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Alveolar Injury in Acute Carbon Tetrachloride Intoxication
Victor E. Gould, MD;
Edward A. Smuckler, MD, PhD
Arch Intern Med. 1971;128(1):109-117.
Abstract
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.
Author Affiliations
Seattle
From the Department of Pathology, University of Washington School of Medicine, Seattle.
Footnotes
Received for publication Oct 21, 1970; accepted April 5, 1971.
Read in part before the Tenth Annual Hanford Biology Symposium on Pollution and Lung Biochemistry, Richland, Wash, June 5, 1970, jointly sponsored by the Battelle Memorial Institute-Pacific Northwest Laboratories, National Air Pollution Control Administration, National Institute of Environmental Health Sciences, and the US Atomic Energy Commission.
Read in part before the International Academy of Pathology, San Francisco, March 11, 1969.
Reprint requests to BB218, University Hospital, Seattle 98105 (Dr. Gould).
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ABSTRACT
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