Inflammatory sequences in acute pulmonary radiation injury.
The histopathologic events in the developing acute pulmonary inflammatory reaction to inhaled particles of Yttrium 90 are detailed. In animals that died or were sacrificed during the first year after inhalation exposure, microscopic findings of acute inflammation predominated and included vascular congestion; stasis, focal hemorrhage; edema; various inflammatory cell infiltrates; cytolysis and desquamation of bronchiolar and alveolar epithelium followed by regeneration; vascular injury and repair; and the eventual development of pulmonary fibrosis. Accumulation of alveolar fibrin deposits was an additional characteristic, though not a constant feature of the early stages of radiation pneumonitis. In addition to the direct effects of radiation on pulmonary cell populations, the histopathologic findings were suggestive of diverse activation of various cellular and humoral mediation systems in their pathogenesis. The potential interrelationships of systems responsible for increased vascular permeability, coagulation and fibrinolysis, chemotaxis, and direct cellular injury were discussed and related to the pathogenesis of the microscopic findings characteristic of early pulmonary radiation injury.
D000336:Aerosols; D000818:Animals; D002199:Capillary Permeability / Q000528:radiation effects; D004781:Environmental Exposure; D005337:Fibrin / Q000378:metabolism; D007249:Inflammation / Q000209:etiology*; D008168:Lung / Q000528:radiation effects*; D011014:Pneumonia / Q000209:etiology / Q000473:pathology; D011650:Pulmonary Alveoli / Q000528:radiation effects; D011833:Radiation Injuries, Experimental / Q000473:pathology*; D015021:Yttrium Radioisotopes
D000336:Aerosols; D015021:Yttrium Radioisotopes; D005337:Fibrin