Hypovolemic shock in acute lethal T-2 mycotoxicosis.

Area of Science:

• Toxicology
• Veterinary Medicine
• Physiology

Background:

• Trichothecene mycotoxins, such as T-2 toxin (T2T), are known for their acute lethal toxicity.
• The precise mechanism underlying T2T-induced lethality, specifically whether it stems from cardiac failure or hypovolemia, remains debated.

Purpose of the Study:

• To investigate the role of hypovolemia versus cardiac failure in the acute lethal toxicity of T-2 toxin (T2T) in cats.
• To elucidate the physiological changes associated with T2T exposure and their contribution to mortality.

Main Methods:

• Experiments were conducted on pentobarbital-anesthetized cats.
• Measurements included mean arterial blood pressure (MAP), arterial pulse pressure (PP), and heart rate (HR).
• Cats received T2T (2 mg/kg iv), with some undergoing plasma and blood transfusions; a control group simulated shock through plasmapheresis and blood removal.

Main Results:

• T-2 toxin administration led to depressed MAP and PP, indicative of mycotoxic shock.
• Transfusions significantly delayed or counteracted the development of shock and prevented/reversed hematocrit increases.
• Heart rate remained stable throughout the experiments; simulated shock effectively mimicked T2T-induced physiological changes.

Conclusions:

• Acute lethal T-2 mycotoxicosis is primarily attributed to hypovolemia and subsequent polycythemia.
• These conditions result from plasma leakage and internal bleeding induced by T-2 toxin.
• The findings challenge the notion of cardiac failure as the primary cause of acute T2T lethality.