Abstract
Paraquat causes focal intracellular oedema of the terminal bronchiolar epithelial cells and focal subpleural atelectasis with thickening of the interalveolar septa 1 hr after the administration of an LD50. These changes are progressive, and lead to panacinar atelectasis with necrosis plus sloughing of epithelial cells in many terminal bronchioles. Radioactive phosphatidyl choline (PC) is recoverable by lavage within 90 s of the administration of tritiated palmitate, which supports previous suggestions that one source of pulmonary surfactant is rapid secretion by the terminal bronchiole. Paraquat causes a reduction in the relative amounts of radioactive PC that are recoverable from the airways within 90 s of giving tritiated palmitate. A deficiency of pulmonary surfactant of bronchiolar origin is implicated, at least in part, in the pathogenesis of the acute phase of the paraquat lesion in mice.
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