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hemostatic defect accompanying aflatoxin B₁ intoxication in rabbits
The hemostatic defect accompanying chronic aflatoxin B(,1) (AFB(,1)) intoxication was evaluated in 3 groups of 6 New Zealand white rabbits. Group A rabbits served as controls, while group B and C rabbits received daily intraperitoneal injections of AFB(,1) at dose rates of 0.06 and 0.09 mg/kg respectively. Rabbits treated with AFB(,1) became progressively depressed and developed hepatotoxicity over the 14 day study period. Hemostatic defects became apparent in AFB(,1) treated rabbits shorty before death. Hemorrhage was evident in necropsy in 1 rabbit receiving AFB(,1), and thrombi were evident histologically in this rabbit and an additional AFB(,1) treated rabbit. The hemostatic defect was characterized by prolongation of activated partial thromboplastin time and prothrombin time with significant reduction in factor V, VII, and VIII activities and factor I concentration. Changes in fibrinogen degradation products, fibrin monomer or platelet count levels were not significant; however, platelet aggregation was impaired in AFB(,1) treated rabbits shortly before death. Significant correlation between albumin concentration and factor I, V, and VIII activities in AFB(,1) treated rabbits suggested that hepatic protein synthesis was impaired. In a similarly designed study, no significant differences between AFB(,1) treated and control rabbits were found with respect to specific incorporation of tritium-labeled amino acids into total serum proteins, fibrinogen, or platelet protein. Also, no significant alterations in fibrinogen half-life were found between groups. The pathogenesis of the hemostatic defect accompanying aflatoxicosis in rabbits was not clearly defined. Fibrinolysis was not evident nor was vitamin K antagonism important in the development of the hemostatic defect. Likewise, disseminated intravascular coagulation only occurred in 1 rabbit and was considered to be a result of acute hepatocellular necrosis. In the remaining AFB(,1) treated rabbits, DIC did not appear important. Impaired hepatic synthesis of proteins appeared to be a partial explanation for the hemostatic defect because of significant correlation between the reductions in albumin and hepatic origin coagulation factor activities. Failure to demonstrate reduced specific incorporation of label into proteins did not preclude reduced synthesis, synthesis of dysfunctional proteins, or interference with synthesis of coagulation factors (other than fibrinogen) in chronic aflatoxicosis of rabbits.
Ph. D. in Philosophy Texas A & M University 1984
Includes bibliographical references (leaves 99-111).