Pulmonary injury in rats following continuous exposure to 60% O2 for 7 days

Hayatdavoudi, G.; O’Neil, John J.; Barry, Brenda E.; Freeman, B. A.; Crapo, J. D.

doi:10.1152/jappl.1981.51.5.1220

Cited by 57 publications

(28 citation statements)

References 17 publications

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“…In the ference of cytochrome oxidase or peroxidase with the assay. In control group and the NDH group subjected to a 5-h period of lysates of rat erythrocytes, we found the CuZnSOD to be 9.7 ventilation with room air or pure oxygen immediately after birth, times more active at pH 10.2 than at pH 7.8, which is in SOD, catalase, and GPX activity remained at about the initial accordance with earlier reports (15). Because manganese SOD level (Table 3).…”

Section: Original Reports By La~hmann El A/ (1 1) On Artificial Ventsupporting

confidence: 90%

Nitrofen-Induced Diaphragmatic Hernias in Rats: Pulmonary Antioxidant Enzyme Activities

et al. 1992

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ABSTRACT. We developed an experimental rat model of sive care and artificial ventilation (I). Mortality still remains at congenital diaphragmatic hernia (CDH) to elucidate the 50% as a result of pulmonary hypoplasia with or without peretiology and pathogenesis of this serious congenital anom-sistent pulmonary hypertension (2). Those infants with severe aly in humans and in particular to study the effects of a respiratory compromise need maximal ventilatory support and short period of artificial ventilation on the CDH lung in are often subjected to high inflation pressures and high percentrelation to antioxidant defense mechanisms. CDH was ages of oxygen. The side effects of respiratory treatment are well induced in about 60% of the offspring by maternal exposure known, (3) and the clinical picture of bronchopulmonary dysplato 2,4-dichlorophenyl-pnitrophenylether (Nitrofen) during sia has become one of the major sequelae of neonatal intensive pregnancy. This herbicide resembles thyroid hormone in care (4). Only a few reports describe defense mechanisms against chemical structure. The lungs of fetal rats (d 19, 20, 21, oxidative stress in the human neonatal lung (5). Most experiand 22) were examined for protein and DNA content and mental studies on the development of AOA have been done in activity of superoxide dismutase, catalase, and glutathione small rodents (6, 7). The effect of artificial ventilation on the peroxidase (GPX). The same parameters were assessed in lung has been studied only in larger animals such as the baboon tracheotomized newborn rats after pressure-controlled ar-(8). tificial ventilation with either room air or pure oxygen We described a model in which CDH was induced in fetal during a short period of 5 h. In both CDH rats and controls, Sprague-Dawley rats by maternal exposure to a single dose of wet lung weight increased during gestation. At term, CDH 2,4-dichlorophenyl-pnitrophenylether (Nitrofen, Wako Chemirats had significantly lower mean lung weights than con-cals, Neuss, Germany) during pregnancy (9, 10). The incidence trols. Neither group differed in protein and DNA content of CDH in the treatment group was up to 60%. The diaphragper mg lung or superoxide dismutase, catalase, and GPX matic defect was mainly right-sided with severe hypoplasia of the activity before and at birth. After artificial ventilation of lung as reflected by decreased lung weight/body weight ratios. neonates with air and pure oxygen, superoxide dismutase No correlation was found between the size of the defect and the activity tended to decrease, whereas catalase activity re-ipsilateral and contralateral lung weights (9). Without artificial mained virtually unchanged in the CDH lung. However, ventilation, more than 80% of the CDH animals died within 2 GPX activity in the CDH lung was reduced to 80% of h after birth as a result of severe respiratory insufficiency. initial activity at term after ventilation with air and to 70%In the present study, we report 1 )

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Section: Original Reports By La~hmann El A/ (1 1) On Artificial Ventsupporting

confidence: 90%

Nitrofen-Induced Diaphragmatic Hernias in Rats: Pulmonary Antioxidant Enzyme Activities

et al. 1992

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“…704 Bitterman et al General concepts ofpulmonaryfibrosis Independent of cause, the fundamental anatomical feature of pulmonary fibrosis is an increased number of fibroblasts within the alveolar wall. Qualitative studies in humans (30,31), as well as morphometric studies in animals (10,11,32), indicate a several-fold increase in fibroblast number in these disorders. As a result of this expansion of the lung fibroblast population, there tration is increased two-to fivefold (40).…”

Section: Discussionmentioning

confidence: 97%

Modulation of alveolar macrophage-driven fibroblast proliferation by alternative macrophage mediators.

Bitterman¹,

Wewers²,

Rennard³

et al. 1986

J. Clin. Invest.

213

108

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Tissue fibrosis results, in part, from an interaction between growth regulatory molecules released by mononuclear phagocytes and fibroblasts. In the chronic interstitial lung disorders, alveolar macrophages, the mononuclear phagocytes of the lung, are known to spontaneously release two growth factors for fibroblasts, fibronectin and alveolar macrophage-derived growth factor (AMDGF) that together stimulate nonreplicating lung fibroblasts to divide. In addition to these two primary growth promoting signals, alveolar macrophages are able to release other mediators that may have a potential role in modulating lung fibroblast replication in response to these primary signals, including interferon y (IFNy), prostaglandin E2 (PGE2), and interleukin 1 (IL-1).To evaluate this possibility, we examined the effect of each of these other mediators on lung fibroblast replication in response to fibronectin and AMDGF in serum-free, defined medium. IFNy had no effect on fibroblast replication. In contrast, PGE2 resulted in a dose-dependent inhibition offibroblast replication in response to fibronectin and AMDGF with 50% of the maximum inhibition observed at a PGE2 concentration of <10 ng/ml. IL-1, while not active as a primary growth promoting signal, at concentrations of 4-10 U/ml, augmented fibroblast replication in response to fibronectin and AMDGF by 10 to 15%. Temporally, the growth augmenting effect of IL-1 occurred early in the GI phase of the cell cycle. These data indicate that lung fibroblast replication in response to two of the primary growth promoting signals spontaneously released by alveolar macrophages in the interstitial lung disorders, while uninfluenced by IFNy, can be inhibited by PGE2 and modestly augmented by IL-1. Understanding the relevant fibroblast growth modulatory signals within the alveolar microenvironment in the chronic interstitial disorders may lead to rational therapeutic strategies designed to interrupt the fibrotic process.

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“…Moreover, several studies have shown that bovine (49), murine (50), and hamster (45) (18)(19)(20)(21)(22)(23)(24). Second, rigorous demonstration of increased numbers of alveolar macrophages by morphometry has been performed in several animal models of inflammatory lung disorders (51)(52)(53) and in small numbers of human smokers (54). Finally, quantitation of the numbers of macrophages recovered by bronchoalveolar lavage indicates that individuals with chronic lung inflammation have a substantial increase in the number of macrophages in the alveolar compartment accessible to that procedure (55).…”

Section: Discussionmentioning

confidence: 99%

Alveolar macrophage replication. One mechanism for the expansion of the mononuclear phagocyte population in the chronically inflamed lung.

et al. 1984

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A s bstract. Within any chronically inflamed tissue, there is an increased number of macrophages, pluripotential phagocytic cells that, while critical to host defenses, are also able to profoundly damage parenchymal structure and function. Because of their central role in the inflammatory response, considerable attention has been focused on the mechanisms resulting in an expansion of the macrophage population within an inflamed tissue. Although recruitment of precursor monocytes from the circulation into inflamed tissues clearly plays an important role in macrophage accumulation, it is also possible that replication of tissue macrophages contributes to the expansion of macrophage numbers in inflammation. Because of the accessibility of tissue macrophages with the technique of bronchoalveolar lavage, the lung provides an ideal opportunity to test this hypothesis in humans. To accomplish this, bronchoalveolar lavage was performed to obtain alveolar macrophages from normals (n = 5) and individuals with chronic lung inflammation (normal smokers [n = 5], idiopathic pulmonary fibrosis [n = 13], sarcoidosis [n = 18], and other chronic interstitial lung disorders [n = 1 1]). Alveolar macrophage replication was quantified by three independent methods: (a) DNA synthesis, assessed by autoradiographic analysis of macrophages cultured for 16 h in the presence of [3H]thymidine; (b) DNA content, assessed by flow cytometric analysis of macrophages fixed immediately after recovery from the lower respiratory tract; and (c) cell division, assessed by cluster formation in semisolid medium. While the proportion of replicating macrophages

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Pulmonary injury in rats following continuous exposure to 60% O2 for 7 days

Cited by 57 publications

References 17 publications

Nitrofen-Induced Diaphragmatic Hernias in Rats: Pulmonary Antioxidant Enzyme Activities

Nitrofen-Induced Diaphragmatic Hernias in Rats: Pulmonary Antioxidant Enzyme Activities

Modulation of alveolar macrophage-driven fibroblast proliferation by alternative macrophage mediators.

Alveolar macrophage replication. One mechanism for the expansion of the mononuclear phagocyte population in the chronically inflamed lung.

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