Location: Forage-Animal Production Research
Title: Dietary exposure to ergot alkaloids decreases contractility of bovine mesenteric vasculature Authors
|Egert, Amanda -|
|Kim, Do Hyung -|
|Schrick, F. Neal -|
|Harmon, David -|
Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 20, 2013
Publication Date: February 3, 2014
Citation: Egert, A.M., Kim, D., Schrick, F., Harmon, D.L., Klotz, J.L. 2014. Dietary exposure to ergot alkaloids decreases contractility of bovine mesenteric vasculature. Journal of Animal Science. 92:1768-1779. Interpretive Summary: Ergot alkaloids associated with fescue toxicosis administered in the diet are recovered in the abomasum, so it is known that ergot alkaloids enter the small intestine. However, little information is available about the effect of these compounds on the small intestine or what interaction alkaloids might have with the midgut. A reduction in contractile response to 5HT and ERV in lateral saphenous veins collected from steers that had grazed high-endophyte tall fescue. Therefore, it was hypothesized that ergot alkaloids cause vasoconstriction in midgut vasculature and that dietary exposure to ergot alkaloids may decrease their vasoactivity. Objectives of this study were to profile the vasoactivity of ergot alkaloids in mesenteric artery and vein and determine if prior dietary exposure to toxic endophyte-infected tall fescue seed affected in vitro vasoactivity of ergot alkaloids and serotonin. This study has demonstrated that ergot alkaloids, with the exception of lysergic acid, were vasoactive in the bovine midgut mesentery in vitro. Steers exposed to endophyte-infected tall fescue seed had diminished or lacked contractility to many ergot alkaloids and serotonin in the small intestinal vasculature. This suggests that dietary exposure to ergot alkaloids could affect absorption of nutrients within the animal by decreased blood flow to and from the midgut due to vasoconstriction. However, because steers which had already been dosed with endophyte-infected tall fescue seed exhibited a reduced contractile response in vitro compared to endophyte-free dosed steers, the vasoactive response to ergot alkaloids and biogenic amines is suppressed in chronically exposed cattle. Prevention of mid-gut absorption of ergot alkaloids is viewed as a viable solution to the fescue toxicosis syndrome. Along with determining the mechanism of ergot alkaloid absorption from the midgut, further research should be directed towards investigating the passage of nutrients through mesenteric vasculature of animals exposed to endophyte-infected and endophyte-free tall fescue seed.
Technical Abstract: Ergot alkaloids are hypothesized to cause vasoconstriction in the midgut, and prior exposure may affect the vasoactivity of these compounds. The objectives of this study were to profile vasoactivity of ergot alkaloids in bovine mesenteric artery (MA) and vein (MV) and determine if previous exposure to endophyte-infected tall fescue seed affected vasoactivity of ergocryptine (ERP), ergotamine (ERT), ergocristine (ERS), ergocornine (ERO), ergonovine (ERN), lysergic acid (LSA), ergovaline (EXT), and 5-hydroxytryptamine (5HT; serotonin). Ruminally cannulated Angus steers (n = 12; BW = 547 ± 31 kg) were paired by weight and randomly assigned to 6 blocks. Steers were ruminally dosed daily with 1 kg of either endophyte-infected (E+; 4.45 mg/kg ergovaline) or endophyte-free (E-) tall fescue seed for 21 d prior to slaughter. Branches of MA and MV supporting the cranial portion of the ileum were collected after slaughter on d 22, placed in a modified Krebs-Henseleit buffer on ice, cleaned, sectioned and mounted in a multimyograph chamber. Contractile response was normalized to a maximum KCl response. Inner diameter (P = 0.04) and outer diameter (P = 0.02) of MA were smaller for E+ steers than E- steers. Maximum contractile responses to 120 mM KCl were not different between seed treatments in MA (P = 0.33; E-: 2.67 ± 0.43 g; E+: 3.33 ± 0.43 g) or MV (P = 0.26; E-: 2.01 ± 0.18 g; E+: 1.81 ± 0.18 g). Steers receiving E+ had smaller (P < 0.01) MA contractile responses than E- steers to ERP, ERT, ERS, ERO, ERN, EXT, and 5HT. Steers receiving E+ had a smaller (P < 0.05) MV contractile response to ERP, ERT, ERS, ERN, EXT, and 5HT than E- steers. Lysergic acid failed to induce a contractile response in MA and MV. The greatest contractile response in MA and MV was produced by serotonin on vessels from E- steers. Ergovaline was the most potent agonist in MV (P < 0.05) and MA of E+ steers having the greatest (P < 0.05) –logEC50 values. These data show that ergot alkaloids were vasoactive in the midgut, and steers exposed to E+ had diminished contractility to some ergot alkaloids in small intestinal vasculature. These data suggest that dietary exposure to ergot alkaloids has potential to alter nutrient absorption from the midgut by decreasing blood flow to and from the midgut due to vasoconstriction.