Advertisement

Cardiovascular changes associated with intravenous administration of fumonisin B1 in horses

Geoffrey W. SmithDepartment of Veterinary Clinical Medicine, University of Illinois, Urbana, IL 61802.

Search for other papers by Geoffrey W. Smith in
Current site
Google Scholar
PubMed
Close
 DVM, MS
,
Peter D. ConstableDepartment of Veterinary Clinical Medicine, University of Illinois, Urbana, IL 61802.

Search for other papers by Peter D. Constable in
Current site
Google Scholar
PubMed
Close
 BVSc, PhD
,
Jonathan H. ForemanDepartment of Veterinary Clinical Medicine, University of Illinois, Urbana, IL 61802.

Search for other papers by Jonathan H. Foreman in
Current site
Google Scholar
PubMed
Close
 DVM, MS
,
Robert M. EppleyFood and Drug Administration, 200 C Street SW, Washington, DC 20204.

Search for other papers by Robert M. Eppley in
Current site
Google Scholar
PubMed
Close
 PhD
,
Amy L. WaggonerDepartment of Pathobiology, University of Illinois, Urbana, IL 61802.

Search for other papers by Amy L. Waggoner in
Current site
Google Scholar
PubMed
Close
 BS
,
Mike E. TumblesonDepartment of Biosciences, University of Illinois, Urbana, IL 61802.

Search for other papers by Mike E. Tumbleson in
Current site
Google Scholar
PubMed
Close
 PhD
, and
Wanda M. HaschekDepartment of Pathobiology, University of Illinois, Urbana, IL 61802.

Search for other papers by Wanda M. Haschek in
Current site
Google Scholar
PubMed
Close
 BVSc, PhD

Abstract

Objective—To determine whether cardiovascular dysfunction is evident in horses with leukoencephalomalacia experimentally induced by administration of fumonisin B1.

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).

Abstract

Objective—To determine whether cardiovascular dysfunction is evident in horses with leukoencephalomalacia experimentally induced by administration of fumonisin B1.

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).