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Biomedical subjects

C G Loosli

Publications and source records attributed to C G Loosli.

At least 19 recordsLinked to original sources
PubMed1978

Ultrastructural evidence concerning the mode of secretion of electron-dense granules by Clara cells.

An ultrastructural study of the secretory activity of non-ciliated bronchiolar epithelial (Clara) cells has been made. Membrane-bound, electron-dense granules were observed in the apical cytoplasm of Clara cells, immediately beneath the terminal web, and within terminal web regions, with their limiting membranes in close association with the plasma membrane of the cell. Granules were also observed in cytoplasmic pockets with varying amounts of their surfaces exposed to the bronchiolar, lumen, or within cytoplasmic projections into the lumen. Granules that were enveloped in a thin, uniform coat of cytoplasm and granules with no associated cytoplasm were both found free in the bronchiolar lumen. The study is consistent with the conclusion that the granules are secretory in nature, being extruded by a merocrine and possibly an apocrine mechanism.

Animals↗
PubMed1977

Electron-microscopic studies of the innervation of the pulmonary veins of the mouse.

The innervation of the pulmonary veins was studied with electron microscopy. The adrenergic and cholinergic nerves were differentiated with potassium permanganate fixation. All three layers of the venous wall, namely, the tunica intima, media and adventitia, contained unmyelinated axons. Adrenergic and cholinergic axons were located near the cardiac muscle in the tunica media and near the smooth muscle in the tunica intima. The morphological relationships may explain the pharmacological and electrophysiological responses of the large pulmonary veins observed by others.

Adrenergic Fibers↗
PubMed1976

Epithelial and surfactant changes in influenzal pulmonary lesions.

Pulmonary epithelial cell destruction in mice infected with PR8-A influenza virus has been studied with light and electron microscopy and enzyme histochemistry, and correlated with pulmonary surfactant activity. All epithelial cell types were infected by the virus, resulting in destruction, pneumonitis, and atelectasis by seven to ten days. Pulmonary surfactant activity decreased progressively following onset of infection, and was minimal by seven to ten days. Before types 1 and 2 alveolar pneumocytes regenerated, the regenerating bronchial cells grew peripherally into some of the denuded alveolar ducts and alveoli to form epithelial nodules. Eventually the types 1 and 2 pneumocytes regenerated to cover the alveolar surfaces that were not invaded by bronchial epithelium. This regeneration was associated with increased surfactant activity in the postinfluenzal lesions, suggesting that the type 2 pneumocytes are a source of surfactant.

Animals↗
PubMed1975

The destruction of type 2 pneumocytes by airborne influenza PR8-A virus; its effect on surfactant and lecithin content of the pneumonic lesions of mice.

Influenzal pneumonia has been studied in mice subjected to sublethal doses of airborne PR8-A influenza virus. Electron microscopy revealed that the virus propagated in and at the same time destroyed the ciliated and nonciliated bronchial cells and the types 1 and 2 alveolar pneumocytes. The regenerating bronchial membranes were metaplastic and grew peripherally into the surrounding alveolar ducts and alveoli to form epithelial nodules which caused obstruction and collapse of the involved lobes. The development of the lung lesions was correlated with phospholipid (lecithin) levels in consolidated and unconsolidated infected and normal lungs. As the lungs became more and more consolidated, there was a corresponding and significant decrease in the amount of phospholipid (dipalmitoyl lecithin) compared to the amount of normal or unconsolidated infected tissue. The destruction of the type 2 pneumocytes by the influenza virus and their failure to regenerate is considered to be the reason for the low phospholipid levels in the involved lobes, and thus an important cause of post-influenzal collapse in mice. The above adds additional evidence to the view that the type 2 pneumocytes are a major source of surfactant in mammalian lungs.

Aerosols↗