The air-blood barrier represents the maturity of developing lung. The development of air-blood barrier in human fetal lung was studied by transmission electron microscopy. The results obtained were as follows. 1. The formation of air-blood barrier started at 16 week of postcoitum, which was the end of pseudoglandular period. The basement membranes began to be fused with each other as the capillaries penetrated between epithelial cells of primitive alveoli. 2. The flattening of the type II alveolar cells was observed only around the site of fused basement membranes, which seemed to be developed not by mechanical force but by induction of the fused basement membrane. 3. The basement membranes of capillaries and alveoli were relatively flat until the fusion occurred, but they showed severe folds with the occurrence of fusion. But with the proceeding of the terminal sac period, the folds greatly decreased. In summary, the air-blood barrier began to develop at the end of pseudoglandular period and was formed as capillaries penetrated the cytoplasms of epithelial cells devoided of the nuclei. The fused basement membranes seems to play an important role in the development of air-blood barrier.
Basement Membrane ; Blood-Air Barrier* ; Capillaries ; Cytoplasm ; Epithelial Cells ; Humans* ; Lung* ; Microscopy, Electron, Transmission ; Pulmonary Alveoli

Industrial glues contain many kinds of organic solvents and glue sniffing by young people has become a social problem in Korea. Glue vapor may induce chronic toxicities different from those induced by exposures to the solvent of single component. We studied the effects of the inhalation of glue vapor on the primary target organ, the pulmonary epithelium of the respiratory system. Vapor samples of glue were collected for analysis; the components were acetone, n-hexane, methyl cyclopentane, c-hexane, and toluene. For the inhalation of glue vapor, experimental mice were exposed in a whole body chamber for 20 min/d for 3, 5, 7, and 14 d. Control groups were exposed to room air. Animals were euthanized and lung tissues were fixed in 10% neutral formalin for light microscopy, and in 2.5% glutaraldehyde plus 1.5% paraformaldehyde for electron microscopy. The results are as follows. 1. Alcianophilic bands were not detected in the normal alveolar epithelium, but weak alcianophilic bands were detected in bronchioles. Alcian blue-PAS and PAS positive cells were found in the mucosae of mice exposed to glue vapor for 5 and 7 d. 2. Types I and II pneumocytes and capillary endothelial cells were found in the normal alveolar epithelium. The blood-air barrier consists of Type I pneumocytes, a common basal lamina, and the capillary endothelium. 3. The alveolar epithelium of vapor-exposed mice showed more type II pneumocytes. In the longerexposed group, Type I pneumocytes and endothelial cells contained many pinocytotic vesicles. 4. The vapor-exposed lungs showed macrophages in the alveolar space, mild interstitial swelling, and increased numbers of collagenous fibers. Clearly, ultrastructural changes in pulmonary epithelia can occur following glue sniffing.
Acetone ; Adhesives ; Animals ; Basement Membrane ; Blood-Air Barrier ; Bronchioles ; Collagen ; Cyclopentanes ; Endothelial Cells ; Endothelium, Vascular ; Epithelium ; Formaldehyde ; Glutaral ; Inhalant Abuse ; Inhalation* ; Korea ; Lung* ; Macrophages ; Mice* ; Microscopy ; Microscopy, Electron ; Mucous Membrane ; Pneumocytes ; Respiratory System ; Social Problems ; Solvents ; Toluene

BACKGROUND: Laminin-1 is known to have regular functions in the development and course of differentiation of the lungs. The morphogenesis and distribution of laminin-1 still remains as a mystery and its distribution and changes in the molecular structure of laminin-1 in the pathogenesis of the lung still is a subject of great controversy. In this study, experiments were done to delineate the distribution and changes in the amount of laminin-1 after inducing inflammation of the lungs by exposing experimental animals to CS gas and especially, to find compositions of laminin-1 within type II pneumocytes. MATERIALS AND METHODS: The experimental subjects of study were newborn rats and the extracted tissue from the experimental rats were viewed under light microscope and electron microscope after the sections were treated with immunohistochemical methods and immunogold reaction methods using bounded gold particles. RESULTS: 1) Lymphocytes and mononuclear phagocytes invaded the alveolar septa in the 2 day group rats after CS gas exposure and intense interstitial inflammation was seen in the 3 day group. 2) Laminin immunoreactions decreased to a moderate degree in the 2 and 3 day group rats after CS gas exposure and strong laminin immunoreactions were seen again in the 5 and 7 day group rats. 3) Gold particles in basal lamina of the lung blood-air barrier decreased and in the type I pneumocytes decreased in the 2 and 3 day group rats after CS gas exposure. 4) Gold particles were seen only on the surface of the cell membranes of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure. 5) Few gold particles around the lamellar bodies and cytoplasm of type II pneumocytes in the control rat group and at 12 hours after CS gas exposure. Gold particles are seen only on the surface of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure and are evenly distributed in small amounts in the cells of the 3 day group after CS gas exposure. CONCLUSION: CS gas exposure in the rats caused inflammation of lung alveolar septa and also induced a decrease in laminin-1 in basal lamina and loss of laminin-1 in the cytoplasm of type II pneumonocytes. As the inflammatory cells disappeared, an increase in the distribution of laminin-1 occurred. This reflects tissue regeneration functions of laminin-1 in the pneumocytes of rats and the distribution of laminin-1 in type II pneumocytes can be seen through the electron microscope using immunogold methods.
Animals ; Basement Membrane ; Blood-Air Barrier ; Cell Membrane ; Cytoplasm ; Humans ; Infant, Newborn ; Inflammation ; Laminin ; Lung* ; Lymphocytes ; Molecular Structure ; Morphogenesis ; Phagocytes ; Pneumocytes ; Rats* ; Regeneration

Calculi ; Humans ; Lung Diseases ; Male ; Middle Aged ; Pulmonary Alveoli ; pathology

We describe a case of pulmonary alveolar proteinosis in a male adult with lung cancer. To achieve the successful operation of lung cancer, we used percutaneous veno-venous extracorporeal membrane oxygenation (ECMO) during whole lung lavage (WLL) of the contralateral lung. We performed successful WLL under ECMO support.
Adult ; Bronchoalveolar Lavage* ; Extracorporeal Membrane Oxygenation* ; Humans ; Lung Neoplasms* ; Lung* ; Male ; Pulmonary Alveolar Proteinosis* ; Pulmonary Alveoli

BACKGROUND: Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. METHODS: From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and 200muM CoCl2 were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. RESULTS: 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-1alpha (HIF-1alpha)was also induced by 2% oxygen. CONCLUSION: Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.
Acute Lung Injury ; Anoxia ; Blood-Air Barrier ; Cell Proliferation ; Immunohistochemistry ; Lung* ; Microscopy ; Microvessels ; Oxygen ; Pericytes* ; Permeability ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A

Humans ; Nitric Oxide ; Carcinoma, Non-Small-Cell Lung/drug therapy* ; Lung Neoplasms ; Lung ; Nitric Oxide Synthase ; Macrophages, Alveolar ; Pulmonary Alveoli

We report a rare cause of lung cavities, occurring in a patient with intrapulmonary cystic teratoma. Computed tomography (CT) provided us more detailed informations about the tumor characteristics containing fat and calcification, which could not be distinguished on the plain radiographs. In addition, CTscans clearly demonstrated the dilated anterior segmental bronchus of the left upper lobe entering the posterior aspect of the cavity.
Bronchi ; Humans ; Lung* ; Teratoma*

Adult ; Haploidy ; Hematopoietic Stem Cell Transplantation ; Hemorrhage ; Humans ; Lung Diseases ; Male ; Pulmonary Alveoli

Adolescent ; Adult ; Female ; Humans ; Lithiasis ; genetics ; Lung Diseases ; genetics ; Male ; Middle Aged ; Pedigree ; Pulmonary Alveoli