© 1996 Oxford University Press
research-article |
Cardiovascular Effects of Fumonisins in Swine
*Departments of Veterinary Pathobiology, University of Illinois Urbana, Illinois 61801
Departments of Clinical Medicine, University of Illinois Urbana, Illinois 61801
Mycotoxin Research Unit, Russell Research Center USDA-ARS, Athens, Georgia 30601
Received August 14, 1995; accepted January 29, 1996
Fumonisins, mycotoxins produced by Fusarium moniliforme, induce hepatic damage and acute lethal pulmonary edema in swine. We examined the cardiovascular effects of short-term fumonisin exposure in anesthetized and conscious male cross-bred pigs weighing 30–36 kg. Culture material containing fumonisins at 
20 mg/kg/day (fumonisin B1 and B2 backbone) was added to the feed of treated pigs (n = 5) for 7 days, while control pigs (n = 5) were fed a diet free of fumonisins. On Day 8, pigs were anesthetized with halothane and instrumented with Swan-Ganz catheters to facilitate hemodynamic measurements. Mean pulmonary artery pressure, central venous pressure, heart rate, cardiac output, and electrocardiographic variables were recorded and stroke volume was calculated. All measurements were repeated at least 18 hr after recovery from anesthesia. Pigs fed fumonisins had a significant increase in mean pulmonary artery pressure, accompanied by decreased heart rate, cardiac output, and mixed venous oxygen tension. The electrocardiogram was normal, and there was no evidence of pulmonary edema formation either histologically or by altered lung wet/dry weights. This study suggests that pulmonary hypertension caused by hypoxic vasoconstriction may be associated with the pulmonary edema observed in fumonisin toxicity.