TY - JOUR
T1 - Ingestion of fumonisin B1-containing culture material decreases cardiac contractility and mechanical efficiency in swine
AU - Constable, Peter D.
AU - Smith, Geoffrey W.
AU - Rottinghaus, George E.
AU - Haschek, Wanda M.
N1 - Funding Information:
This study was supported by an American Heart Association Grant-in-Aid (97-GB-01). Dr. Smith is supported by an American Heart Association Fellowship Award (9804717X).
PY - 2000/2/1
Y1 - 2000/2/1
N2 - Fumonisins are mycotoxins produced primarily by Fusarium verticillioides, a fungus that commonly contaminates corn. Fumonisin ingestion increases plasma and tissue sphingosine and sphinganine concentrations and causes porcine pulmonary edema, which has been attributed to acute left-sided heart failure or increased vascular permeability. We investigated the effect of short-term ingestion of fumonisin B1-containing culture material on cardiac function in pigs. Treated male pigs (n = 7) received fumonisin-containing culture material which was mixed into the grower diet at 20 mg fumonisin B1/kg body weight each day, while control pigs (n = 7) were fed only the grower diet on the same schedule as the treated pigs. Pigs were anesthetized after 3 days of receiving either diet and instrumented to accurately characterize the cardiovascular effects of fumonisin ingestion. Fumonisin-treated pigs had lower cardiac outputs and heart rates than control pigs. Fumonisin-treated pigs also had a marked reduction in cardiac contractility, as indicated by decreased values for endsystolic elastance (the gold standard in vivo measure of cardiac contractility), V0 (the intercept value for the end-systolic pressure-volume relationship), and mechanical efficiency. These data indicate that in pigs, short-term ingestion of fumonisin B1-containing culture material produces negative inotropic and chronotropic effects and decreases mechanical efficiency of the left ventricle. Theses cardiovascular effects are consistent with fumonisin-induced, sphingosine-mediated L-type Ca2+ channel blockade and suggest that pulmonary edema in pigs fed fumonisin is primarily due to acute left-sided heart failure instead of increased vascular permeability. (C) 2000 Academic Press.
AB - Fumonisins are mycotoxins produced primarily by Fusarium verticillioides, a fungus that commonly contaminates corn. Fumonisin ingestion increases plasma and tissue sphingosine and sphinganine concentrations and causes porcine pulmonary edema, which has been attributed to acute left-sided heart failure or increased vascular permeability. We investigated the effect of short-term ingestion of fumonisin B1-containing culture material on cardiac function in pigs. Treated male pigs (n = 7) received fumonisin-containing culture material which was mixed into the grower diet at 20 mg fumonisin B1/kg body weight each day, while control pigs (n = 7) were fed only the grower diet on the same schedule as the treated pigs. Pigs were anesthetized after 3 days of receiving either diet and instrumented to accurately characterize the cardiovascular effects of fumonisin ingestion. Fumonisin-treated pigs had lower cardiac outputs and heart rates than control pigs. Fumonisin-treated pigs also had a marked reduction in cardiac contractility, as indicated by decreased values for endsystolic elastance (the gold standard in vivo measure of cardiac contractility), V0 (the intercept value for the end-systolic pressure-volume relationship), and mechanical efficiency. These data indicate that in pigs, short-term ingestion of fumonisin B1-containing culture material produces negative inotropic and chronotropic effects and decreases mechanical efficiency of the left ventricle. Theses cardiovascular effects are consistent with fumonisin-induced, sphingosine-mediated L-type Ca2+ channel blockade and suggest that pulmonary edema in pigs fed fumonisin is primarily due to acute left-sided heart failure instead of increased vascular permeability. (C) 2000 Academic Press.
KW - End-systolic elastance
KW - Mechanical energetics
KW - Pressure-volume area
KW - Stroke work
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U2 - 10.1006/taap.1999.8831
DO - 10.1006/taap.1999.8831
M3 - Article
C2 - 10652243
AN - SCOPUS:0034142108
SN - 0041-008X
VL - 162
SP - 151
EP - 160
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
IS - 3
ER -