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ARS Home » Midwest Area » Lexington, Kentucky » Forage-animal Production Research » Research » Publications at this Location » Publication #359218

Research Project: Optimizing the Biology of the Animal-Plant Interface for Improved Sustainability of Forage-Based Animal Enterprises

Location: Forage-animal Production Research

Title: Ergot alkaloid exposure during gestation alters: II. Uterine and umbilical artery vasoactivity

item Klotz, James
item BRITT, JESSIE - Clemson University
item MILLER, MARKUS - Clemson University
item SNIDER, MIRIAM - University Of Kentucky
item Aiken, Glen
item LONG, NATHAN - Clemson University
item PRATT, SCOTT - Clemson University
item ANDRAE, JOHN - Clemson University
item DUCKETT, SUSAN - Clemson University

Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/11/2019
Publication Date: 2/14/2019
Citation: Klotz, J.L., Britt, J.L., Miller, M.F., Snider, M.A., Aiken, G.E., Long, N.M., Pratt, S.L., Andrae, J.G., Duckett, S.K. 2019. Ergot alkaloid exposure during gestation alters: II. Uterine and umbilical artery vasoactivity. Journal of Animal Science. 97(4):1891-1902.

Interpretive Summary: Exposure of pregnant livestock to ergot alkaloids, the toxins responsible for fescue toxicosis, can cause a growth restriction that results in reduced birth weights. We have shown in other blood vessels that prior exposure to ergot alkaloids cause decreased blood flow (vasoconstriction) and a significant decrease in the ability to respond to external stimuli. Thus, it was hypothesized that maternal exposure to ergot alkaloids during gestation will reduce vasoactivity of uterine and umbilical vasculature and result in reduced blood flow causing intra-uterine growth restriction and lower birth weights of the lambs. A study was conducted that evaluated contractile responses of uterine and umbilical arteries collected from ewes consuming ergot alkaloids during gestation. The umbilical (fetal) blood vessels were much more reactive to direct exposure to serotonin and ergot alkaloids compared to the uterine (maternal) blood vessel. The activity of both blood vessels tested were significantly reduced in the treatments where the ewes were receiving ergot alkaloids in the diet. This combined with the fetal weight also being lower in these treatments compared to controls, indicate that a compromised blood supply is a responsible factor. These findings are of value to both researchers and producers interested in minimizing the negative effects that ergot alkaloids can have on livestock productivity.

Technical Abstract: Previous research has shown that livestock exposed to ergot alkaloids results in decreased vasoactivity of gastrointestinal and peripheral vasculature. Little is known regarding the effect ergot alkaloid exposure during gestation may have on vasculature supporting the fetus. The objective of this study was to evaluate contractile responses of uterine and umbilical arteries collected from ewes consuming ergot alkaloids during gestation. On d 35 of gestation, 36 Suffolk ewes (78.24 ±9.5 kg) were randomly assigned to endophyte-infected (E+) or endophyte-free (E-) tall fescue seed treatments that were fed either throughout or switched on d 86 of gestation, creating four seed treatments E+E+, E+E-, E-E+, E-E-. Ewes were fed E+ tall fescue seed to provide 1.77 mg of total ergovaline/head/d with E- ewes receiving the same quantity of E- seed. Gestation was terminated on d 133, and sections of uterine artery and umbilical cord were surgically collected. Only collections from 28 ewes (n=7/treatment) were of sufficient viability to proceed with the contractility experiments. Arteries were cleaned, sliced into 2-mm cross sections, and suspended in multi-myograph chambers containing 5 mL of continuously oxygenated Krebs-Henseleit buffer. Vessels were exposed to increasing concentrations (5x10-8 to 1x10-4 M) of norepinephrine, serotonin, ergotamine, and ergovaline (5x10-9 to 1x10-5 M; extract of tall fescue seed) in 15-min intervals. Increasing concentrations of norepinephrine generated a moderate contractile response by the uterine artery (P< 0.05), but no response in the umbilical artery. Increasing concentrations of serotonin resulted in negligible responses in uterine preparations, whereas umbilical artery preparations were very responsive (P<0.05) to serotonin. Ewes receiving E+E+ and E-E+ treatments had decreased vasoactivity in umbilical arteries to serotonin with a dextral shift in concentrations where the response curve initiated (P< 0.05). Interestingly, uterine arteries were not responsive to exposure to ergotamine or ergovaline, whereas umbilical arteries were very responsive. Umbilical arteries collected from ewes receiving E-E- and E+E- were more vasoactive to ergot alkaloids (P<0.05) than other treatments. These findings indicate that maternal blood supply to the placenta appears protected from negative effects of ergot alkaloids; however, umbilical vasculature is not, and this could adversely affect fetal growth.