The Journal of Cell Biology · 1967 · 396 citations · 28 references
The study examines why alveolar epithelium and pulmonary endothelium respond differently to toxic oxygen exposure. Rats were exposed to 98.5 % oxygen at 765 torr for 6–72 h, and the resulting pulmonary changes were examined by electron microscopy and morphometric analysis. High‑oxygen exposure produced progressive thickening of the air‑blood barrier, loss of ~50 % of capillaries, extensive endothelial cytoplasmic degeneration and fragmentation, while epithelial damage remained limited, resulting in measurable impairment of lung function.
Rats were exposed to 98.5% oxygen at 765 torr for 6–72 hr. The pulmonary changes were investigated by electron microscopy and by morphometric methods. A progressive thickening of the air-blood barrier, from the normal 1.5 to 3 µ after 3 days, was due primarily to enlargement of the interstitial space by accumulation of edema which was replaced secondarily by cells and fibrin. This was accompanied by destruction of about 50% of the capillaries. Morphometric data allowed an estimate of the degree of impairment of lung function. The primary cellular damage was located in endothelial cells which underwent cytoplasmic changes and, finally, fragmentation. In contrast, the damage to the epithelial lining of alveoli was relatively scarce compared to the extensive endothelial changes. This pertained even to severely damaged lungs with 65% of the alveoli obliterated by a heterogeneous exudate. Possible causes for this apparently different reaction of epithelium (the first target cell) and endothelium to toxic oxygen effects are discussed.
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IMPROVEMENTS IN EPOXY RESIN EMBEDDING METHODS
John H. Luft · The Journal of Cell Biology · 1961 · 10.2K citations · Full text
Materials Science, Tissue Engineering, Methacrylate Embedding +15
JUNCTIONAL COMPLEXES IN VARIOUS EPITHELIA
Marilyn G. Farquhar, George E. Palade · The Journal of Cell Biology · 1963 · 3.6K citations · Full text
Cytoskeleton, Low Density, Anatomy +18