ABSTRACT
This chapter describes the cardiovascular toxicity of trichothecene mycotoxins in mammals and is organized according to the species in which the trichothecene toxicoses (either accidental or experimental) have been observed. In vivo effects and in vitro experiments (if any) are described and interpreted. A common observation in most species after sufficient exposure to trichothecene has been initial tachycardia followed by bradycardia and hypotension. In cases of severe toxicosis, a shock-like syndrome has often been described. The available experimental evidence indicates that the effects of trichothecenes on the cardiovascular system are both direct and indirect (mediated through reflex mechanisms, hormones, shock, other tissues damaged, etc.). In laboratory tests, initial tachycardia and increased arterial blood pressure were prevented by either sympathetic blockers or brain stem ablation, indicating that these effects were centrally reflexively mediated. At very high degrees of exposure trichothecene-induced hypotension, bradycardias and/or tachycardias, and arrhythmias have been demonstrated in vivo. These effects could not be reversed by drugs and were not present after brain stem ablation. Therefore, these cardiovascular effects resulted, at least in part, from trichothecene-induced central nervous system dysfunction. Alternate hypotheses, that trichothecenes interfere with myocyte transmembrane ion fluxes and that trichothecenes inhibit protein synthesis, are discussed in the context of observed cardiovascular effects.
