Development of Fine Structural Damage to Alveolar and Capillary Lining Cells in Oxygen-poisoned Rat Lungs
نویسندگان
چکیده
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 micro 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.
منابع مشابه
Existence, functional impairment, and lung repair potential of endothelial colony-forming cells in oxygen-induced arrested alveolar growth.
BACKGROUND Bronchopulmonary dysplasia and emphysema are life-threatening diseases resulting from impaired alveolar development or alveolar destruction. Both conditions lack effective therapies. Angiogenic growth factors promote alveolar growth and contribute to alveolar maintenance. Endothelial colony-forming cells (ECFCs) represent a subset of circulating and resident endothelial cells capable...
متن کاملUltrastructural immunoperoxidase demonstration of autologous albumin in the alveolar capillary membrane and in the alveolar lining material in normal rats
The location of autologous serum albumin within the alveolar-capillary membrane was studied in the rat under physiological conditions using antialbumin antibodies labeled with peroxidase. Albumin was detected in the lung interstitium, and in numerous pinocytic vesicles within endothelial cells and type I alveolar epithelial cells. The immunoreaction was also positive at the level of plasmalemma...
متن کاملHypoxia causes permeability oedema in the constant-pressure perfused rat lung.
Alveolar hypoxia causes pulmonary oedema associated with increased lung capillary pressure and decreased alveolar fluid reabsorption. However, the role of altered permeability is unclear. The aim of the present study was to test whether hypoxia affects alveolar permeability and induces pulmonary oedema in rat lungs, and whether terbutaline affects oedema formation. Isolated lungs of normoxic ra...
متن کاملIntravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.
Intravascular activation of the complement system with cobra venom factor results in acute lung injury, which has been quantitated by increases in lung vascular permeability. Cobra venom factor preparations devoid of phospholipase A2 activity retain full lung-damaging capacity. The lung injury is associated with the preceding appearance of chemotactic activity in the serum coincident with the d...
متن کاملLECTIN HISTOCHEMISTRY OF CHOLESTEROL CLEFT GRANULOMAS IN NON-SPECIFIC INTERSTITIAL PNEUMONIA (NSIP)
ABSTRACT Background: Cholesterol cleft granulomas with clusters of giant cells were noted to be a common feature of non-specific interstitial pneumonia (NSIP). Objective: This study aimed to define the cell populations involved in the granulomas. Methods: The granulomas of 16 patients with cryptogenic fibrosing alveolitis (five cases with the histological features ofNSIP, five with those ofUIP...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- The Journal of Cell Biology
دوره 32 شماره
صفحات -
تاریخ انتشار 1967