Relationship of whole body nitrogen utilization to urea kinetics in growing steers.

Urea kinetics were measured in 2 experiments, with treatments designed to change protein deposition by the animal. Our hypothesis was that increased protein deposition by cattle (Bos taurus) would reduce urea production and recycling to the gastrointestinal tract. Urea kinetics were measured by continuous intravenous infusion of (15)N(15)N-urea followed by measurement of enrichment in urinary urea at plateau. In Exp. 1, 6 steers (139 kg) were maintained in a model in which leucine was the most limiting AA. Treatments were arranged as a 2 × 3 factorial and were provided to steers in a 6 × 6 Latin square design. Leucine treatments included 0 or 4 g/d of abomasally supplemented L-leucine, and energy treatments included control, abomasal glucose infusion (382 g DM/d), or ruminal VFA infusion (150 g/d of acetic acid, 150 g/d of propionic acid, and 50 g/d of butyric acid). Leucine supplementation increased (P < 0.01) N retention, and energy supplementation tended to increase (P = 0.09) N retention without differences between glucose and VFA supplements (P = 0.86). Energy supplementation did not strikingly improve the efficiency of leucine utilization. Although both leucine and energy supplementation reduced urinary urea excretion (P ≤ 0.02), treatments did not affect urea production (P ≥ 0.34) or urea recycling to the gut (P ≥ 0.30). The magnitude of change in protein deposition may have been too small to significantly affect urea kinetics. In Exp. 2, 6 steers (168 kg) were maintained in a model wherein methionine was the most limiting AA. Steers were placed in 2 concurrent 3 × 3 Latin squares. Steers in one square were implanted with 24 mg of estradiol and 120 mg trenbolone acetate, and steers in the other square were not implanted. Treatments in each square were 0, 3, or 10 g/d of L-methionine. Implantation numerically improved N retention (P = 0.13) and reduced urea production rate (P = 0.03), urinary urea excretion (P < 0.01), and urea recycling to the gastrointestinal tract (P = 0.14). Effects of methionine were similar to implantation, but smaller in magnitude. When protein deposition by the body is increased markedly, ruminally available N in the diet may need to be increased to offset reductions in urea recycling.

Effects of ruminal casein and glucose on forage digestion and urea kinetics in beef cattle.

Effects of supplemental glucose and degradable intake protein on nutrient digestion and urea kinetics in steers (Bos taurus) given ad libitum access to prairie hay (4.7% CP) were quantified. Six ruminally and duodenally cannulated steers (initial BW 391 kg) were used in a 4 × 4 Latin square with 2 extra steers. Treatments were arranged as a 2 × 2 factorial and included 0 or 1.2 kg of glucose and 240 or 480 g of casein dosed ruminally once daily. Each period included 9 d for adaptation, 4 d for total fecal and urine collections, and 1 d for ruminal and duodenal sampling. Jugular infusion of (15)N(15)N-urea with measurement of enrichment in urine was used to measure urea kinetics. Glucose reduced forage intake by 18% (P < 0.01), but casein did not affect forage intake (P = 0.69). Glucose depressed (P < 0.01) total tract NDF digestion. Glucose supplementation decreased ruminal pH 2 h after dosing, but the effect was negligible by 6 h (treatment × time; P = 0.01). Providing additional casein increased the ruminal concentration of NH(3), but the increase was less when glucose was supplemented (casein × glucose; P < 0.01). Plasma urea-N was increased (P < 0.01) by additional casein but was reduced (P < 0.01) by glucose. Microbial N flow to the duodenum and retained N increased (P ≤ 0.01) as casein increased, but neither was affected by glucose supplementation. Urea-N entry rate increased (P = 0.03) 50% with increasing casein. Urinary urea-N excretion increased (P < 0.01) as casein increased. The proportion of urea production that was recycled to the gut decreased (P < 0.01) as casein increased. Glucose supplementation decreased (P < 0.01) urinary urea excretion but did not change (P ≥ 0.70) urea production or recycling. The amount of urea-N transferred to the gut and captured by ruminal microbes was less for steers receiving 480 g/d casein with no glucose than for the other 3 treatments (casein × glucose interaction, P = 0.05), which can be attributed to an excess of ruminally available N provided directly to the microbes from the supplement. Overall, the provision of supplemental glucose decreased forage intake and digestibility. Increasing supplemental casein from 240 to 480 g/d increased urea production but decreased the proportion of urea-N recycled to the gut.

Effects of supplemental energy and protein on forage digestion and urea kinetics in growing beef cattle.

Effects of supplemental energy sources on nutrient digestion and urea kinetics at 2 levels of degradable intake protein were evaluated in cattle (Bos taurus). Six ruminally and duodenally cannulated steers (208 ± 17 kg) were used in a 6 × 6 Latin square with treatments arranged as a 3 × 2 factorial. Energy treatments included a control, 600 g glucose dosed ruminally once daily, and 480 g VFA infused ruminally over 8 h daily. Casein (120 or 240 g) was dosed ruminally once daily. Steers had ad libitum access to prairie hay (5.8% CP). Jugular infusion of (15)N(15)N-urea with measurement of enrichment in urine was used to measure urea kinetics. Infusing VFA decreased (P < 0.01) forage intake by 27%. Supplementing glucose decreased (P < 0.01) total tract NDF digestibility and tended to decrease ruminal NDF digestibility; depressions in response to glucose tended to be greater at the lower level of casein. Increasing casein decreased (P < 0.02) ruminal pH. Infusing VFA decreased pH only during infusions, whereas glucose decreased pH 2 h after dosing. Ruminal concentrations of NH(3), acetate, and propionate decreased and butyrate concentration increased when glucose was supplemented. Increasing casein supplementation increased (P < 0.01) ruminal concentrations of NH(3), acetate, and propionate. Supplemental energy decreased (P = 0.03) plasma urea-N concentration, but casein level did not affect it (P = 0.16). Microbial N flow was greater (P < 0.04) for 240 than for 120 g/d casein but was not affected by supplemental energy (P = 0.23). Urea-N entry rate and gut entry of urea-N were not affected (P ≥ 0.12) by supplemental energy or casein, but the proportion of urea production that was recycled to the gut was less (P = 0.01) when 240 g/d rather than 120 g/d casein was provided. Compared with VFA, glucose tended (P = 0.07) to increase the proportion of urea-N entry rate that was recycled to the gut. Supplementation with glucose led to more (P = 0.01) microbial uptake of recycled urea than did supplementation with VFA. Urea recycling did not differ greatly among treatments despite impacts on ruminal pH and NH(3) and on plasma urea-N that were expected to alter urea transport across ruminal epithelium. Lack of treatment effects on urea production indicate that the complete diets did not provide excessive amounts of N and that increases of intestinally available AA were used efficiently by cattle for protein deposition.

Effect of nitrogen supplementation and zilpaterol-HCl on urea kinetics in steers consuming corn-based diets.

We studied effects of zilpaterol-HCl on steers consuming corn-based diets with nitrogen (N) supplementation provided by dried distillers grains with solubles (DDGS) or urea. Two sets of six steers (approximately 350 kg) were used in two replicates of similarly designed trials. Within each replicate, three steers were fed 60 mg/day of zilpaterol-HCl throughout the trial and three steers received no zilpaterol-HCl. Within zilpaterol treatment, three corn-based dietary N treatments were offered in Latin square designs: control (9.6% crude protein), urea (UREA; 12.4% crude protein) or DDGS (13.7% crude protein). Total feed intake was unexpectedly greater (p < 0.01) with zilpaterol feeding but was not affected by dietary N (p = 0.76). Nitrogen intake was greater (p < 0.01) when zilpaterol was fed and was greater (p < 0.05) for DDGS and UREA than for control. Despite greater N intake, zilpaterol did not affect urea entry rate (p = 0.80) or urea-N recycled to the gastrointestinal tract (GER; p = 0.94). As a percentage of N intake, urea entry rate (p = 0.19) tended to be less when zilpaterol was fed (91 vs. 123% of N intake), and GER was numerically (p = 0.34) less (72 vs. 92% of N intake). Microbial N flow was greater (p = 0.02) for zilpaterol than for control but did not differ (p = 0.78) among dietary N treatments. As a percentage of N intake, microbial N flow was unaffected by zilpaterol (p = 0.97), but was greater (p < 0.05) for control than DDGS or UREA. The lack of change in urea entry and GER in response to zilpaterol, despite greater N intake, as well as lower urea entry and GER when expressed as proportions of N intake provide some evidence that the amount of N available for urea production and recycling was reduced by zilpaterol.

Effect of nitrogen supplementation on urea kinetics and microbial use of recycled urea in steers consuming corn-based diets.

We studied the effects of supplementing N as distillers dried grains with solubles (DDGS) or urea to steers consuming corn-based diets. Six ruminally and duodenally cannulated steers (244 kg) were used in 2 concurrent 3 x 3 Latin squares and fed 1 of 3 corn-based diets: control (10.2% CP), urea (13.3% CP), or DDGS (14.9% CP). Periods were 14 d, with 9 d for adaptation and 5 d for collection of urine and feces. Urinary (15)N(15)N-urea enrichments, resulting from venous infusions of (15)N(15)N-urea, were used to measure urea kinetics. Dry matter intake (6.0 kg/d) was not affected by treatment, but N intake differed (99, 151, and 123 g/d for the control, DDGS, and urea treatments, respectively). Urea-N synthesis tended to be greater (P = 0.09) for DDGS (118 g/d) than for the control treatment (52 g/d), with the urea treatment (86 g/d) being intermediate. Urea-N excreted in the urine was greater (P < 0.03) for the DDGS (35 g/d) and urea treatments (29 g/d) than for the control treatment (13 g/d). Gastrointestinal entry of urea-N was not statistically different among treatments (P = 0.25), but was numerically greatest for DDGS (83 g/d), intermediate for urea (57 g/d), and least for the control (39 g/d). The amount of urea-N returned to the ornithine cycle tended to be greater (P = 0.09) for the DDGS treatment (47 g/d) than for the urea (27 g/d) or control treatment (16 g/d). The fraction of recycled urea-N that was apparently used for anabolism tended (P = 0.14) to be greater for the control treatment (0.56) than for the DDGS treatment (0.31), with the urea treatment (0.45) being intermediate, but no differences were observed among treatments in the amount of urea-N used for anabolism (P = 0.66). Urea kinetics in cattle fed grain-based diets were largely related to the amount of N consumed. The percentage of urea production that was captured by ruminal bacteria was greater (P < 0.03) for the control treatment (42%) than for the DDGS (25%) or urea treatment (22%), but the percentage of duodenal microbial N flow that was derived from recycled urea-N tended (P = 0.10) to be greater for the DDGS treatment (35%) than for the urea (22%) or control treatment (17%). Thus, ruminal microbes were more dependent on N recycling when the protein supplement was largely resistant to ruminal degradation.

The cost and value of pre-registration clinical placements for Project 2000 students.

The research outlined in this article was commissioned by the Sheffield and North Trent College of Nursing and Midwifery to explore the cost implications of pre-registration clinical placements in the context of Project 2000. The authors outline the methodology and findings of an exercise designed to collect relevant cost information which was not readily available. On the basis of these findings, they suggest that: at 1995/1996 pay and prices, clinical placements cost the education provider approximately pound 890 per student per annum; in terms of real resources, the value to service providers of the service contribution made by second- and third-year nursing and midwifery students on ward-based placements outweighs the value of the time spent by qualified staff on their supervision and education. Once the funding assumptions underlying the introduction of Project 2000 have been taken into account, second- and third-year nursing and midwifery students benefit the service provider by on average pound 3.46 for every hour they spend in an unrostered ward-based placement. The service contribution made by students in community-based clinical placements cannot free staff time in the same way as on the wards and, because qualified staff in these areas are generally more highly graded, the value of the time they spend on the supervision and education of students on placement is higher than in ward-based placements. Second- and third-year students therefore appear to cost the service provider on average pound 0.48 for each hour they spend in a community-based placement. It was not possible to determine whether this cost translates into a reduction in patient contacts.

Protection of calves against cryptosporidiosis with immune bovine colostrum induced by a Cryptosporidium parvum recombinant protein.

The purpose of the study was to determine if immunization with a recombinant protein (rC7) of Cryptosporidium parvum would induce immune bovine colostrum that protected calves against cryptosporidiosis following oral challenge with C. parvum oocysts. Late gestation Holstein cows with low titers of antibody to the p23 antigen of C. parvum were immunized three times with 300 microg affinity purified rC7 C. parvum recombinant protein (immune cows), or left nonimmunized (control cows). Colostrum was obtained from each cow in both groups and partitioned into identical aliquots of pooled immune colostrum or pooled control colostrum. Twelve calves obtained at birth received either immune or control colostrum within the first 2 h, and again at 12 and 24 h of age. Each calf was challenged orally with 10(7) C. parvum oocysts at 12 h of age and monitored for signs of cryptosporidiosis. All six calves administered pooled control colostrum developed severe diarrhea (mean total fecal volume = 8447+/-5600 ml) and shed an average of 1.87+/-1.66 x 10(12) C. parvum oocysts. None of the six calves administered pooled immune colostrum developed diarrhea (mean total fecal volume = 740+/-750 ml, p < 0.05), and shed significantly fewer oocysts (3.05+/-2.26 x 10(9), p < 0.05). The absence of diarrhea and 2.79 log10 (99.8%) reduction in oocyst excretion indicates that immune bovine colostrum induced by immunization with C. parvum recombinant protein rC7 provided substantial protection against cryptosporidiosis in neonatal calves.

Disparate effects of nitric oxide on lung ischemia-reperfusion injury.

BACKGROUND: Inhaled nitric oxide (.NO) has been found to be a potent pulmonary vasodilator. We assessed whether .NO, through this function or others, could alleviate lung reperfusion injury. METHODS: Rats underwent thoracotomy, with clamps used to create left lung ischemia. After 90 minutes of ischemia, clamps were released, permitting reperfusion for either 30 minutes or 4 hours. Additional animals received inhaled .NO via the ventilator to determine its effects on reperfusion injury. RESULTS: Lung injury, measured by increased vascular permeability using iodine-125-labeled bovine serum albumin leakage, was significantly increased in ischemic-reperfused animals compared with time-matched shams not undergoing ischemia. Inhaled .NO delivered at the start of reperfusion worsened injury at 30 minutes but was protective at 4 hours. The increased injury could be avoided either by delaying .NO for 10 minutes or by treating the animals with superoxide dismutase before reperfusion. .NO reversed postischemic pulmonary hypoperfusion at 4 hours, as measured by labeled microspheres. Lung neutrophil content was significantly reduced at 4 hours in .NO-treated animals. CONCLUSIONS: .NO is toxic early in reperfusion, due to its interaction with superoxide, but is protective at 4 hours of reperfusion, due to reversal of postischemic lung hypoperfusion and reduction of lung neutrophil sequestration.