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Vasoconstriction is a known effect associated with ergot alkaloid consumption. The vascular contractile responses are often sustained for an extended period after exposure. Ergot alkaloids exist in two molecular configurations, the C-8-(R)-isomer (R -epimer) and the C-8-(S)-isomer (S -epimer). The sustained vascular contractile response to the R -epimers has been studied previously, unlike the S -epimers which are thought to be biologically inactive. Additionally, antagonists have been utilized to attenuate the vascular contraction associated with the R- epimers of ergot alkaloids utilizing ex vivo techniques. This study utilized an arterial tissue bath to examine and compare the sustained vascular contractile response attributed to ergocristine (R) and ergocristinine (S) using dissected bovine metatarsal arteries. The contractile blocking effect of a noncompetitive alpha-adrenergic antagonist, phenoxybenzamine (POB), was also investigated in precontracted arteries. Arteries (n = 6/epimer) were exposed to a single dose of ergocristine or ergocristinine (1 × 10−6 M in buffer). Each of the epimer doses was followed by a POB (1 × 10−3 M) or methanol (control) treatment at 90 min and the response was observed for another 90 min. Both epimers produced a sustained contractile response over the 180-min incubation period in the control groups. The R -epimer caused a greater sustained contractile response from 60 to 180 min post epimer exposure, compared to the S -epimer (P < 0.05, generalized estimating equations, independent t-test). Phenoxybenzamine caused a decrease in the contractile response induced by ergocristine and ergocristinine from 105 to 180 min, compared to the control (P < 0.05, generalized estimating equations, paired t-test). Overall, these results demonstrate the presence of a sustained vascular contractile response attributed to the R- and S -epimer of an ergot alkaloid with differences in contractile response between the epimers, suggesting differences in receptor binding mechanisms. Furthermore, this study demonstrated that a noncompetitive antagonist could attenuate the sustained arterial contractile effects of both ergot configurations ex vivo. Additional investigation into S -epimers of ergot alkaloids is needed. This research contributes to the understanding of the ergot epimer-vascular receptor binding mechanisms, which may support the investigation of different approaches of minimizing ergot toxicity in livestock. [ABSTRACT FROM AUTHOR]

Ergot alkaloids are produced by the fungus Claviceps purpurea and their levels are carefully monitored in animal and human diets due to their harmful effects and widespread contamination of cereal crops. Ergot alkaloids exist in two forms known as the (R)- and (S)-epimers with only the former being monitored in diets in North America. The (S)-epimers of ergot alkaloids are thought to be biologically inactive and, therefore, harmless. A major mechanism by which the (R)-epimers of ergot alkaloids produce their toxic effect is through vasoconstriction. Therefore, the objective of this study was to examine the vasoactivity potential (contractile response) of four (S)-epimers, namely ergocryptinine, ergocristinine, ergocorninine, and ergotaminine utilizing an in vitro arterial tissue bath system. Bovine metatarsal arteries (n = 6, ergocryptinine and ergocorninine; n = 6, ergocristinine and ergotaminine; n = 6 arteries/(S)-epimer, total n = 12) were collected from healthy mixed-breed beef steers immediately after slaughter, cut into 3-mm arterial cross sections, and suspended in a tissue bath with continuously oxygenated Krebs–Henseleit buffer. To assess the contractile response of each (S)-epimer, a cumulative contractile dose–response curve was constructed by incubating arteries with increasing concentrations (1 × 10−11 to 1 × 10−6 M) of that (S)-epimer. Contractile responses were recorded as grams of tension and were normalized to an initial contraction of phenylephrine. Contrary to the widespread belief, all tested (S)-epimers were found vasoactive and produced a concentration-dependent arterial contractile response similar to what has been reported for the (R)-epimers. The arterial contractile response to ergotaminine was strongest and was significantly greater than that of ergocryptinine and ergocristinine at the highest concentration used (P ≤ 0.01). Our results indicate that the (S)-epimers are biologically active and are likely harmful similar to the (R)-epimers. The levels of (S)-epimers should be carefully monitored in human and animal diets worldwide. [ABSTRACT FROM AUTHOR]

The rumen simulation technique (RUSITEC) was used to investigate the effect of ergot alkaloids (EA) and a mycotoxin deactivating product (Biomin AA; MDP) on nutrient digestion, ruminal fermentation parameters, total gas, methane, and microbial nitrogen production. Ruminal fermentation vessels received a feedlot finishing diet of 90:10 concentrate:barley silage (DM basis). Using a randomized complete block design, treatments were assigned (n = 4 vessels/treatment) within two RUSITEC apparatuses in a 2 × 2 factorial arrangement. Treatments included: (1) control (CON) diet (no EA and no MDP); (2) CON diet + 1 g/d MDP; (3) CON diet + 20 mg/kg EA; and (4) CON diet + 20 mg/kg EA + 1 g/d MDP. The study was conducted over 14 d with 7 d of adaptation and 7 d of sample collection. Data were analyzed in SAS using PROC MIXED including fixed effects of EA, MDP, and the EA×MDP interaction. Random effects included RUSITEC apparatus and cow rumen inoculum (n = 4). Ergot alkaloids decreased dry matter (DMD) (P = 0.01; 87.9 vs. 87.2%) and organic matter disappearance (OMD) (P = 0.02; 88.8 vs. 88.4%). Inclusion of MDP increased OMD (P = 0.01; 88.3 vs. 88.9%). Neutral detergent fiber disappearance (NDFD) was improved with MDP; however, an EA×MDP interaction was observed with MDP increasing (P < 0.001) NDFD more with EA diet compared to CON. Acetate proportion decreased (P = 0.01) and isovalerate increased (P = 0.03) with EA. Consequently, acetate:propionate was reduced (P = 0.03) with EA. Inclusion of MDP increased total volatile fatty acid (VFA) production (P < 0.001), and proportions of acetate (P = 0.03) and propionate (P = 0.03), and decreased valerate (P < 0.001), isovalerate (P = 0.04), and caproate (P = 0.002). Treatments did not affect (P ≥ 0.17) ammonia, total gas, or methane production (mg/d or mg/g of organic matter fermented). The inclusion of MDP reduced (P < 0.001) microbial nitrogen (MN) production in the effluent and increased (P = 0.01) feed particle-bound MN. Consequently, total MN decreased (P = 0.001) with MDP. In all treatments, the dominant microbial phyla were Firmicutes, Bacteroidota, and Proteobacteria, and the major microbial genus was Prevotella. Inclusion of MDP further increased the abundance of Bacteroidota (P = 0.04) as it increased both Prevotella (P = 0.04) and Prevotellaceae_UCG-003 (P = 0.001). In conclusion, EA reduced OMD and acetate production due to impaired rumen function, these responses were successfully reversed by the addition of MDP. [ABSTRACT FROM AUTHOR]

This study evaluated the effect of feeding pelleted or mash ergot contaminated grain fed continuously or intermittently on the growth performance, blood serum variables, and carcass quality of finishing beef steers. Sixty black angus steers (442 ± 36.7 kg) were used in a complete randomized finishing (90% concentrate:10% barley silage DM basis) 126-d study. Steers were randomly assigned to 4 different treatments and individually housed. Treatments included: 1) control ration [CON; no added ergot alkaloids (EA)], 2) continuous ergot mash (CEM; fed continuously at 2 ppm total EA), 3) intermittent ergot mash (IEM; fed at 2 ppm EA during the first week of each 21-d period and control diet for the remaining 2 weeks), and 4) intermittent ergot pellet (IEP; fed at 2 ppm EA incorporated into a pelleted supplement during the first week of each 21-d period and control diet for the other 2 weeks). Steers were weighed every 21 d and blood samples were collected on day 0, 42, 84, and 126. Steer DMI (P < 0.01, 9.95 vs. 11.05 kg/day) and ADG (P = 0.04) decreased for all EA treatments compared with the CON. Total shrunk BW gain (P = 0.03, 202.5 vs. 225.2 kg), final BW (P = 0.03, 617.9 vs. 662.2 kg), and carcass weight (P = 0.06) decreased for all EA steers compared with the CON steers. No treatment effects (P > 0.05) were observed for carcass dressing percentage, ribeye area, marbling score, or liver abscess. The percent of carcasses graded AAA decreased for all EA steers compared CON steers (P < 0.01, 46.7 vs. 93.3%). Steers fed EA had increased rectal temperature compared with CON steers (P < 0.01, 39.8 vs. 39.4 °C). Hair cortisol concentrations were less in steers fed IEP (P = 0.05, 1.23 vs. 1.76 pg/mg) than CON. No treatment effects (P > 0.05) were observed for complete blood count, and serum prolactin, haptoglobin, albumin, alkaline phosphatase, alanine transaminase, amylase, calcium, creatine, glucose, lipase, total bilirubin, total protein, or globulin. Blood urea nitrogen was less for EA steers compared with CON (P = 0.01, 3.48 vs. 4.10 mmol/L). The IEM steers had decreased concentrations of serum gamma-glutamyl transferase compared with IEP steers (P = 0.04, 23.4 vs. 28.5 IU). Pelleting ergot contaminated grain did not reduce the impact of ergot alkaloids on any of the measured parameters. Results suggest that continuously or intermittently feeding an ergot contaminated diet (2 ppm EA) can significantly reduce intake, growth performance, and carcass weight, with minimal impact on blood serum variables in finishing steers. Pelleting was not an effective method of reducing ergot toxicity. [ABSTRACT FROM AUTHOR]

The objective of this study was to evaluate the effect of feeding pelleted or mash ergot contaminated grain continuously or intermittently on performance and blood parameters of backgrounding steers. Sixty black angus steers (300 ± 29.4 kg) were used in a complete randomized backgrounding (60% barley silage:40% concentrate DM basis) 84 d study. Steers were randomly assigned to 4 different treatments and housed individually. Treatments included: 1) control ration (CON; no added ergot), 2) continuous ergot mash (CEM; fed continuously at 2 ppm), 3) intermittent ergot mash (IEM; fed at 2 ppm on the first wk of each 21 d period and control diet for the remaining 2 wk), and 4) intermittent ergot pellet (IEP; fed at 2 ppm during the first wk of each 21 d period and control diet for the other 2 wk). Calves were weighed every 21 days and blood samples were collected on d 0, 42, and 84. No treatment effects (P>0.05) were observed for complete blood count. Steer DMI was reduced for all ergot diets compared to the CON diet (P< 0.01, 7.45 vs. 8.05 kg/d). Steer ADG was reduced for all ergot diets compared to the CON diet (P< 0.01). CEM fed steers had lower ADG (P< 0.01, 0.980 vs. 0.735 kg) and shrunk final weight (P< 0.01, 366 vs. 350 kg) than CON calves, but CEM and IEM were no different. CEM fed steers had lower Gain:Feed (P< 0.07, 0.130 vs. 0.142) than CON calves. Pelleting ergot contaminated grain did not reduce the impact of ergot alkaloids on any of the measured parameters. Results suggest that continuously or intermittently feeding an ergot contaminated TMR (2 ppm) can significantly reduce the growth performance of backgrounded feedlot steers but no effects were observed for blood parameters. Pelleting was not an effective method of reducing ergot toxicity. [ABSTRACT FROM AUTHOR]

This study evaluated the effects of feeding ergot alkaloids (EA) at increasing levels (0, 0.75, 1.5, and 3.0 ppm) to feedlot beef cattle over backgrounding (BG) and finishing (FS) phases on growth performance and carcass quality. Steers (n=240; 280±32 kg) were blocked by weight and randomly allocated to 16 pens (4 pens/treatment; 15 steers/pen). Treatments included: no added EA (CTL); or EA added at 0.75 (EA075); 1.50 (EA150); and 3.0 ppm (EA300). Steers were fed barley-based BG diets containing 40% concentrate: 60% silage (DM basis) for 84 d, then stepped up over 28 d to a 90% concentrate:10% silage (DM basis) FS diet for 119 d. Steers fed EA300 received CTL in FS after 77 days on feed (DOF). In the BG phase, a quadratic decrease (P=0.05) in ADG and a linear decrease in final BW (P=0.03) and total BW gain (P=0.02) were observed with increasing EA. In the FS phase, up to 77 DOF, there was a linear decrease in steers DMI (P=0.04), ADG (P=0.01), and total BW gain (P=0.01) with increasing levels of EA. Over the full FS phase (119 DOF), a quadratic response was observed for ADG (P=0.05), final BW (P=0.05), total BW gain (P=0.02) and carcass weight (P=0.05) with steers fed EA150 showing the lowest performance. Gain:feed was not affected (P>0.20) by EA in the BG or FS phase. Dressing percentage (P=0.02) showed a quadratic effect with EA300 being the lowest. Additionally, a linear increase in lean meat yield (P< 0.001) was observed with increasing EA. Including EA in the diet promoted a linear increase in rectal temperature (P< 0.01). In conclusion, increasing levels of EA in the diet reduced growth performance, but when EA was removed, steers showed compensatory weight gain. [ABSTRACT FROM AUTHOR]

A rumen simulation technique (RUSITEC) investigated effects of ergot alkaloids (E) and a mycotoxin deactivating product (Biomin® AA; B) on nutrient digestion, rumen fermentation, total gas and methane emissions. Fermenters received a finishing diet of 90:10 concentrate:barley silage. Using a randomized complete block design, treatments were assigned (4 vessels/treatment) within two RUSITECs in a 2 × 2 factorial. Treatments included: 1) control diet, 2) control + 1 g B, 3) control + 20 ppm E, and 4) control + 20 ppm E + 1 g B. The study had a 14-d experimental period, with 7-d adaptation and 7-d sample collection. Data were analyzed in SAS using PROC mixed including fixed effects of E, B, and E×B interaction. Random effects included RUSITEC apparatus and cow rumen inoculum (n = 4). Ergot decreased dry matter disappearance (DMD) (P < 0.05; 87.9 vs. 87.2%) and organic matter disappearance (OMD) (P < 0.05; 88.8 vs. 88.4%). Adding B increased OMD (P < 0.05; 88.3 vs. 88.9%) and neutral detergent fiber disappearance (NDFD) (P < 0.01); however, an E×B interaction was observed for NDFD (P < 0.01) with B promoting greater increases with E. Ergot decreased acetate proportions (P < 0.01) and increased isovalerate (P < 0.05). Consequently, acetate:propionate was reduced (P < 0.05) with E. Inclusion of B increased total volatile fatty acids (P < 0.01), and proportions of acetate (P < 0.05) and propionate (P < 0.05), and decreased valerate (P < 0.01), isovalerate (P < 0.01), and caproate (P < 0.01). Treatments did not affect (P = 0.17) ammonia-N, total gas, or methane production (mg/d or mg/g of OM fermented). In conclusion, E reduced OMD and acetate production, but these responses were reversed by the addition of B. [ABSTRACT FROM AUTHOR]