Alveolar epithelial lesions induced by angiotensin in rabbit lungs.
We slowly administered a bolus of 10 micrograms/kg of angiotensin II in saline to anesthetized rabbits. Their lungs are fixed by vascular perfusion of fixatives 2-3 minutes after the end of the infusion. Electron-microscopic examination of the lung parenchyma did not reveal signs of hemodynamic edema, but several epithelial alterations were observed that could be interpreted as the result of incorporation of plasmalemmal vesicles into the plasma membrane: these included undulating membrane profiles, transcellular channels formed by coalescing vesicles, and/or deep infoldings of the cell membrane. These appear to have the capability of causing demarcations in the cellular cytoplasm of Type I epithelial cells, which result in cell fractionation and localized destruction of the squamous alveolar epithelium, which leads to denudation of the basement membrane from the air side. These epithelial lesions were often associated with intracapillary platelet-fibrin aggregates, and cell destruction was most apparent in the presence of substantial amounts of fibrin. Morphologic signs of damage of the capillary endothelial cells existed but were less pronounced; in particular, there was no endothelial denudation under the platelet aggregates.
D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D002458:Cell Fractionation; D002462:Cell Membrane / Q000648:ultrastructure; D004727:Endothelium / Q000648:ultrastructure; D004848:Epithelium / Q000648:ultrastructure; D008168:Lung / Q000648:ultrastructure; D010974:Platelet Aggregation / Q000187:drug effects; D011650:Pulmonary Alveoli / Q000648:ultrastructure*; D011817:Rabbits
D000804:Angiotensin II