Taylor-Edwards C C, Elam N A, Kitts S E, McLeod K R, Axe D E, Vanzant E S, Kristensen N B, Harmon D L
Department of Animal and Food Sciences, University of Kentucky, Lexington 40546-0215, USA.
J Anim Sci. 2009 Jan;87(1):209-21. doi: 10.2527/jas.2008-0913. Epub 2008 Sep 26.
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.
进行了两项试验，以评估缓释尿素（SRU）与饲料级尿素对育肥牛门静脉引流内脏（PDV）养分通量、养分消化率和总氮平衡的影响。使用多导管牛来确定瘤胃内给药（试验1；n = 4；体重319±5 kg）或饲喂（试验2；n = 10；4头荷斯坦牛，体重236±43 kg，6头安格斯牛，体重367±46 kg）SRU或尿素对给药后10 h内PDV养分通量和血液变量的影响。试验1中瘤胃内给予SRU可防止尿素给药时瘤胃氨浓度的快速升高（处理×时间P = 0.001）。尽管干物质、有机物、中性洗涤纤维和酸性洗涤纤维的表观全肠道消化率不受处理影响（P>0.53，试验2），但SRU增加了粪便氮排泄（49.6对45.6 g/d；P = 0.04）并降低了表观全肠道氮消化率（61.7对66.0%；P = 0.003）。试验1和2中，两种处理在所有时间点均发生了尿素从血液向胃肠道的转移，但试验1中尿素给药后0.5 h除外，此时尿素实际上是从胃肠道转移到血液中。试验1和2中，尿素和SRU处理均使采食后0.5至6 h动脉血尿素浓度升高，但SRU处理的动脉血尿素浓度始终较低（处理×时间P<0.001，试验1；P = 0.007，试验2）。SRU处理时，整个采样期门静脉净氨释放相对稳定，而尿素处理在试验1中增加了门静脉氨释放，试验2中也有类似趋势（处理×时间P分别为0.003和0.11）。尿素处理还使0.5 h内肝脏氨摄取增加（处理×时间P = 0.02，试验1）；然而，尿素处理给药后2 h内氨的总内脏释放增加，表明PDV氨通量可能超过了肝脏的清除能力。缓释尿素降低了氨氮释放的速度，并可能减少与氨处理相关的氮代谢变化。然而，SRU增加了粪便氮排泄，并增加了尿素向胃肠道的转移，这可能是由于SRU水解减少或对消化模式的影响。尽管如此，SRU防止尿素饲喂负面影响的能力在某些饲喂应用中可能是有效的。
