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Biomedical subjects

P Soler

Publications and source records attributed to P Soler.

At least 91 records · Page 5Linked to original sources
PubMed1987

Pulmonary fibrosis following pneumonia due to acute Legionnaires' disease. Clinical, ultrastructural, and immunofluorescent study.

During a recent nosocomial outbreak, 20 critically ill patients with acute Legionnaires' disease were admitted to the intensive care unit of Hopital Bichat, Paris. Pulmonary specimens were obtained at surgery or immediately after death in 12 patients and were examined by light, immunofluorescent, and electron microscopy. Five of these 12 patients showed evidence of pulmonary fibrosis. In all of these five patients, infection with Legionella pneumophila was evidenced by bacteriologic methods, and other diseases known to cause fibrosis were excluded. The condition of four patients deteriorated rapidly with respiratory failure, and they died with pulmonary fibrosis. Only one patient finally recovered but was left with pulmonary sequelae. Two distinctive morphologic patterns were observed, one in which interstitial fibrosis was predominant and one in which intra-alveolar organization and fibrosis were also present. The alveolar epithelial lining and the basement membranes were disrupted in all patients, as evidenced by ultrastructural observations and by immunofluorescent studies showing gaps in the distribution of type 4 collagen and laminin. Types 1 and 3 collagen accumulated in areas corresponding to thickened interstitium and intra-alveolar fibrosis. Thus, some patients who survive the acute pneumonia of Legionnaires' disease may develop pulmonary fibrosis, and this process may lead to functional impairment or death despite prompt and appropriate treatment.

Adult↗
PubMed1986

Sarcoid-like lymphocytosis of the lower respiratory tract in patients with active Crohn's disease.

To re-evaluate the relationship between Crohn's disease and sarcoidosis, we compared the numbers and types of cells recovered by bronchoalveolar lavage from normal volunteers and patients with Crohn's disease, with other forms of inflammatory bowel disease, and with sarcoidosis. Patients with Crohn's disease, but not patients with other inflammatory bowel disorders, had an increase in the number of T lymphocytes on the surface of the lower respiratory tract similar to that seen in patients with sarcoidosis. As in sarcoidosis, this lymphocytosis results from an expansion of the T4+ T-lymphocyte subset, is characteristic of patients with active disease only, and is not associated with similar abnormalities in the peripheral blood. Thus, patients with apparently localized Crohn's disease have sarcoid-like lymphocytosis of the lower respiratory tract, a finding that emphasizes the systemic nature of Crohn's disease and the disorder's close relationship to sarcoidosis.

Adolescent↗
PubMed1986

Intraluminal fibrosis in interstitial lung disorders.

The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8). Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized. All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment. Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause. Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis. Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved. Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue.

Alveolitis, Extrinsic Allergic↗
PubMed1985

Cytochrome b-245 in human alveolar macrophages.

To kill microorganisms, phagocytes exhibit an oxidative burst with, in particular, a NADPH-dependent, superoxide-generating system that consists, in polymorphonuclear leukocytes (PMN), of a flavin enzyme and cytochrome b-245 (cyt b-245). We investigated the existence of this cytochrome in human alveolar macrophages (AM) because its presence would support its wide-spread occurrence in phagocytes and would raise the possibility of similarities in the oxygen-dependent killing mechanisms in AM and PMN. Moreover, we compared the amount of cyt b-245 in AM from patients with lung disorders with that from healthy subjects, by a differential spectroscopic measurement of its 558 to 559 nm characteristic band. This spectrum showed that cyt b-245 was present in AM. In AM of healthy subjects, the amount was similar to that found in PMN of blood. In AM of patients with miscellaneous lung diseases and in Am of infected lungs, the data were not modified.

Cytochrome b Group↗
PubMed1985

Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats.

The mechanisms by which intermittent positive-pressure ventilation with high inflation pressure (HIPPV) induces pulmonary edema remain uncertain. In this study we investigated the physiologic and anatomic changes related to HIPPV at 45 cmH2O peak inspiratory pressure in rats. Edema was quantified by the extravascular lung water obtained from postmortem weighing and by 22Na distribution space. Pulmonary microvascular permeability was assessed by dry lung weight and fractional albumin uptake. After only 5 min of HIPPV, there was a significant increase in Na space, dry lung weight, and fractional albumin uptake when compared with that in control rats mechanically ventilated at 7 cmH2O peak inspiratory pressure. These changes suggest that edema may be due at least in part to alterations in microvascular permeability. Moderate peribronchovascular edema was present. At the ultrastructural level, some endothelial cells were found detached from their basement membrane. This lesion has been previously described in other types of pulmonary microvascular injury. The above findings remained almost unchanged after 10 min of HIPPV. After 20 min of HIPPV, we observed the outpouring of a high protein content alveolar flooding accompanied by a further significant increase in fractional albumin uptake and dry lung weight. Additional anatomic damage appeared including epithelial lesions and hyaline membranes. Thus, HIPPV edema presents all the features of high permeability edema. These results may be of concern in the ventilatory management of patients with acute respiratory failure in order to avoid additional damages induced by local overinflation.

Animals↗
PubMed1985

Immunocytochemical characterization of pulmonary histiocytosis X cells in lung biopsies.

Morphologic and immunohistochemical studies were made of open lung biopsies from 9 patients with pulmonary histiocytosis X (HX) and 12 patients with other conditions, and of skin biopsies from patients with cutaneous sarcoidosis, Chester-Erdheim disease, and eruptive histiocytoma. The monoclonal antibody OKT6 was detected with the use of goat anti-mouse IgG labeled with fluorescein (FITC) for light microscopy, and sheep antimouse Fab'2 fragment of IgG labeled with horseradish peroxidase (HRP) for immunoelectron microscopy. The presence of S-100 protein was revealed by an antibody prepared against bovine S-100 protein, using sheep anti-rabbit IgG labeled with FITC for light microscopy and with HRP for immunoelectron microscopy. OKT6 antibody and S-100 protein were detected simultaneously by double labeling with FITC and rhodamine. In all patients with pulmonary HX, the major cellular components (HX cells) of the granulomas showed labeling of the plasma membranes by OKT6 and of the cytoplasm by the anti S-100 protein antibody. The double-labeling technique demonstrated that the same cells carried both reactivities. Immunoelectron microscopy showed that the reactive cells had all the structural characteristics of Langerhans cells, including Langerhans cell granules. Cells reacting with OKT6 showed discrete internal labeling in some of the Langerhans granules, especially those in continuity with the plasma membranes. However, internal labeling of Langerhans granules was not demonstrated in preparations for the localization of S-100 protein. Control samples of sarcoid lesions and other pulmonary lesions unrelated to HX did not show any reactivity except in Langerhans cells; a skin lesion from a patient with eruptive histiocytoma contained OKT6-positive cells which did not have Langerhans granules.

Antibodies, Monoclonal↗
PubMed1984

[Exploratory bronchoalveolar lavage].

Bronchoalveolar lavage is a simple technique, complementary to fiberoptic bronchoscopy. The material yielded comprises cells and supernatant, and both components may provide information about the distal lung structures. A few counter-indications should be respected. Normally, the cell differential comprises: 93 +/- 5% alveolar macrophages, 7 +/- 1% lymphocytes and about 1% neutrophils, eosinophils and basophils. Total cellularity and cell differentials are altered in many conditions, according to different patterns, which permits a classification. The increase in numbers may relate to macrophages (smokers, pneumoconiotic disorders...), to lymphocytes (sarcoidosis, hypersensitivity pneumonitis...) and to neutrophils and/or eosinophils (fibrotic disorders, chronic eosinophilic pneumonia, histiocytosis X...). In the last disease, the diagnosis may be established by detecting Langerhans cells. In other conditions, bronchoalveolar lavage mostly provides a trend to diagnosis. Usually well tolerated, bronchoalveolar lavage may usefully be repeated for monitoring patients with chronic interstitial lung disorders. It also gives an insight into the pathogenesis of many pulmonary pathological processes.

Bronchi↗
PubMed1984

Lung alterations in guinea-pigs infected with influenza virus.

Guinea-pigs were infected intranasally with influenza A Hong Kong 68 (H3N2) virus. Infective particles were re-isolated from lung homogenates up to 3 days after inoculation and indicated local replication. The subsequent lung inflammatory stages were studied by light microscopy, scanning and transmission electron microscopy (TEM). Lung alterations appeared after 24 h and intensified up to 7 days after virus inoculation, progressively decreasing until 3 weeks thereafter. The damage was reversible and complete restoration of structure was obtained within 5 weeks. The lesions commenced with the infiltration of bronchiolar and alveolar walls by polymorphonuclear cells, histiocytes and macrophages. A purulent exudate was seen to occupy the bronchiolar lumen. Cilia disappeared from tracheal and bronchiolar epithelia. Tracheal epithelium desquamated in some animals. TEM examination showed deterioration in type I pneumocytes, an increase in type II pneumocytes and concomitant damage to alveolar capillaries. Alveolar oedema and fibrinous deposits were seen. The pleura presented slight modifications. These results show that infection of guinea-pigs with influenza virus is a useful model for the study of lung pathology associated with a non-lethal respiratory viral infection.

Animals↗
PubMed1984

Acute pneumonitis with bilateral pleural effusion after talc pleurodesis.

We describe a patient who developed acute pulmonary distress with bilateral interstitial infiltrates and pleural effusion following talc pleurodesis. Talc particles, obtained by bronchoalveolar lavage, were identified by transmission electron microscopy and chemical analysis. The patient improved with corticosteroid therapy. Acute respiratory failure can be a potential hazard of talc pleurodesis.

Adult↗
PubMed1984

Diagnosis of pulmonary histiocytosis X by immunodetection of Langerhans cells in bronchoalveolar lavage fluid.

Based on the finding that Langerhans cells and histiocytosis X cells react with the monoclonal antibody OKT6, raised against a subset of thymocytes, we used this antibody to study the cells collected by bronchoalveolar lavage (BAL) from 131 patients, including 18 with pulmonary histiocytosis X, 43 with pulmonary sarcoidosis, 67 with miscellaneous pulmonary disorders, and 3 controls. Immunofluorescence studies demonstrated the presence of OKT6-reactive cells in all patients with pulmonary histiocytosis X (mean +/- SEM, 5.29% +/- 1.14% of all cells in BAL fluid). Immunoelectron microscopic studies revealed that the cells labeled in these patients (n = 13) contained Langerhans granules. The number of fluorescent cells in the other 113 patients was significantly smaller (mean +/- SEM, 0.20% +/- 0.04% of all cells; P less than 0.001). In the 3 control patients, in the 43 patients with sarcoidosis, and in 61 of the 67 patients with miscellaneous disorders unrelated to histiocytosis X, no cells or less than 1% of the total were labeled; however, in the 6 remaining patients in this miscellaneous group, 1.3 to 2.8% of all cells in BAL were labeled. In 3 of these 6 patients, immunoelectronmicroscopic examination showed that the cells labeled by OKT6 had the general characteristics of Langerhans cells but lacked Langerhans granules. OKT3, OKT4, and OKT8 monoclonal antibodies did not stain histiocytosis X cells in BAL fluid.

Antibodies, Monoclonal↗
PubMed1983

Detection of pulmonary venous flow by pulsed Doppler echocardiography in children.

Parasternal pulsed Doppler echocardiographic examinations of the left atrium were prospectively performed in 14 pediatric patients, aged 2 weeks to 8 years, in order to characterize the left atrial flow pattern in children. None of the patients had clinical or cardiac catheterization evidence (9 of 14 patients) of either mitral regurgitation, right-to-left shunts at the atrial level, or anomalies of pulmonary venous drainage. In all 14 patients, a systolic-diastolic positive velocity pattern could be recorded within the left atrium. Furthermore, this pattern was more readily detected in those children with left-to-right shunts. We conclude that continuous positive velocity patterns are commonly recorded in the left atria of children and probably represent pulmonary venous return. Demonstration of this signal is contingent on proper orientation of the transducer with respect to pulmonary venous flow.

Child↗
PubMed1983

Pulmonary NO2 toxicity in neonate and adult guinea pigs and rats.

The pulmonary effects of NO2 were investigated in two animal species. Rats and guinea pigs aged from 5 to 60 days or more were exposed for 3 days either to 2 ppm or to 10 ppm NO2. Lung histology or superoxide dismutase (SOD) determination in alveolar macrophages was assessed in air and NO2-exposed animals. Results demonstrated that the lung histological alterations are different for both NO2-exposed species. Rats were more tolerant than guinea pigs, but rat and guinea pig newborns were less affected than adults. The enzyme response to NO2 exposure was similar in both species and a decrease in SOD activity was noted in animals of all ages. These observations support the conclusion that NO2 exposure leads to increased lung damage during the life span, but on the contrary, exposure to oxygen does not involve SOD induction. This suggests that the defense mechanisms against NO2 are different from those of O2.

Animals↗