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Systemic distribution of blood flow during T-2 toxin induced shock in swine

1986Fundamental and Applied ToxicologyJournal Article
10.1016/0272-0590(86)90161-2PubMed
CardiovascularEndocrine (ADH/ACTH/MSH)Immune/InnateNeurologicalRespiratory/Sinus
Indoor Mold (Stachybotrys, Aspergillus, etc.)MycotoxinsWater-Damaged Buildings (WDB)

Abstract

Three groups of swine (6 per group) were used to determine hemodynamic and blood flow alterations induced by T-2 toxin. Two groups were dosed at 0.6 or 2.4 mg/kg T-2 toxin, and one group served as a vehicle control (70% ethanol). Organ blood flow was determined at 0 hr (predosing) and at 90-min intervals for 6 hr postdosing using 15-micron diameter radionuclide labeled microspheres injected into the left atrium. Hemodynamic parameters were obtained at the same time points. The infusion of T-2 toxin resulted in reductions in cardiac output. This trend appeared to reverse itself in the low dose animals after 3 hr, whereas in the high dose group, cardiac output continued to decline. Mean aortic pressure (MAP) declined in a dose dependent fashion which tended to parallel the reduction observed in cardiac output. Heart rate was increased in both groups treated with T-2 toxin. Blood flow, to the brain, heart, and kidneys decreased following exposure to the toxin. The relative percentage of cardiac output received by these organs, however, was maintained despite the drop in blood flow. Pancreatic and splenic blood flows were the most severely compromised as a result of T-2 toxicosis. Consequently, the percentage of cardiac output going to the pancreas and spleen was dramatically reduced. Adrenal, hepatic, and total gastrointestinal blood flows increased or did not change from control values. As a result, the percentage of cardiac output supplying these organs increased.

Key Biomarkers

Abnormal QEEG with alpha and theta band increasesAbnormal T and B cell populationsAntinuclear autoantibodies (ANA)Autoantibodies against smooth muscle (ASM)CNS and PNS myelin autoantibodiesDecreased cardiac outputDecreased NK cellsElevated autoantibodies to neural antigens (IgA, IgM, IgG)Reduced mean aortic pressureTrichothecene toxin in urine and serum

Symptom Clusters

Autonomic nervous system dysfunctionCardiovascular instabilityCognitive impairment similar to mild traumatic brain injuryMood and emotional disturbances (depression, anxiety)Neurobehavioral dysfunction (balance impairment, reaction time slowing)Neuropsychological impairment (memory, concentration, executive function)Peripheral neuropathy (numbness, tingling, tremors, muscle weakness)Respiratory symptoms (asthma, airway irritation, wheezing, rhinorrhea)

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