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

The systemic administration of O,S,S-trimethyl phosphorodithioate (OSS), a contaminant of various organophosphorus insecticides, induces delayed damage to rat and mouse lung tissue. The lesion, particularly in the rat, closely resembles that produced by butylated hydroxytoluene (BHT) in mice. Although the time course of cell damage and repair has been studied in both species, it is not clear whether excess collagen, indicative of fibrosis, is deposited. Changes in pulmonary hydroxyproline content and synthesis, indices of collagen metabolism, were analysed in mice treated with 45 mg/kg OSS. A significant increase in total lung hydroxyproline was evident 21 days after treatment compared to both pair-fed and ad libitum controls. This increase was not augmented by subsequent treatment with 35 mg/kg 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or exposure to 70% oxygen for 7 days. The rate at which lung tissue synthesized hydroxyproline was increased 7-14 days after treatment with OSS. These data demonstrate that treatment of mice with OSS results in changes indicative of pulmonary fibrosis. However, in contrast to some other lung-toxic chemicals, this lesion was not enhanced by subsequent treatment with BCNU or hyperoxia.
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PMID:Pulmonary hydroxyproline content and production following treatment of mice with O,S,S-trimethyl phosphorodithioate. 366 Apr 35

To detect whether pulmonary vascular responsiveness is a factor which can aggravate the pulmonary hypertension induced by irreversible pulmonary fibrosis, we examined the acute hemodynamic effects of low-flow oxygen and of nifedipine both at rest and during exercise in 8 patients with idiopathic pulmonary fibrosis (IPF). During exercise, the increments in pulmonary artery pressure, pulmonary vascular resistance (PVR), and right ventricular stroke work index relative to resting values were blunted by both treatments. During exercise, both systemic vascular resistance and PVR decreased more significantly after nifedipine than on oxygen (p less than 0.001). At exercise, nifedipine administration induced a greater increment in oxygen delivery (CaO2 X CI) than that produced by oxygen breathing (p less than 0.01). Our results in patients with IPF seem to confirm that active vasoconstriction of pulmonary vessels may contribute to the pulmonary hypertension during exercise. The evaluation of reversibility of pulmonary hypertension by nifedipine in IPF deserves further long-term studies.
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PMID:Pulmonary vascular responsiveness at rest and during exercise in idiopathic pulmonary fibrosis: effects of oxygen and nifedipine. 374 13

A wide variety of types of pulmonary diseases and respiratory symptoms have been associated with gastroesophageal reflux (GER). Asthma, chronic bronchitis, bronchiectasis, and pulmonary fibrosis have all been linked to GER, but causal mechanisms have been difficult to establish. To characterize pulmonary function abnormalities in older children and young adults (age 7-23 years) with GER, lung function was evaluated in 22 patients being treated for reflux. The patients were divided into two groups: nine subjects (Group 1) had no history of pulmonary symptoms. Thirteen subjects (Group 2) had known pulmonary disease; all had diagnosed asthma, and five had a history of recurrent pneumonia. Lung volumes and spirometry were measured. Airway reactivity was assessed by measuring change in flows following isocapneic hyperventilation of subfreezing air. The presence of "small airway" disease was assessed by air-helium flow volume curves and the single breath oxygen test. Lung size, as indicated by measurement of total lung capacity, was normal in all patients. Flow rates, density dependence of maximal expiratory flow, single breath oxygen test, and tests of airway reactivity were abnormal only in Group 2 patients and were normal in the Group 1 patients. That not all children with GER have abnormal pulmonary function suggests that, if there is a causal relationship between GER and lung disease, it is multi-factorial in nature. Children with GER who do have lung disease have evidence of airway obstruction, maldistribution of ventilation, and increased airway reactivity, but do not have restricted lung volumes.
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PMID:Pulmonary function in older children and young adults with gastroesophageal reflux. 376 70

Groups of male rats were exposed to acute doses of oxygen, ozone, or paraquat which produced equivalent mortality (25-30%) over a 28 day post-exposure period. Quantitative evaluation of morphological changes indicated the primary response to be edema and inflammation with only slight fibrosis being apparent by the end of the observation period. Aerobic pulmonary metabolism was inhibited in lungs from animals exposed to oxygen and ozone as evidenced by decreased oxygen consumption; however, this was transient and O2 consumption returned to normal within 24 hours after removal from the exposure chamber. Conversely, treatment with paraquat caused an immediate, transient stimulation of O2 consumption. Glucose metabolism was unaltered by the gas exposures and, as previously reported, was initially stimulated by paraquat treatment. In vitro, only paraquat altered both O2 consumption and glucose metabolism when added to lung slice preparations; ozone had no effect. Oxygen did not alter O2 consumption but caused a slight biphasic response in glucose metabolism. Aerobic metabolism is relatively unchanged by these doses of oxygen and ozone which result in the death of 25-30% of all treated animals. Even though paraquat produces similar morphologic changes, it may represent a more severe metabolic insult than "equivalent" doses of oxygen or ozone. Also, if interstitial pulmonary fibrosis is a desired result of experimental exposure, rats may not be a suitable model for oxidant induced lung injury.
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PMID:Severe acute oxidant exposure: morphological damage and aerobic metabolism in the lung. 379 10

Bronchoalveolar lavage fluid (BAL) was obtained from patients with adult respiratory distress syndrome (ARDS). Controls included BAL from normal subjects and from patients with sarcoidosis or pulmonary fibrosis. Neutrophil elastase measured immunologically was found in all BAL samples, but it was strikingly greater in BAL from patients with ARDS than in the BAL from normal subjects or patients with sarcoidosis. There was no significant difference in the neutrophil elastase antigen concentrations in BAL samples from patients with ARDS and those with pulmonary fibrosis. No elastolytic activity was found in either group. The alpha-1-antitrypsin and the bronchial mucus inhibitor were greater in BAL from patients with ARDS. There was a highly significant correlation between the alveolar-arterial oxygen tension difference and the neutrophil elastase concentration in BAL from the patients with ARDS. Kallikrein, prekallikrein, factor XIa-like activity, and high molecular weight kininogen antigen were found in BAL of patients with ARDS, suggesting that the kallikrein-kinin cascade may be activated in the lungs of patients with ARDS. Kallikrein-like activity in the BAL from the patients with ARDS was significantly correlated with the number of neutrophils in the BAL, the neutrophil elastase concentration, and the ability of the BAL to release elastase from cytochalasin-B-treated neutrophils. There was no correlation between these variables and C5a concentration. These studies demonstrated an association between BAL neutrophil elastase and the clinical state of patients with ARDS.
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PMID:Neutrophil elastase-releasing factors in bronchoalveolar lavage from patients with adult respiratory distress syndrome. 387 83

The respirator lung is characterized histologically in the first exudative phase by capillary congestion, intra-alveolary edema, hyaline membranes and in most cases by concomitant inflammatory alterations. In the following irreversible phase, fibrous organization processes dominate and show a variable tendency towards pulmonary fibrosis. In 27 cases with long-term artificial respiration from 4 days to 12 weeks, mainly the proliferative alterations were investigated. In 18 cases, the histopathological findings indicated fibrosis of the alveolar septa with disseminated distribution. In 9 cases, focal fibrosis with obliterations of alveoli prevailed. The extent of pathological results in the lungs does not correlate with the duration of artificial respiration. In cases of artificial respiration with pure oxygen, there is a special toxic component, which is illustrated by a young woman with polytraumatism who was administered artificial respiration for 5 weeks with pure oxygen. She died from respiratory insufficiency with severe pulmonary fibrosis. As different pathogenetic factors may cause irreversible pulmonary fibrosis, histomorphological classification is difficult later and, moreover, forensic problems result.
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PMID:[Histomorphologic lung findings in long-term artificial respiration with special reference to extreme continuous artificial respiration using pure oxygen]. 392 60

Two parturients with severe pulmonary disease had cardiopulmonary hemodynamics assessed by invasive techniques, and vaginal delivery was conducted under continuous epidural anesthesia. Both patients demonstrated hypoxemia (F1O2 = 0.21%) by arterial blood gas analysis. Supplemental oxygen was administered throughout the last trimester of pregnancy. The patient with chronic pulmonary fibrosis had dyspnea at rest prior to pregnancy and delivered a viable, 1,400-gm infant prematurely. She died suddenly three weeks postpartum. The second patient, 41 years old, had a twin gestation. A pneumonectomy had been performed previously for tuberculosis. The patient demonstrated numerous bouts of acute pulmonary embarrassment and pneumonia, developed gestational diabetes and dyspnea late in gestation and spontaneously delivered two viable, 1,600-gm infants prematurely. All did well. Swan-Ganz catheters were used to assess cardiopulmonary hemodynamics in both patients. Epidural anesthesia was used successfully in both.
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PMID:Assessment of severe pulmonary disease in pregnancy with Swan-Ganz monitoring. A report of two cases. 398 92

The hemodynamic effects of nifedipine s.l. (20 mg) on pulmonary hypertension following chronic obstructive pulmonary disease (COPD) and advanced pulmonary fibrosis (PF) have been studied in 6 patients under stable conditions (3 patients with COPD and 3 patients with PF). Nifedipine induced a significant reduction in mean arterial pressure, right atrial pressure and systemic vascular resistances, with a significant increase in heart rate, right ventricular stroke work index and cardiac index. There was no significant change in mean pulmonary artery pressure, pulmonary arteriolar resistances and oxygen delivery. Individual analysis showed that in 2 patients with COPD there was a real direct vasodilating effect of nifedipine on the pulmonary circulation. In 2 patients with PF, the drug induced an increase in mean pulmonary artery pressure and pulmonary arteriolar resistances. In the last 2 patients, the effect of the drug on the pulmonary circulation was associated with an increase in driving pressure concomitantly with a rise in cardiac output, suggesting recruitment of the pulmonary vessels. In conclusion, nifedipine can dilate pulmonary vessels constricted by hypoxia in patients with COPD, but deleterious effects are observed in patients with pulmonary hypertension following PF.
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PMID:[Variable hemodynamic response to nifedipine in pulmonary hypertension secondary to chronic obstructive bronchopathy and pulmonary fibrosis]. 407 Oct 9

The modification of early and late radiation damage to the mouse lung by oxygen and WR 2721 has been studied by measurement of breathing rate, lethality, pleural fluid and hydroxyproline content. Protection by hypoxia and sensitization by hyperoxia of early radiation pneumonitis were demonstrated. There was a tendency for the protective effect of WR 2721 to decrease as the breathed oxygen concentration was raised above normal levels. WR 2721 protection of the late damage was higher (PF = 1.6-1.65) than was seen for early pneumonitis (PF = 1.3-1.35) when either breathing rate or lethality were used. Protection factors (PF) gained from measurements of pleural fluid at a year after treatment were similar to those for other endpoints of late damage (PF = 1.7). In contrast, the measurement of fibrosis through determination of lung hydroxyproline at 1 year gave a somewhat lower protection factor for WR 2721. In the same experiments the degree of epilation on the dorsal thorax was scored at 6 weeks. One hundred per cent oxygen gave enhancement (dose enhancement factor (DEF) = 1.2), 9 per cent oxygen reduced damage (DEF less than 0.7) and WR 2721 gave PF values in excess of 1.4 at all oxygen concentrations used. This showed that the radiation response of hair follicles was more sensitive to WR 2721 or to changes of oxygen than the lung. The results presented indicate a competitive interaction between WR 2721 and oxygen for the same injury site causing a shift in the oxygen K curve to higher oxygen concentrations. The validity of applying functional or survival measurements to assess the extent of pulmonary fibrosis is discussed.
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PMID:Oxygen-dependent protection of radiation lung damage in mice by WR 2721. 609 59

Plasma thromboxane A2, a vasoconstrictor, and plasma prostacyclin (epoprostenol), a vasodilator, were assessed by double-antibody radioimmunological assay of their respective stable circulating metabolites, thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha, in 9 patients with severe diffuse pulmonary fibrosis (DPF), who were known to become hypo-oxaemic during exercise, and in 9 healthy volunteers. In the 7 patients with the most severe DPF, mean arterial PO2 fell from 68 mm Hg at rest to 51 mm Hg at peak aerobic exercise, and mean TxB2 increased to twice the value at rest. The 9 controls remained oxygen saturated throughout exercise; their mean TxB2 did not change during aerobic exercise, but during anaerobic exercise increased to twice the value at rest, and increased further during recovery. There were no significant changes in 6-keto-prostaglandin F1 alpha in either group. The selective release of TxB2 during aerobic exercise in hypo-oxaemic patients suggests that thromboxane mediates hypoxic pulmonary vasoconstriction. Its release in normal man during anaerobic exercise may reflect a more general response to the metabolic changes of tissue hypoxia.
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PMID:Thromboxane and prostacyclin (epoprostenol) during exercise in diffuse pulmonary fibrosis. 612 94


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