Submitted to: Fundamental and Applied Toxicology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/29/1996
Publication Date: N/A
Citation: Interpretive Summary: The fumonisins are toxins produced by specific molds referred to as Fusarium moniliforme. These toxins damage the liver and produce excessive accumulations of fluids in the lungs of pigs. The mechanism through which this accumulation occurs is unknown. Studies were conducted to determine the effect the fumonisins have on the heart and circulatory system of pigs. Scientists at RRC provided toxic corn with graded amounts of fumonisins for use in a collaborative study with scientist at the University of Illinois. The corn was mixed in a diet and fed for eight days. The results indicated pigs receiving the toxins had increased pulmonary artery pressure, decreased heart rate and cardiac output, and decreased pulmonary arterial oxygen tension. This study indicates that pulmonary hypertension caused by vasoconstriction of the blood vessels may be associated with the excessive accumulation of fluid observed in the lungs of pigs.
Technical Abstract: Fumonisins are mycotoxins produced by Fusarium moniliforme that 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 weighting 30-36 kg. Culture material containing fumonisins at <20mg/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 calculated. All measurements were repeated at least 18 hrs after recovery from anesthesia. Pigs fed fumonisins had a significant increase in mean pulmonary artery pressure, accompanied by decreased heart rate, cardiac output, and pulmonary arterial 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.