Blood coagulation variations induced by carbon tetrachloride inhalation in Wistar rats.

Research into the development of chronic hepatic failure induced by CCl4 inhalation and the effect of this damage on blood coagulation was performed on Wistar rats. Exposure to CCl4 (325 ppm) consisted of the administration of 22, 26, 29, 31, 34, 39, 40, 45, and 49 doses, respectively. To determine and evaluate the nature and degree of CCl4-induced lesions at different stages of the treatment, histological alterations in liver samples were evaluated. Fatty infiltration in the centrilobular parenchymal cells observed after administration of the first doses was seen to spread toward mid- and peripheral zones of the lobules at the highest doses, accompanied by necrosis and nonelastic fibrosis. A causal relationship between liver failure and decrease in plasma fibrinogen levels was not observed, even though CCl4 does reduce protein synthesis. A lack of correlation between changes in reptilase time and quantitative variations in fibrinogen was seen. This finding was confirmed by observations of qualitative modifications in the fibrinogen caused by CCl4 inhalation, such as an increase in sialic acid content, which has been previously described. Activated partial thromboplastin time seems to be a good marker for benign liver damage in carbon tetrachloride intoxication. Nevertheless, prothrombin time does reliably reflect the degree of hepatic degeneration. These results suggest that prothrombin time may be considered a valuable prognostic index.