A novel temporary prostatic stent for the relief of prostatic urethral obstruction.

OBJECTIVES: To determine the effect of a novel temporary prostatic stent (The Spanner, AbbeyMoor Medical, Inc., Minnesota, USA) on variables of voiding function and quality of life among patients with prostatic urethral obstruction. PATIENTS AND METHODS: The stent design is very similar to the proximal 4-6 cm of a Foley catheter; this includes a proximal balloon to prevent distal displacement, a urine port situated cephalad to the balloon, and a reinforced stent of various lengths to span most of the prostatic urethra. There is also a distal anchor mechanism attached by sutures, and a retrieval suture which extends to the meatus and deflates the proximal balloon when pulled. The stent was inserted under topical anaesthesia in 30 patients. The maximum flow rate (Qmax), voided volume (W), postvoid residual (PVR), the International Prostate Symptom Score (IPSS) and stent position were assessed. RESULTS: Stents remained in situ for a mean (range) of 57 (1-98) days. The mean overall Qmax at baseline and after insertion were 8.2 and 11.6 mL/s, representing a 42% improvement (P < 0.001); the respective mean overall Ws were similar, at 219.7 and 221.6 mL (0.9% increase, not significant) and the PVRs were 312.1 and 112.3 mL, representing a 64% decrease (P = 0.004). The overall mean IPSS declined from 22.3 before to 7.1 after insertion, representing a 68% decrease (P < 0.001). There were only minor adverse events. The stability, patency and lack of migration of the device were confirmed radiographically up to 12 weeks of use. CONCLUSIONS: This early study shows that this temporary prostatic stent is easily inserted and removed, remains anchored in position, and significantly improves the Qmax, PVR and IPSS while preserving volitional voiding and continence.

Efficacy of laidlomycin propionate in low-protein diets fed to growing beef steers: effects on steer performance and ruminal nitrogen metabolism.

We conducted two experiments to evaluate the effect of the ionophore laidlomycin propionate (LP) on steer performance and ruminal N metabolism. Experiment 1 was a 91-d growth study evaluating the growth and ruminal characteristics of steer calves consuming supplemental LP. Steers (n = 96; 255 +/- 3 kg; four steers/pen; six pens/treatment) were used in a randomized complete block design with a 2 x 2 factorial arrangement of treatments consisting of two levels of dietary CP (formulated to be 10.5 and 12.5% of DM) with and without LP (11 mg/kg diet DM). Ruminal fluid was collected via stomach tube on d 91 from one steer randomly selected from each pen. No CP x LP interactions were observed with performance data (P > .64). Final weight and total gain were greater (P < .07) for 12.5% CP and LP compared with 10.5% CP and control steers, respectively. Also, DMI was increased (P = .08) with 12.5% CP but not with LP supplementation (P = .36). In addition, ADG and gain:feed ratio were greater (P < .03) for both 12.5% CP and supplemental LP. Ruminal NH3 N concentration was greater (P < .09) with 12.5% CP and LP. Total VFA concentration and molar proportion of acetate were not affected by treatment (P > .11). However, propionate concentration was increased (P < .09) with 12.5% CP and LP, and acetate:propionate was lower (P = .02) with LP supplementation. In Exp. 2, six steers were used in a replicated 3 x 3 Latin square design to compare ruminal fermentation and protein degradation in steers without ionophore feeding or adapted to LP or monensin. In vitro deamination of amino acids by adapted ruminal microbes was also assessed. Ionophore supplementation decreased (P = .07) ruminal NH3 N concentration compared with control steers, and LP increased (P = .02) ruminal NH3 N compared with monensin. Molar proportion of acetate was decreased (P = .02) and propionate increased (P = .01) with ionophore treatment. Consequently, ionophore supplementation depressed the acetate:propionate ratio (P = .01). In situ degradation rate of soybean meal (SBM) CP was greater (P = .09) with ionophore treatment, but estimates of SBM undegradable intake protein were not altered by treatment (P > .25). Microbial specific activity of net NH3 N release and alpha-amino N degradation were decreased (P < .04) with ionophores. Based on this study, LP and monensin did not affect the extent of ruminal degradation of SBM CP but decreased amino acid deamination.

Influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide on ruminant nitrogen metabolism: I. In vitro urea kinetics and substrate digestion.

Two in vitro digestion experiments were conducted to evaluate the influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide (NBPT) on in vitro urea kinetics, substrate digestion, and fermentation characteristics. In Exp. 1, in vitro incubations were conducted in 50-mL test tubes containing .25 g of ground fescue hay to which 0, 6.5, 13, 26, or 52 mg of NBPT in a buffered ruminal fluid innoculum was added. Tubes were incubated in triplicate at 39 degrees C and replicated on consecutive days, with NH3 N and urea concentrations measured at 0, 10, 30, 60, 120, 240, and 360 min. Samples for VFA analysis were collected at 6 h, and incubations were continued through 48 h to estimate true digestibility (based on NDF analysis). Increasing the dose of NBPT tended (P < .12) to linearly depress the rate of urea hydrolysis and decreased (P < .0004) subsequent NH3 N formation. Although total VFA concentration at 6 h increased linearly (P < .03), acetate:propionate and estimated true digestibility decreased (P < .01) with increasing NBPT concentration. In Exp. 2, we compared in vitro urea kinetics and digestion of forage-only or mixed forage-grain substrates in response to addition of NBPT. In vitro incubations were conducted in 50-mL test tubes containing either .5 g of ground fescue hay or .5 g of a ground fescue hay and ground corn mixture (50:50, DM basis) to which 0, 6.5, 13, 26, or 52 mg of NBPT in a buffered ruminal fluid innoculum was added. Tubes were incubated in triplicate at 39 degrees C and replicated on consecutive days, with NH3 N and urea concentrations measured at 0, .5, 1, 2, 4, 8, 12, 24, and 48 h. At 48 h, samples for VFA analysis were collected and true digestibility (based on NDF analysis) was estimated. No (P > .10) NBPT dose x substrate interactions were detected. Increasing the dose of NBPT depressed (P < .003) the rate of urea hydrolysis and subsequent NH3 N formation, regardless of substrate. Although total VFA concentration was unaffected (P > .10), the acetate:propionate and estimated true digestibility decreased (P < .002) with higher NBPT addition. In both experiments, the rate of urea degradation was not different (P > .20) from zero for the 26 and 52 mg NBPT treatments, indicating that nearly complete inhibition of urease had been achieved. We conclude that NBPT can be used to reduce the rate of NH3 N release from dietary urea and, thereby, offers the potential to improve nonprotein nitrogen utilization in ruminants.

Influence of the novel urease inhibitor N-(n-butyl) thiophosphoric triamide on ruminant nitrogen metabolism: II. Ruminal nitrogen metabolism, diet digestibility, and nitrogen balance in lambs.

Three lamb metabolism experiments were conducted to investigate the effects of chronic administration of the novel urease inhibitor N (n-butyl) thiophosphoric triamide (NBPT) on ruminal N metabolism, fermentation, and N balance. In Exp. 1, ruminally cannulated wethers (n = 28; 45.0 +/- .9 kg) were administered one of seven doses of NBPT (0 [control], .125, .25, .5, 1, 2, or 4 g of NBPT daily) and fed a common cracked corn/cottonseed hull-based diet twice daily containing 2% urea at 2.5% of initial BW for the duration of the 15-d experiment. Overall, NBPT decreased (linear P < .0001; quadratic P < .001) ruminal urease activity, resulting in linear increases (P < .0001) in ruminal urea and decreases in ruminal NH3 N concentrations. However, the detection of an NBPT x day interaction (d 2 vs 15; P < .01) indicated that this depression in urea degradation diminished as the experiment progressed. Increasing NBPT linearly decreased (P < .01) total VFA concentrations on d 2 of the experiment, but it had no effect (P > .10) on d 15. Increasing NBPT had no effect (P > .10) on DM or ADF digestibilities, but it linearly decreased (P < .01) N digestibility. Supplementing NBPT produced a linear increase (P < .05) in urinary N excretion and a linear decrease (P < .01) in N retention. In Exp. 2, ruminally cannulated wethers (n = 30; 46.8 +/- .6 kg) were fed one of two basal diets (2.0 vs 1.1% dietary urea) at 2.5% of initial BW and dosed with either 0 (control), .25, or 2 g of NBPT daily for the duration of the 15-d experiment. There were no NBPT x dietary urea interactions (P > .10) for Exp. 2. Increasing NBPT depressed (linear and quadratic P < .0001) ruminal urease activity, producing linear (P < .0001) increases in urea N and linear decreases in NH3 N in the rumen. As in Exp. 1, an NBPT x day interaction (P < .05) was noted for urea, NH3 N, and total VFA concentrations; the maximum response to NBPT occurred on d 2 but diminished by d 15 of the experiment. Administration of NBPT did not influence (P > .10) DM, ADF, or N digestibilities in Exp. 2. In Exp. 3, wether lambs (n = 30; 26.4 +/- .7 kg) were subjected to the same treatment regimen as in Exp. 2 for a 14-d N balance experiment. Although several NBPT x dietary urea interactions (P < .05) were noted, increasing NBPT did not affect (P > .10) N digestibility. Administration of NBPT quadratically increased (P < .10) urinary N excretion, producing a linear decrease (P < .05) in N retention. These results suggest that although NBPT is capable of inhibiting ruminal urease short-term, the ruminal microflora may be capable of adapting to chronic NBPT administration, thereby limiting its practical use in improving the utilization of dietary urea.

Net nutrient flux in visceral tissues of lambs fed diets differing in supplemental nitrogen source.

Eight multicatheterized wethers (35.9 +/- .8 kg BW) were used in a replicated 4 x 4 Latin square design to measure N retention and net uptake and release of plasma metabolites across the portal-drained viscera (PDV), hepatic (HEP), and total splanchnic (TS) tissues in response to changes in supplemental N source. Treatments selected to provide different amounts of undegradable intake protein (UIP) were urea, soybean meal (SBM), poultry by-product meal (PBM), and bloodmeal:corn gluten meal (BMCGM; 50:50 CP basis). Diets (urea, SBM, PBM, and BMCGM) contained 12.9, 13.8, 13.6, and 13.2% CP, respectively. Periods were 10 d, with total feces and urine collected on d 7 to 10 and blood sampled on d 10. Wethers were fed at 2% of BW in 12 daily portions. Nitrogen retention was 2.2, 3.3, 4.1, and 4.4 g/d for urea, SBM, PBM, and BMCGM, respectively. Urea had less (P < .01) N retention than SBM, PBM, and BMCGM; SBM had less N retention (P < .01) than PBM and BMCGM. Arterial, portal, and hepatic plasma flows were greater (P < .09) for SBM than for PBM and BMCGM (21 vs 16, 17; 84 vs 72, 72; 105 vs 87, 88 L/h). Portal plasma flow was greater (P < .10) for urea than for SBM, PBM, and BMCGM (85 vs 84, 72, 72 L/h). Portal-drained viscera and TS alpha-amino N (AAN) fluxes were less (P < .05) for PBM than for BMCGM (20.5 vs 26.6 and 7.2 vs 15.1 mmol/h), but TS AAN flux was less (P < .05) for urea than for SBM, PBM, and BMCGM (6.9 vs 16.9, 7.2, 15.1 mmol/h). Portal-drained viscera flux and HEP removal of NH3 N were greater (P < .001) for SBM than for PBM and BMCGM (27.7 vs 19.4, 20.6; -28.1 vs -20.0, -21.4 mmol/h). Gut use was less (P = .07) and HEP and TS fluxes of urea N were greater (P < .01) for SBM than for PBM and BMCGM (-4.92 vs -8.32, -7.93; 25.87 vs 16.54, 20.00; 20.95 vs 8.22, 12.07 mmol/h). These data suggest that PBM and BMCGM improved efficiency of N use compared with urea and SBM by reducing urinary N loss.

Ergocryptine and other ergot alkaloids stimulate the release of [3H]dopamine from rat striatal synaptosomes.

Ergocryptine is an ergot alkaloid that affects dopaminergic activity principally by interacting with D2-type receptors. In this study the ability of ergocryptine and several other ergot alkaloids to release [3H]dopamine from isolated nerve endings was demonstrated using in vitro superfusion of rat striatal synaptosomes. Ergocryptine, ergocristine, and bromocryptine produced an elevation in baseline dopamine release of approximately 400% with effective concentrations (EC50) of approximately 30 microM. Ergotamine, ergonovine, ergovaline, and ergocornine were devoid of activity. The time-course of the ergocryptine-stimulated release was relatively slow compared with amphetamine, nicotine, or K+-stimulated [3H]dopamine release; the maximal increase in release required a 5-min treatment. A number of receptor antagonists were examined for their ability to block ergocryptine-stimulated release. Of the dopaminergic, adrenergic, serotonergic, GABA-ergic, and cholinergic antagonists examined, only phentolamine produced a moderate attenuation in evoked release. Omission of Ca++ from the medium did not affect ergocryptine-evoked release. Following ergocryptine treatment, the synaptosomes were fully responsive to other stimulant. The results indicate that, in addition to interacting with dopamine receptors, several ergot alkaloids may produce dopaminergic effects by increasing the release of dopamine from central nerve endings. Several mechanisms to account for the evoked neurotransmitter release are discussed.

Estimating true digestibility of nonstructural carbohydrates in the small intestine of steers.

Four Angus steers (318 +/- 16 kg) fitted with ruminal, duodenal, and ileal cannulas were used in a 4 x 4 Latin square design to determine carbohydrate disappearance from the small intestine (SI). Steers were fed fescue hay at 1.8% of BW and abomasally infused with starch hydrolysate (SH) at 10, 20, or 40 g/h or glucose (G) at 30 g/h. Starch hydrolysate was raw cornstarch digested by a heat-stable alpha-amylase. Experimental periods were 10 d with 6 d of adaptation, 3 d of digesta and feces collection, and 1 d of rest. Glucose (% of infused) had greater (P < .001) apparent small intestinal and postruminal disappearance (% of infused) compared with 20 and 40 g/h SH. Starch hydrolysate infusion linearly increased (P < .001) apparent SI, large intestinal (LI), and total intestinal starch disappearance (g/d) and quadratically increased (P < .003) apparent SI and total intestinal starch disappearance (% of infused). Ileal starch flow from infusion increased quadratically (P < .03) as SH infusion increased. True SI and total intestinal starch disappearance increased linearly (P < .001; g/d) with SH infusion. However, SH infusion quadratically decreased (P < .02) efficiency of true SI starch disappearance (% of infused). True LI starch disappearance (g/d and % of infused) quadratically increased (P < .03) as SH infusion increased. These data demonstrate that, even in animals fed all-forage diets, there is a significant flow of alpha-glucosides, and these need to be considered when evaluating intestinal carbohydrate digestion.

Alkaloid binding and activation of D2 dopamine receptors in cell culture.

Ergot and pyrrolizidine alkaloids, either extracted from endophyte-infected tall fescue, synthesized, or purchased commercially, were evaluated in cultured cells to estimate their binding to the D2 dopamine receptor and subsequent effects on cyclic AMP production in GH4ZR7 cells, transfected with a rat D2 dopamine receptor. Ergopeptide alkaloid (alpha-ergocryptine, bromocryptine, ergotamine tartrate, and ergovaline) inhibition of the binding of the D2-specific radioligand, [3H]YM-09151-2, exhibited inhibition constants (K(I)) in the nanomolar range, whereas dopamine was less potent (micromolar). The lysergic acid amides (ergine and ergonovine) were 1/100th as potent as the ergopeptide alkaloids. Ergovaline and ergotamine tartrate were equally effective in inhibiting vasoactive intestinal peptide (VIP)-stimulated cyclic AMP production, with consistent nanomolar effective concentration (EC50) values. The remaining ergopeptide alkaloids (alpha-ergocryptine and bromocryptine), lysergic acid amides (ergonovine and ergine), and dopamine were 1/100th as potent. Two representative pyrrolizidines, N-formylloline and N-acetylloline, exhibited no binding activity at the D2 dopamine receptor or effects on the cyclic AMP system within the concentration ranges of nanomolar to millimolar. Our results indicate that the commercially available ergot alkaloids ergotamine tartrate and ergonovine may be used interchangeably in the D2 dopamine receptor system to simulate the effects of extracted ergovaline and ergine and to examine responses in receptor binding and the inhibition of cyclic AMP.

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.

Injection of a dopamine antagonist into Holstein steers to relieve symptoms of fescue toxicosis.

Two experiments were conducted to determine whether administering a dopamine antagonist to steers fed endophyte-infected (E+) tall fescue would increase serum prolactin (PRL) and reduce rectal temperature. Steers in both experiments were housed in environmentally controlled chambers (32 degrees C; 50% relative humidity). In Exp. 1, 10 steers were allotted randomly to receive s.c. injections of either 0, .006, .03, or .06 mg of Ro 24-0409 (dopamine antagonist)/kg BW. The experiment was designed in four phases: endophyte-free seed (E-) without antagonist (d -11 to 0); E- with antagonist (d 0 to 7); E+ with antagonist (d 7 to 28); E+ without antagonist (d 28 to 38). In Exp. 2, 22 Holstein steers were allotted randomly to the same treatments and design, except three steers were maintained on E- without antagonist. Steers were fed individually with intakes measured daily. In Exp. 1, feed intake and rectal temperature were not improved (P > .05) by antagonist injection. In Exp. 2, antagonist injections increased (P < .05) PRL. Ingestion of E+ decreased (P < .05) feed intake and serum PRL. Antagonist injection decreased (P < .05) rectal temperature and increased (P < .05) serum PRL.

Effects of endophyte-infected tall fescue, environmental temperature and prazosin injection on the rat.

Effects of an alpha 1 antagonist, prazosin, injection on the rat (Rattus rattus) exposed to warm vs normal environments and fed endophyte-infected (E+) or -free (E-) tall fescue seed were studied. Rats were injected IP daily with placebo or prazosin (1 mg/kg BW). Daily skin and rectal temperatures and food intake measurements were recorded. Selected brain tissues were dissected to determine treatment effects on monoamine receptor density. Rats fed E+ and injected with placebo had reduced (P < 0.01) food intake compared with all other treatments. By day 5 of injection, an endophyte x temperature interaction for increased (P < 0.03) skin and rectal temperatures was measured when rats were fed E+ and housed at 32 degrees C. Also by day 5, injection of rats consuming E+ with prazosin reduced (P < 0.01) skin and rectal temperatures 0.4 degree C compared with those consuming E+ and injected with placebo. Monoamine receptor (alpha 1, alpha 2, and D2) densities were similar (P > 0.10) among treatments. Prazosin injection reduced E+ induced body temperature increases chronically and increased food intake acutely to E- levels. Monoamine receptor densities were unchanged; therefore, E+ effects via monoamine receptors may be due to acute modulation of receptor-associated activity.

Ergovaline binding and activation of D2 dopamine receptors in GH4ZR7 cells.

Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and ergot alkaloid inhibition of vasoactive intestinal peptide (VIP)-stimulated cyclic AMP production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated. Ergovaline inhibition of the binding of the D2-specific radioligand, [3H]YM-09151-2, exhibited a KI (inhibition constant) of 6.9 +/- 2.6 nM, whereas dopamine was much less potent (370 +/- 160 nM). Ergot alkaloids were also effective in inhibiting VIP-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively. Inhibition of cyclic AMP production by ergovaline was blocked by the dopamine receptor antagonist, (-)-sulpiride (IC50, 300 +/- 150 nM). Our results indicate that ergot compounds, especially ergovaline, bind to D2 dopamine receptors and elicit second messenger responses similar to that of dopamine. These findings suggest that some of the deleterious effects of consumption of endophyte-infected tall fescue, which contains several ergot alkaloids including ergovaline, may be due to D2 dopamine receptor activation.

Growth, livability, and feed conversion of 1957 vs 1991 broilers when fed "typical" 1957 and 1991 broiler diets.

The relative contributions of genetic selection and dietary regimen on the performance of broilers was assessed. Body weight, feed consumption, mortality (M), and the degree of tibial dyschondroplasia (TD) were measured in the 1957 Athens-Canadian Randombred Control (ACRBC) strain of broilers and in the 1991 Arbor Acres (AA) feather-sexable strain when fed "typical" 1957 and 1991 diets. Energy and protein levels, vitamin and mineral packs, and the coccidiostats used in the two dietary regimens were chosen to be representative of those in use by the industry for the two time periods. Eight treatment groups, i.e., two strains, two sexes, and two dietary regimens, were assigned into four blocks of eight litter floor pens for grow out. The 1957 diets were fed as mash, and the 1991 starter and grower diets were fed as crumbles and pellets, respectively. Feed consumption and BW were recorded at 21, 42, 56, 70, and 84 d of age, a period covering the normal marketing ages for the two broilers. Mortality and the cause of death was recorded daily. The incidence and severity of TD was assessed using a Lixiscope at 42 d of age. Average BW were 190, 508, 790, 1,087, and 1,400 g for the ACRBC on the 1957 diets vs 700, 2,132, 3,108, 3,812, and 4,498 g for the AA on the 1991 diets at 21, 42, 56, 70, and 84 d of age, respectively. The 1991 diets increased the BW of the AA by an average of 14% (20% at 42 d, but only 8% at 84 d) and of the ACRBC by 22%. The BW advantage for the 1991 diet over the 1957 diet for the AA was less for males than for females after 42 d of age, and the advantage decreased with age, probably due to the increasing incidence of leg problems. The M for AA was 9.1% vs 3.3% for the ACRBC at 42 d. Most of the ACRBC M occurred before 21 d, whereas M occurred throughout for the AA, with most after 21 d due to flip-overs and ascites. The feed conversion at 42 d for the ACRBC on the 1957 diet was 3.00 vs 2.04 for the AA on the 1991 diet. The AA on the 1991 diet had a 48.6% incidence of TD vs 25.6% on the 1957 diet. The ACRBC had approximately 1.2% TD on both diets. The TD was more severe with the 1991 diet.

D2 dopamine receptor response to endophyte-infected tall fescue and an antagonist in the rat.

Effects on rat brain D2 dopamine receptors by endophyte-infected tall fescue seed consumption and antagonist injection were characterized. Forty-eight male Wistar rats (225 g) in three separate trials were exposed to either 22 or 32 degrees C. Diets, to maintain similar concentrations of ergovaline, contained 10% (Trial 1) or 15% (Trials 2 and 3) endophyte-infected (E+; 325 average ppb of ergovaline) or uninfected (E-; 0 ppb of ergovaline) tall fescue seed. Rats were injected i.p. daily with either placebo (PL) or an experimental D2 dopamine antagonist (DA, .0375 mg/kg BW). No effects (P > .10) on diet DM intake by E+ ingestion or DA injection were detected at 22 degrees C. However, ingestion of E+ reduced (P < .01) and injection of DA improved (P < .05) DM intake of rats housed in 32 degrees C (11.1 vs 15.4 g of DM/d for E+ vs E-, respectively). Whole brain D2 dopamine receptor density (Bmax) and mRNA were reduced (P < .05) by E+ and increased (P < .05) by DA in Trial 1. No treatment effects (P > .10) on cerebral cortex alpha 1- and alpha 2-adrenergic or striatal D2 dopamine receptor Bmax were measured in Trials 2 and 3. In summary, dietary E+ reduced whole brain D2 dopamine mRNA and Bmax, whereas injection of DA increased D2 dopamine mRNA. Thus, long-term regulation of monoamine receptors seems to be affected by E+ ingestion or DA injection.