Pathophysiology of Acute T-2 Intoxication in the Cynomolgus Monkey and Comparison to the Rat as a Model
ARMY RESEARCH INST OF ENVIRONMENTAL MEDICINE NATICK MA
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The reported pathophysiologic studies of acute T-2 intoxication reported are most compatible with widespread tissue and organ injury including hematologic, hepatic, renal, pancreatic, muscular, and cardiac effects. The mechanism of death during acute intoxication seems to be cardiovascular with a decreased cardiac contractility, decreased cardiac output, and ultimately shock and death. Although changes in cardiac conductivity do occur, they appear to play only an ancillary role in the acute deaths. Secondary cellular effects in addition to direct cellular toxin effects from poor tissue perfusion, shock, tissue hypoxia and acidosis are a prominent part of the picture. The connection between the above responses and the known inhibition of protein synthesis remains to be elucidated. In addition to inhibition of protein synthesis, cellular toxic effects could include cell wall or organelle injury or impaired cellular energy utilization. These have not yet been proven. Therapy for high dose acute intoxication may need to be directed toward cardiovascular support as well as toward T-2 metabolism, binding and excretion. Both the rat and monkey models are useful in studying acute T-2 intoxication.