during exercise in younger subjects after pneumonectomy (PNE) resemble the situation with UPAO provided the remaining lung is intact. In older patients after PNE the same rise of blood flow is associated with a considerably greater rise of Ppa. PNE patients compared to healthy individuals increase their cardiac output during exercise more by increasing stroke volume. Patients with pulmonary fibrosis show a disproportionate rise in Ppa in relation to flow. This is due to reduced distensibility of the pulmonary system. Hypoxia also seems to be involved in pulmonary hypertension during exercise. Pulmonary wedge pressure rises at work but remains within the normal range, even in patients having marked hypoxaemia at rest and during exercise. In idiopathic intersitial pulmonary fibrosis (IIPF), pulmonary hypertension during exercise is greater than in other forms of pulmonary fibrosis. Inhalation of oxygen during exercise in patients IIPF leads to a reversal of hypoxaemia but the decrease of Ppa is small and due to a passive decrease of cardiac output. Finally right ventricular function in restrictive pneumopathies is discussed.
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PMID:Central haemodynamics during exercise in patients with restrictive pulmonary disease. 88 Mar 98

Eleven patients with severe influenza viral pneumonia were seen over a six-week interval. Five patients survived after prolonged respirator and oxygen therapy. Follow-up chest roentgenograms and pulmonary function testing one year after recovery showed development of diffuse pulmonary fibrosis in the four survivors reexamined.
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PMID:Clinical course, management, and long-term sequelae of respiratory failure due to influenza viral pneumonia. 89 55

Physiological conditions of respiration in children are defined especially by - relative hyperventilation because of high oxygen uptake per body surface, - relative narrow and soft airways with high tendency to obstruction, causing atelectasis, pneumonia or severe bronchiolitis. It is useful to differentiate between bronchiolitis and spastic or asthmatoid bronchitis, the latter being sensible to Adrenalin and developing to asthma of adults. Characteristical signs of asthmatoid bronchitis are bronchial hyperreactivity, increased airway-resistance and residual volume, decreased FEV 1, pulmonary compliance, arterial PO2 and PCO2 with signs of pulmonary inhomogeneity. Mucviscidosis, starting from abnormal viscosity of bronchial secretion, is functionally characterized by similar signs, so are increased RV with air-trapping, decreased FEV 1, VC, PO2a and pulmonary inhomogeneity. Diffuse progressive interstitial pulmonary fibrosis (HAMMAN-RICH) of acute type being mostly lethal in children up to 2 years of age and of subacute type in older children shows diffusion disturbance and characteristical ventilation disturbance with reduction of inspiratory reserve volume and enlargement of functional residual capacity but normal FEV 1. Disturbances are sensible to corticoid-therapy.
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PMID:[Pathophysiology of respiratory disturbances in children (author's transl)]. 96 Jul 65

A light and electron microscopic study was carried out in 21 infants in whom the pathologic diagnosis of bronchopulmonary dysplasia had been made. All the infants except two had the respiratory distress syndrome at birth, and all 21 had been treated with respirator and oxygen therapy for various periods of time. The pathologic alterations observed in all the infants studied were primarily damage of the bronchial and bronchiolar ciliary apparatus and mucous membranes, severe necrotizing bronchiolitis, and marked bronchiolar and alveolar fibrosis. These changes were more pronounced in infants who survived the longest period of time. Such inflammatory and fibrotic changes are known to predispose to destruction of lung tissue, emphysema, and pulmonary hypertension. Six of these 21 infants developed symptoms and signs of cardiac atrial or ventricular stress, including cor pulmonale, prior to their demise. These infants were among those that survived the longest periods of time, had the longest exposure to supplemental oxygen, and showed histopathologically severe pulmonary fibrosis and emphysema.
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PMID:Bronchopulmonary dysplasia: the pulmonary pathologic sequel of necrotizing bronchiolitis and pulmonary fibrosis. 99 46

Ingestion or injection of the herbicide paraquat (1,1'-dimethyl-4,4'-dipyridylium dichloride) has caused more than 120 deaths in humans. Most have been due to respiratory failure caused by pulmonary edema, hemorrhage, and atelectasis, or subsequent pulmonary fibrosis. Paraquat is concentrated in lung tissue and is believed to cause superoxide radical formation in the presence of oxygen and suitable electron donors. Exposure to increased concentrations of oxygen has been reported to accelerate the toxicity of paraquat. The therapeutic efficacy of a reduced oxygen environment was investigated by exposing paraquat-poisoned mice to 10% oxygen after stepwise drops from 14% oxygen. Sixty-one mice were given intraperitoneal injections of 27 mg. per kg. of paraquat. The 25 mice in hypoxia for 7 days had a 32% mortality rate versus a 78% mortality rate for the remainder of the mice in room air, p less than 0.01. After a dose of 20 mg. per kg. of paraquat administered intraperitoneally, 24 mice in hypoxia had a 25% mortality rate versus 51% for 35 animals in room air. Brief exposures of the hypoxic group to "normoxia" (room air) led to pulmonary edema and death. The continuous exposure of paraquat-poisoned animals to hypoxic environments was protective. This approach may be useful in other oxidant lung injuries.
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PMID:Hypoxic protection in paraquat poisoning. 99 61

Following near-drowning in fresh water, a 19-year-old man experienced severe adult respiratory distress syndrome, necessitating ventilatory support with positive end-expiratory pressure and high oxygen concentrations. Post-extubation, his course was highlighted by persistent hypoxemia and interrupted by a lung abscess which responded promptly to antibiotics. Pulmonary function tests were consistent with severe restrictive disease and chest radiograph revealed persistent bilateral alveolar and interstitial infiltrates. An open lung biopsy on the 26th hospital day showed interstitial fibrosis. Over the ensuing two months, the chest radiograph and pulmonary function tests returned towards normal. We attribute the pulmonary fibrosis to incomplete resolution of the alveolar interstitial pathology secondary to the near-drowning and exposure to high oxygen mixtures.
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PMID:Pulmonary interstitial fibrosis following near-drowning and exposure to short-term high oxygen concentrations. 115 46

In our previous papers we reported characteristic morphological changes of the capillary endothelium in the lung and of the arterial endothelium. These changes were induced by administration of various soluble immune complexes. In this paper we have induced pulmonary fibrosis in guinea pigs under allergic procedures. Administration of soluble immune complexes alone produces interstitial pneumonia. However, these changes would not normally result in diffuse pulmonary fibrosis. The administration of soluble immune complexes to guinea pigs plus exposure to a 60% oxygen-rich atmosphere yielded diffuse pulmonary fibrosis.
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PMID:Experimental pulmonary fibrosis induced by soluble immune complex and 60% oxygen atmosphere. 115 25


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