Alteration of fasting heat production during fescue toxicosis in Holstein steers.

This study was designed to examine alteration of fasting heat production (FHP) during fescue toxicosis. Six ruminally cannulated Holstein steers (BW = 348 ± 13 kg) were BW-matched into pairs and used in a 2 period crossover design experiment. Each period consisted of 2 temperature segments, one each at 22 and 30°C. During each period, 1 steer per pair was ruminally dosed twice daily with 0.5 kg of ground endophyte-infected fescue seed (E+) and the other with ground endophyte-free fescue seed (E-) for 7 d. Steers on E- treatment were pair-fed to E+ steers offered alfalfa cubes at 1.5 × NEm. On d 8 of each segment, steers were moved to individual metabolism stalls fitted with indirect calorimetry head boxes. Ruminal contents were removed, weighed, and subsampled for DM determinations. The reticulorumen was washed and filled with a buffer (NaCl = 96; NaHCO3 = 24; KHCO3 = 30; K2HPO4 = 2; CaCl2 = 1.5; MgCl2 = 1.5 mmol·kg buffer(-1)) that was gassed with a 75% N2 and 25% CO2 mixture before rumen incubation. During buffer incubation, an E+ or E- fescue seed extract was added at 12 h intervals to maintain treatment presentation to the animal. After a 12-h wait, heart rate, O2 consumption, CO2 production, and urinary output were recorded for 16 h. There was no difference (P = 0.931) in DMI/kg(0.75) between endophyte treatments by design; however, intake decreased (P = 0.004) at 30°C. Increased temperature had no effect (P > 0.10) on other measurements and there were no significant interactions (P > 0.11) of temperature and endophyte treatment. Heart rate was unaffected by fescue treatment or environmental temperature. Percent DM of ruminal contents as well as total rumen DM/kg(0.75) was increased (P < 0.0001) in E+ steers. Respiratory quotient was elevated (P = 0.02) in E+ steers. Oxygen consumption decreased (P = 0.04) and CO2 production tended to be reduced (P = 0.07) during E+ treatment. Calculated FHP (kcal/kg BW(0.75)) was also less (P = 0.006) in steers receiving E+ treatment. These data suggest that consumption of endophyte-infected tall fescue by cattle results in a reduction in basal metabolic rate.

Ergot alkaloids from endophyte-infected tall fescue decrease reticuloruminal epithelial blood flow and volatile fatty acid absorption from the washed reticulorumen.

An experiment was conducted to determine if ergot alkaloids affect blood flow to the absorptive surface of the rumen. Steers (n=8) were pair-fed alfalfa cubes and received ground endophyte-infected (Neotyphodium coenophialum) tall fescue (Lolium arundinaceum; E+) seed (0.015 mg ergovaline·kg BW(-1)·d(-1)) or endophyte-free tall fescue (E-) seed via the rumen cannula 2x daily for 7 d at thermoneutral (TN; 22°C) and heat stress (HS; 32°C) conditions. On d 8, the rumen was emptied and rinsed. A buffer containing VFA was incubated in the following sequence: control (CON), 15 µg ergovaline·kg BW(-1) (1×EXT) from a tall fescue seed extract, and 45 µg ergovaline·kg BW(-1) (3×EXT). For each buffer treatment there were two 30-min incubations: a 30-min incubation of a treatment buffer with no sampling followed by an incubation of an identical sampling buffer with the addition of Cr-EDTA and deuterium oxide (D2O). Epithelial blood flow was calculated as ruminal clearance of D2O corrected for influx of physiological water and liquid outflow. Feed intake decreased with dosing E+ seed at HS but not at thermoneutral conditions (TN; P<0.02). Dosing E+ seed decreased serum prolactin (P<0.005) at TN. At HS, prolactin decreased in both groups over the 8-d experiment (P<0.0001), but there was no difference in E+ and E- steers (P=0.33). There was a seed treatment×buffer treatment interaction at TN (P=0.038), indicating that E+ seed treatment decreased reticuloruminal epithelial blood flow at TN during the CON incubation, but the two groups of steers were not different during 1×EXT and 3×EXT (P>0.05). Inclusion of the extract in the buffer caused at least a 50% reduction in epithelial blood flow at TN (P=0.004), but there was no difference between 1×EXT and 3×EXT. There was a seed × buffer treatment interaction at HS (P=0.005), indicating that the reduction of blood flow induced by incubating the extract was larger for steers receiving E- seed than E+ seed. Volatile fatty acid flux was reduced during the 1×EXT and 3×EXT treatments (P<0.01). An additional experiment was conducted to determine the effect of time on blood flow and VFA flux because buffer sequence could not be randomized. Time either increased (P=0.05) or did not affect blood flow (P=0.18) or VFA flux (P>0.80), indicating that observed differences are due to the presence of ergot alkaloids in the rumen. A decrease in VFA absorption could contribute to the signs of fescue toxicosis including depressed growth and performance.

Evaluation of a ruminally dosed tall fescue seed extract as a model for fescue toxicosis in steers.

Tall fescue (Lolium arundinaceum) toxicosis research is often complicated by a reduction in intake of infected forage or seed, making treatment comparisons difficult. This study was conducted to develop a fescue toxicosis model that would allow for variations in DMI without altering the quantity of alkaloids consumed over the course of the experiment. Ground tall fescue seed and a tall fescue seed extract were used in two 2-period crossover experiments to determine the effectiveness of ruminal dosing of a tall fescue seed extract to induce fescue toxicosis. This experiment used 4 growing Holstein steers (BW = 337 ± 24 kg) surgically fitted with ruminal cannulas. Steers were maintained on a diet of endophyte-free fescue hay fed ad libitum throughout the experiment. Endophyte-infected (E+; 4.1 mg/kg of ergovaline) and uninfected (E-; 0.0 mg/kg of ergovaline) KY-31 tall fescue seed was ground and dosed or extracted with ethanol, concentrated, and lyophilized before ruminal dosing. Ergovaline concentration of the final extract was 102 mg/kg. Animals were given a minimum of a 3-wk washout period between treatments. Physiological indicators were measured over 7 d at 22°C (d 1 to 3) and 32°C (d 4 to 7) during both seed and extract dosing. Seed and extract E+ dosing reduced serum prolactin concentrations such that they were not different from zero (P < 0.10). Treatment with E+ reduced feed intake (P < 0.05) and heart rate (P < 0.001), and increased respiration rate (P < 0.01) and core temperature (P < 0.05) during both seed and extract dosing. Increasing environmental temperature from 22 to 32°C reduced total intake (P < 0.05) and increased core temperature (P < 0.001) and respiration rate (P < 0.001) during both seed and extract dosing. Diastolic blood pressure tended (P < 0.09) to be increased during E+ extract dosing and reduced during heat stress. These physiological alterations are consistent with those reported for cattle grazing or consuming seed from endophyte-infected tall fescue. These data indicate that a ruminally dosed ethanol extract of tall fescue seed is efficacious in inducing fescue toxicosis in cattle.

Constriction of bovine vasculature caused by endophyte-infected tall fescue seed extract is similar to pure ergovaline.

Ergovaline has been extensively used to study vasoactive effects of endophyte- (Neotyphodium coenophialum) infected tall fescue (Lolium arundinaceum). However, initial results indicated that an extract of toxic tall fescue seed (E+EXT) is more potent than ergovaline alone in a right ruminal artery and vein bioassay. The E+EXT induced a greater contractile response than an equal concentration of ergovaline alone in the ruminal artery of heifers (P = 0.018). This led to a hypothesis that other compounds in the seed extract contribute to vasoconstriction. Thus, experiments were conducted to determine if vasoactivity of an E+EXT is different from a mixture of ergot alkaloids (ALK; ergovaline, ergotamine, ergocristine, ergocryptine, ergocornine, ergonovine, and lysergic acid) of similar concentrations and to determine if the vasoactivity of an E+EXT differs from an endophyte-free tall fescue seed extract (E-EXT). Segments of lateral saphenous vein and right ruminal artery and vein were collected from Holstein steers (n = 6) shortly after slaughter. Vessels were cleaned of excess connective tissue and fat and sliced into segments that were suspended in a multimyograph chamber with 5 mL of continually oxygenated Krebs-Henseleit buffer, equilibrated for 90 min, and exposed to a reference compound (120 mM KCl for ruminal vessels and 0.1 mM norepinephrine for saphenous vein). Increasing concentrations of each treatment (E+EXT, E-EXT, ALK, and ergovaline) were added to the respective chamber every 15 min after buffer replacement. Data were normalized as a percentage of maximal contractile response of the reference compound and fit to a sigmoidal concentration response curve. Ergovaline, ALK, and E+EXT induced similar responses in the saphenous vein, ruminal artery, and ruminal vein. The E+EXT displayed a smaller EC(50) (half maximal effective concentration) than ergovaline or ALK in the saphenous vein and ruminal vein (P < 0.008), but not the ruminal artery (P = 0.31). Extrapolated maximum response was greatest in the saphenous vein for ergovaline, least for E+EXT, and intermediate for ALK (P < 0.0001). The E-EXT did not induce a contractile response in any vessel tested (P > 0.1). Data from this study indicate that ergovaline is largely responsible for the locally induced vasoconstriction of bovine vasculature observed with endophyte-infected tall fescue.

Influence of slow-release urea on nitrogen balance and portal-drained visceral nutrient flux in beef steers.

Two experiments were conducted to evaluate the effects of slow-release urea (SRU) versus feed-grade urea on portal-drained visceral (PDV) nutrient flux, nutrient digestibility, and total N balance in beef steers. Multi-catheterized steers were used to determine effects of intraruminal dosing (Exp. 1; n = 4; 319 +/- 5 kg of BW) or feeding (Exp. 2; n = 10; 4 Holstein steers 236 +/- 43 kg of BW and 6 Angus steers 367 +/- 46 kg of BW) SRU or urea on PDV nutrient flux and blood variables for 10 h after dosing. Intraruminal dosing of SRU (Exp. 1) prevented the rapid increase in ruminal ammonia concentrations that occurred with urea dosing (treatment x time P = 0.001). Although apparent total tract digestibilities of DM, OM, NDF, and ADF were not affected by treatment (P > 0.53, Exp. 2), SRU increased fecal N excretion (49.6 vs. 45.6 g/d; P = 0.04) and reduced apparent total tract N digestibility (61.7 vs. 66.0%; P = 0.003). Transfer of urea from the blood to the gastrointestinal tract occurred for both treatments in Exp. 1 and 2 at all time points with the exception for 0.5 h after dosing of urea in Exp. 1, when urea was actually transferred from the gastrointestinal tract to the blood. In both Exp. 1 and 2, both urea and SRU treatments increased arterial urea concentrations from 0.5 to 6 h after feeding, but arterial urea concentrations were consistently less with SRU (treatment x time P < 0.001, Exp. 1; P = 0.007, Exp. 2). Net portal ammonia release remained relatively consistent across the entire sampling period with SRU treatment, whereas urea treatment increased portal ammonia release in Exp. 1 and tended to have a similar effect in Exp. 2 (treatment x time P = 0.003 and P = 0.11, respectively). Urea treatment also increased hepatic ammonia uptake within 0.5 h (treatment x time P = 0.02, Exp. 1); however, increased total splanchnic release of ammonia for the 2 h after urea treatment dosing suggests that PDV ammonia flux may have exceeded hepatic capacity for removal. Slow-release urea reduces the rapidity of ammonia-N release and may reduce shifts in N metabolism associated with disposal of ammonia. However, SRU increased fecal N excretion and increased urea transfer to the gastrointestinal tract, possibly by reduced SRU hydrolysis or effects on digestion patterns. Despite this, the ability of SRU to protect against the negative effects of urea feeding may be efficacious in some feeding applications.

Effects of slow-release urea on ruminal digesta characteristics and growth performance in beef steers.

Two experiments were conducted to evaluate the effects of slow-release urea (SRU) versus feed-grade urea on ruminal metabolite characteristics in steers and DMI, gain, and G:F in growing beef steers. Experiment 1 used 12 ruminally cannulated steers (529 +/- 16 kg of BW) to monitor the behavior of SRU in the ruminal environment. Compared with feed-grade urea, SRU decreased ruminal ammonia concentration (P = 0.02) and tended to increase ruminal urease activity (P = 0.06) without affecting ruminal VFA molar proportions or total concentrations (P > 0.20). After 35 d of feeding, the in situ degradation rate of SRU was not different between animals fed urea or SRU (P = 0.48). Experiment 2 used 180 Angus-cross steers (330 +/- 2.3 kg) fed corn silage-based diets supplemented with urea or SRU for 56 d to evaluate the effects on feed intake, gain, and G:F. The design was a randomized complete block with a 2 x 4 + 1 factorial arrangement of treatments. Treatments included no supplemental urea (control) or urea or SRU at 0.4, 0.8, 1.2, or 1.6% of diet DM. Over the entire 56 d experiment, there were interactions of urea source x concentration for gain (P = 0.04) and G:F (P = 0.01) because SRU reduced ADG and G:F at the 0.4 and 1.6% supplementation concentrations but was equivalent to urea at the 0.8 and 1.2% supplementation concentrations; these effects were due to urea source x concentration interactions for gain (P = 0.06) and G:F (P = 0.05) during d 29 to 56 of the experiment. The SRU reduced DMI during d 29 to 56 (P = 0.01) but not during d 0 to 28, so that over the entire experiment there was no difference in DMI for urea source (P = 0.19). These collective results demonstrate that SRU releases N slowly in the rumen with no apparent adaptation within 35 d. Supplementation of SRU may limit N availability at low (0.4%) concentrations but is equivalent to urea at 0.8 and 1.2% concentrations.

Effects of a dietary Aspergillus oryzae extract containing alpha-amylase activity on performance and carcass characteristics of finishing beef cattle.

Three experiments were conducted to examine the effects of an Aspergillus oryzae extract containing alpha-amylase activity on performance and carcass characteristics of finishing beef cattle. In Exp. 1, 120 crossbred steers were used in a randomized complete block design to evaluate the effects of roughage source (alfalfa hay vs. cottonseed hulls) and supplemental alpha-amylase at 950 dextrinizing units (DU)/kg of DM. Significant roughage source x alpha-amylase interactions (P < 0.05) were observed for performance. In steers fed cottonseed hulls, supplemental alpha-amylase increased ADG through d 28 and 112 and tended (P < 0.15) to increase ADG in all other periods. The increases in ADG were related to increased DMI and efficiency of gain during the initial 28-d period but were primarily related to increased DMI as the feeding period progressed. Supplemental alpha-amylase increased (P = 0.02) the LM area across both roughage sources. In Exp. 2, 96 crossbred heifers were used in a randomized complete block design with a 2 x 3 factorial arrangement of treatments to evaluate the effects of corn processing (dry cracked vs. high moisture) and supplemental alpha-amylase concentration (0, 580, or 1,160 DU/kg of DM). Alpha-amylase supplementation increased DMI (P = 0.05) and ADG (P = 0.03) during the initial 28 d on feed and carcass-adjusted ADG (P = 0.04) across corn processing methods. Longissimus muscle area was greatest (quadratic effect, P = 0.04), and yield grade was least (quadratic effect, P = 0.02) in heifers fed 580 DU of alpha-amylase/kg of DM across corn processing methods. In Exp. 3, 56 crossbred steers were used in a randomized complete block design to evaluate the effects of supplemental alpha-amylase (930 DU/kg of DM) on performance when DMI was restricted to yield a programmed ADG. Alpha-amylase supplementation did not affect performance when DMI was restricted. We conclude that dietary alpha-amylase supplementation of finishing beef diets may result in increased ADG through increased DMI under certain dietary conditions and that further research is warranted to explain its mode of action and interactions with dietary ingredients.

Influence of fiber fermentability on nutrient digestion in the dog.

Eight mature dogs (17.2 +/- 0.2 kg) surgically fitted with ileal T-cannulas were used in a replicated 4-x-4 Latin-square-design experiment to evaluate nutrient disappearance at the terminal ileum and through the digestive tract. Two fiber types, cellulose, a crystalline, slowly fermented fiber, and pectin, a soluble, rapidly fermented fiber, were fed in different increments, and the effects on nutrient availability were assessed. Treatments included 1) 100% cellulose, 2) 66% cellulose and 33% pectin, 3) 66% pectin and 33% cellulose, and 4) 100% pectin. Fiber was added at 10% of diet dry matter (DM). Diets were fed at 100% of ME for maintenance and offered at 0730 and 1730 h. All periods were 21 d, which included 3 d of diet transition and 7 d of adaptation. Daily DM intake was 210 +/- 5 g. Total tract and large-intestine DM digestibility increased linearly (P < 0.01) with increased pectin. These changes in DM digestion were largely the result of changes in fiber digestion. Fermentation of total dietary fiber in the large intestine went from less than zero to 39% of ileal flow (linear, P < 0.01). Total-tract crude-protein digestibility decreased linearly (P < 0.01) with increased pectin. This study demonstrated that fiber fermentability significantly affects digestion in the dog. Increasing fermentable fiber increased the digestion of DM and energy. However, increased fiber fermentability inversely affects crude protein digestibility. The lower crude-protein digestibility could be attributed to larger microbial protein excretion as a result of greater fermentation of pectin versus cellulose.

Nutritional evaluation of poultry by-product meal as a protein source for ruminants: small intestinal amino acid flow and disappearance in steers.

Six Angus steers (260+/-4 kg initial BW) fitted with ruminal, duodenal, and ileal cannulas were used in a 6 x 6 Latin square design to evaluate the effect of feeding poultry by-product meal (PBM) on small intestinal flow and disappearance of amino acids. The diets were provided at 2% of BW on a DM basis, formulated to contain 11.5% CP, and consisted of 49% corn silage, 36% cottonseed hulls, and 15% supplement on a DM basis. Supplements were formulated to contain 37% CP with sources of supplemental N being soybean meal (100% SBM) and 0, 25, 50, 75, and 100% PBM, with urea used to balance for N. Duodenal flow of all amino acids increased linearly (P < .07) as PBM increased in the diet and, except for His, increased (P < .09) for 100% PBM compared with 100% SBM. Similar results were observed for duodenal flow of nonbacterial amino acids, which linearly increased (P < .05) with PBM and were greater (P < .05) for 100% PBM than for 100% SBM. Soybean meal increased (P < .09) the duodenal flow of nonbacterial Lys compared with 0% PBM, and 0% PBM increased (P < .04) flow of Val, Ala, and Pro compared with 100% SBM. Duodenal bacterial essential, nonessential, and total amino acid flows were not affected (P > .80) by PBM; however, they were greater (P < .02) for 100% SBM than for 100% PBM. In addition, nonessential and total bacterial amino acid flows were increased (P < .06) for 100% SBM compared with 0% PBM. Small intestinal disappearance of Lys and Pro increased linearly (P < .09) as PBM increased, and 100% PBM increased (P < .07) disappearance of Arg and Ala compared with 100% SBM. Supplemental N source had no effect (P > .31) on apparent small intestinal disappearance of essential, nonessential, and total amino acids. These data suggest that when PBM, SBM, and urea were used as sources of supplemental N, the daily disappearance of amino acids from the small intestine of steer calves consuming a corn silage- and cottonseed hull-based diet was similar.

Nutritional evaluation of poultry by-product meal as a protein source for ruminants: effects on performance and nutrient flow and disappearance in steers.

We conducted three studies with steers to evaluate poultry by-product meal (PBM) as a supplemental N source for ruminants. An in situ study compared the solubility, degradation rate, and ruminal escape of PBM N with blood meal (BM), corn gluten meal (CGM), and soybean meal (SBM) N. Additionally, an 84-d growth study (n = 95, 228+/-5 kg BW) and a digestion trial (6 x 6 Latin square) were conducted. The basal diet for the growth and digestion studies consisted of 49% corn silage, 36% cottonseed hulls, and 15% supplement (DM basis). Sources of supplemental N (% of total supplemental N) were 100% SBM and 0, 25, 50, 75, and 100% PBM, with urea used to balance for N. In situ ruminal escape N (25.2, 55.3, 86.7, and 98.9% for SBM, PBM, CGM, and BM, respectively) was greater (P < .05) for PBM than for SBM; however, a greater (P < .05) proportion of BM and CGM N escaped ruminal degradation compared with PBM. Dry matter intake, ADG and gain/ feed increased linearly (P < .003) as PBM increased; however, no differences (P > .48) were observed in these variables for 100% PBM compared with 100% SBM. Duodenal N flow and small intestinal N disappearance increased linearly (P < .05) as PBM increased in the diet. Bacterial N flow to the small intestine was not affected (P > .19) by treatment; however, 100% SBM decreased (P < .04) bacterial CP synthesis (g bacterial N/kg OM disappearance from the stomach) compared with 0 and 100% PBM. In vivo ruminal escape N of PBM and SBM was 40.6 and 13.7%, respectively. Ruminal NH3 N decreased linearly (P < .001) as PBM increased. These data suggest that PBM can replace SBM as a source of supplemental N for steer calves that consume a diet based on corn silage and cottonseed hulls.