Objective—To determine whether cardiovascular
dysfunction is evident in horses with leukoencephalomalacia
experimentally induced by administration of
Animals—11 healthy horses of various breeds (body
weight, 252 to 367 kg).
Procedure—Horses were randomly assigned to 3
groups and administered fumonisin B1 daily. Horses
received IV injections of 0 (control horses; n = 4), 0.01
(3), or 0.20 mg (4) of fumonisin B1/kg for 7 to 28 days.
Horses were examined daily for evidence of neurologic
disease. When neurologic signs consistent with
leukoencephalomalacia were evident, horses were
anesthetized, and catheters were inserted for evaluation
of the cardiovascular system. After recovery from anesthesia,
hemodynamic measurements were obtained.
Results—Fumonisin-treated horses with clinical
signs of neurologic disease had evidence of cardiovascular
dysfunction manifested as decreases in
heart rate, cardiac output, right ventricular contractility
(assessed by measuring the maximal rate of
change of right ventricular pressure), coccygeal artery
pulse pressure, and pH and base excess in venous
blood as well as increases in systemic vascular resistance,
compared with values for control horses.
Fumonisin-treated horses with and without clinical
signs of neurologic disease also had higher serum
and right ventricular sphinganine and sphingosine
concentrations than control horses.
Conclusions and Clinical Relevance—An association
was detected among fumonisin-induced neurologic
disease, increased serum and myocardial sphinganine
and sphingosine concentrations, and decreased cardiovascular
function in horses. Fumonisin-induced
decreases in cardiovascular function may contribute to
the pathophysiologic development of leukoencephalomalacia
in horses. (Am J Vet Res 2002;63:538–545).