Rats receiving orally 0.25 mg of carbon tetrachloride per 100 gm of body weight were killed after 1, 4, 8, 12, and 24 hours. Light microscopy disclosed focal perivascular edema, atelectasis, and hermorhages. Ultrastructurally, earliest changes occurred in inclusions of granular pneumocytes with lamellar attenuation and decreased osmiophilia. Disruption of ribosomal aggregates, endoplasmic reticulum, and mitochondria and decrease in multivesicular bodies occurred at four hours. Small vesicles in granular pneumocytes, increased endothelial pinocytosis, and septal edema appeared later. Subsequently there was granular pneumocyte necrosis, endothelial sloughing, denudation of endothelial basal lamina, intracapillary platelet aggregation, formation of mural thrombi, and intraalveolar fibrin. Early changes are the result of pulmonary CCl4 excretion, the latter substance acting as a lipid solvent upon elements of alveolar wall. Possible formation of a proximate toxin through a xenobiotic enzyme system remains speculative.
Gould VE, Smuckler EA. Alveolar Injury in Acute Carbon Tetrachloride Intoxication. Arch Intern Med. 1971;128(1):109-117. doi:10.1001/archinte.1971.00310190113014