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  • Title: Ultrastructural evidence of pulmonary capillary endothelial damage from paraquat.
    Author: Dearden LC, Fairshter RD, Morrison JT, Wilson AF, Brundage M.
    Journal: Toxicology; 1982; 24(3-4):211-22. PubMed ID: 6927641.
    Abstract:
    Because of lack of agreement concerning the toxicity of paraquat to the pulmonary microvasculature, we have undertaken an electron microscopic study of lungs of paraquat-treated rats. Rats were injected with paraquat or sterile water (controls) intraperitoneally; the animals were then killed at 24-h intervals for 10 days post-injection. In the control animals, lung ultrastructure remained normal throughout the study. In treated animals, the initial evidence of alveolar epithelial injury occurred 24 h post-paraquat. By 48 h, severe fragmentation and desquamation of membranous pneumocytes occurred, and both alveolar and interstitial edema were present. Epithelial damage was maximal 72-96 h post-paraquat. Pulmonary capillary endothelial abnormalities were less extensive than the alveolar epithelial lesions. Endothelial damage was first observed 48 h post-paraquat. In endothelial cells on the septal (thick) side of the capillaries, the number of pinocytotic vesicles was significantly increased (P less than 0.05) from 48 to 96 h post-paraquat. In endothelium adjacent to damaged epithelium, abnormalities included hydration, fragmentation, discontinuity, and widened intercellular junctions; these were maximal 72-96 h post-paraquat. Although other mechanisms are probably important, damaged pulmonary capillary endothelium seems to be a factor favoring paraquat-induced pulmonary edema.
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