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

Abstract

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.