Biomedical subjects

K W Beers

Publications and source records attributed to K W Beers.

At least 37 records · Page 2Linked to original sources

PubMed1995

All-trans-retinoic acid stimulates synthesis of cyclic ADP-ribose in renal LLC-PK1 cells.

Cyclic adenosine diphospho-ribose (cADPR) triggers Ca2+ release from intracellular stores and is therefore proposed to function as a second messenger in cellular signaling; however, an extracellular stimulus, i.e., first messenger (hormone or autacoid) that modulates cADPR metabolism has not been identified. We discovered that all-trans-retinoic acid (atRA) is a potent stimulus to increase cADPR synthesis by cultured LLC-PK1 cells. The stimulation of cADPR synthesis by atRA is dose dependent between 0.1 nM and 1 microM (maximum increase approximately delta + 600%), while atRA does not alter the rate of cADPR hydrolysis by LLC-PK1 cells. The activity of other intrinsic apical membrane enzymes was not significantly altered. The stimulation of cADPR synthesis by atRA occurs after a lag period of 6-8 h, and the stimulation is inhibited by actinomycin D and by cycloheximide. Our results therefore demonstrate that atRA in physiological concentrations is a potent extracellular stimulus, first messenger, that enhances cADPR synthesis, and the effect of atRA requires de novo protein synthesis. We suggest that some of the diverse biologic actions of atRA such as morphogenetic and cell differentiation may be mediated via cADPR.

ADP-ribosyl Cyclase↗

PubMed1994

Acute N-(3,5-dichlorophenyl)succinimide nephrotoxicity in female Fischer 344 rats.

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is an established nephrotoxicant in male Fischer 344 rats at i.p. doses of > or = mmol/kg. Since gender differences often exist in the susceptibility to toxicants, the nephrotoxic potential of NDPS was examined in female Fischer 344 rats. Rats (4-5/group) were administered NDPS (0.1, 0.2, 0.4, or 1.0 mmol/kg, i.p.) or vehicle (sesame oil, 2.5 ml/kg) and renal function monitored for 48 h. At a dose of 0.1 mmol/kg, NDPS had no effect on renal function. However, administration of NDPS at a dose of 0.2 or 0.4 mmol/kg resulted in marked nephrotoxicity characterized by diuresis, increased proteinuria, glucosuria, hematuria, elevated blood urea nitrogen (BUN) concentration and kidney weight, decreased organic ion accumulation and proximal tubular necrosis. NDPS treatment of 1.0 mmol/kg resulted in oliguric renal failure rather than polyuric renal failure in 3 of 4 rats. Proximal tubular damage was observed primarily in the S3 segment of the proximal tubule in NDPS-treated female rats, while in male rats the S1 and S2 segments are the initial renal targets. These results demonstrate that female Fischer 344 rats are more susceptible to NDPS nephrotoxicity than male Fischer 344 rats and that the site of the renal lesion is gender dependent.

Animals↗

PubMed1994

CNP is present in canine renal tubular cells and secreted by cultured opossum kidney cells.

C-type natriuretic peptide (CNP) is a vasoactive and antimitogenic peptide that is structurally similar but genetically distinct from atrial natriuretic peptide. While first discovered in the brain, CNP has been shown to be produced by endothelial cells and may function in a paracrine and autocrine fashion in the control of vascular tone. Recently, CNP immunoreactivity and B-type natriuretic peptide receptors (NPR-B), for which CNP is a specific ligand, have been identified in the kidney. The present study was designed to determine whether renal epithelial cells produce and secrete CNP and whether CNP immunoreactivity is present in canine kidney. Opossum kidney (OK) cells that express proximal tubular cell characteristics were incubated for 6 h in fetal calf serum-free Dulbecco's modified Eagle's medium (DMEM). CNP immunoreactivity was measured in the preincubation and 6-h conditioned media by radioimmunoassay (RIA) using a specific antibody to CNP-22. Furthermore the molecular form of this CNP-like protein was determined by reverse-phase high-performance liquid chromatography (HPLC), and intracellular localization of the CNP immunoreactivity was determined by immunohistochemical staining. CNP immunoreactivity was also determined in renal tissue from dogs subjected to saline or endothelin infusion. Six-hour incubation in DMEM resulted in accumulation of CNP immunoreactivity (baseline below detection level vs. 6 h = 117.3 +/- 8.3 pg/ml, P < 0.001). Intracellular CNP concentration determined after sonication was 1.9 +/- 0.2 micrograms/g protein, and immunohistochemical staining for CNP was markedly positive in the cytoplasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Effect of microsomal enzyme modulators on N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS)-induced nephrotoxicity in the Fischer 344 rat.

We have previously reported that phenobarbital (PB) pretreatment enhances and piperonyl butoxide (PIBX) pretreatment or cobalt chloride (CoCl2) pretreatment decreases the nephrotoxicity induced by the model nephrotoxicant N-(3,5-dichlorophenyl)succinimide (NDPS) in the Fischer 344 rat. The objective of this study was to determine the effect of a microsomal enzyme inducer (PB) or microsomal enzyme inhibitor (PIBX or CoCl2) on a single intraperitoneal (i.p.) injection of N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS, 0.05, 0.1 or 0.2 mmol/kg), a nephrotoxicant metabolite of NDPS, or vehicle (sesame oil, 2.5 ml/kg). Renal function was monitored at 24 and 48 h post-NDHS for PB pretreated rats and at 24 h only for PIBX and CoCl2 pretreated rats, due to lethality at 48 h in PIBX pretreated rats. PB pretreatment potentiated the renal toxicity induced by a non-toxic dose of NDHS (0.05 mmol/kg), inducing diuresis and elevated proteinuria, hematuria, glucosuria, blood urea nitrogen (BUN) concentration and kidney weight. PB pretreatment also enhanced some monitored renal effects of a toxic dose (0.1 mmol/kg) of NDHS, including reduced organic ion transport by renal cortical slices. PIBX and CoCl2 pretreatments did not markedly affect the increased kidney weight, proteinuria, glucosuria, BUN concentration or altered organic ion transport induced by NDHS (0.2 mmol/kg) treatment. We conclude that PB potentiates NDHS-induced nephrotoxicity via a mechanism not influenced by CoCl2 or PIBX.

Animals↗

PubMed1993

Renal and hepatic toxicity of monochloroacetanilides in the Fischer 344 rat.

Chlorinated anilines are widely used chemical intermediates which have been shown to be nephrotoxicants and hepatotoxicants. A major metabolic pathway for the chloroanilines is via acetylation of the amino group to form chlorocetanilides. The purpose of this study was to examine the hepato- and nephrotoxic potential of the three monochloroacetanilides to determine if N-acetylation is an important biotransformation step for activation or detoxification of the chloroanilines in organ-directed toxicity. In one set of experiments, male Fischer 344 rats (4 rats/group) were injected intraperitoneally (i.p.) with a chloroacetanilide (CAA) (0.5, 1.0 or 1.5 mmol/kg) or vehicle and renal function monitored for 24 or 48 h. Liver function and tissue morphology also were determined at 24 or 48 h. None of the CAA were marked nephrotoxicants at doses of 0.5 or 1.0 mmol/kg. However, 4-CAA (1.5 mmol/kg) induced an increase in blood urea nitrogen concentration and kidney weight at 24 h and 3-CAA (1.5 mmol/kg) was lethal within 24 h. The decreasing order of in vivo nephrotoxic potential was found to be 4-CAA > or = 3-CAA > 2-CAA. Based on the elevation of ALT/GPT activity at 48 h, the order of hepatotoxic potential was found to be 4-CAA > 3-CAA, 2-CAA. In a second set of experiments, the in vitro effect of the chloroacetanilides on organic ion transport by renal cortical slices was examined. Both 3- and 4-CAA decreased organic ion accumulation at bath concentrations of 10(-5) M or greater, while 2-CAA had no effect at concentrations up to 10(-3) M. These results demonstrate that the order of nephrotoxic and hepatotoxic potential among the chloroacetanilide isomers is different than among the chloroanilines and that the chloroacetanilides were generally less potent as hepatotoxicants or nephrotoxicants than the corresponding chloroaniline. In addition, N-acetylation appears to be a detoxification rather than a bioactivation step in chloroaniline-induced liver or kidney injury.

Acetylation↗

PubMed1993

Effect of N-(3,5-dichlorophenyl)-2-hydroxysuccinimide on renal function and hemodynamics in the anesthetized rat.

The experimental agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is a nephrotoxicant in the Fischer 344 rat. NDPS induces nephrotoxicity via metabolic bioactivation to one or more metabolites. Both N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (NDHSA), oxidative metabolites of NDPS, are more potent nephrotoxicants than the parent compound. Preliminary studies in our laboratory indicate that altered renal hemodynamics may contribute to the mechanism of NDPS-induced nephrotoxicity. However, it is not known if NDPS affects renal hemodynamics prior to or after altering tubular function. In this study, male Fischer 344 rats (275-300 g) were anesthetized with urethane (1.5 g/kg, i.p.) and prepared for renal function experiments. Renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (V) and fraction of GFR excreted as urine (V/GFR) were determined during eight 30 min intervals following NDHS (0.2 or 0.4 mmol/kg, i.p.) or vehicle (sesame oil, 2.5 ml/kg, i.p.) treatment. NDHS (0.2 or 0.4 mmol/kg) decreased GFR while urine flow rate and V/GFR were increased compared to vehicle-treated controls. These alterations in renal function were evident by 2 h post NDHS (0.4 mmol/kg) and by 3 h post-NDHS (0.2 mmol/kg) treatment. RBF of rats receiving NDHS (0.2 or 0.4 mmol/kg) tended to decrease post-NDHS treatment; however, this decrease was not significant. Results of this study indicate that NDHS (0.2 or 0.4 mmol/kg) initially alters renal function by reducing the tubular reabsorption of glomerular filtrate prior to a reduction of GFR and RBF.

Animals↗

PubMed1993

Thyroid hormone stimulates the Na(+)-PO4 symporter but not the Na(+)-SO4 symporter in renal brush border.

In our previous studies we established that thyroid hormones [L-thyroxine (T4) or 3,5,3'-triiodothyronine (T3)] elicit an increase in Na(+)-Pi symport in rat and mouse renal brush-border membrane (BBM) vesicles (BBMV), but the Na(+)-coupled symports of other solutes were not influenced. However, a recent report [H. S. Tenenhouse, J. Lee, and N. Harvey. Am. J. Physiol. 261 (Renal Fluid Electrolyte Physiol. 30): F420-F426, 1991]claimed that T3 increases to a similar degree both Na(+)-Pi symport and Na(+)-SO4 symport in murine renal BBM. Adult male rats were fed either normal (0.7% Pi; NPD) or high-phosphate (1.4% Pi; HPD) diet and received T3 (0.2 mg/100 g body wt ip) for 3 days before the kidneys were removed, BBMV were prepared, and the transport rates were determined. Although the Na(+)-Pi symport significantly increased (delta = +35%) in both NPD and HPD rats treated with T3, the Na(+)-35SO4 symport and Na(+)-D-[3H]glucose symports were not influenced by T3. Furthermore, treatment of NPD-fed mice with T3 using a similar protocol as rats resulted in a significant increase (delta = +26%) of Na(+)-(Pi)4 symport, but did not alter Na(+)-SO4 symport or Na(+)-glucose symport. Our findings thus document that T3 regulates selectively the Na(+)-Pi symporter in BBM without having any effect on other major divalent anions, such as SO4.

Animals↗

PubMed1992

Acute renal and hepatic toxicity of 2-haloanilines in Fischer 344 rats.

Aniline and its halogenated derivatives are widely used as chemical intermediates. The purpose of this study was to determine the hepatotoxic and nephrotoxic potential of the 2-haloanilines. Male Fischer 344 rats (n > or = 4) were injected (i.p.) with 1.0 or 1.25 mmol/kg of: aniline (A), 2-fluoroaniline (2-FA), 2-chloroaniline (2-ClA), 2-bromoaniline (2-BrA), 2-iodoaniline (2-IA) or vehicle (0.9% saline, 2.5 ml/kg). All compounds were injected as hydrochloride salts. Renal and hepatic function was monitored 24 h after treatment. All of the 2-haloanilines induced oliguria, diminished kidney weight, tubular casts and decreased renal cortical slice accumulation of organic anions. Blood urea nitrogen (BUN) levels were increased (P < 0.05) by treatment with 1.0 or 1.25 mmol/kg of 2-FA, 2-ClA or 2-BrA. Hepatic alterations were also observed and characterized by elevated plasma ALT/GPT activity and altered morphology in the centrilobular region. The nephrotoxic and hepatotoxic potentials were similar among the 2-haloanilines but aniline was less toxic than its 2-halo derivatives. These results demonstrated that halogen substitution at the 2-position of aniline increased hepatic and renal toxicity. However, the severity of toxicity was not influenced by the nature of the halogen substituent.

Acute Disease↗

PubMed1992

Renal effects of N-(3,5-disubstitutedphenyl)-succinimides in the Fischer 344 rat.

Previous studies have demonstrated the importance of substitution at the 3- and 5-positions of the phenyl ring in N-phenylsuccinimides for the production of nephrotoxicants in this series of compounds. The purpose of this study was to determine if the electronic nature of the 3,5-substituents is an important determinant for nephrotoxic potential. Male Fischer 344 rats (four rats per group) were administered a single intraperitoneal injection of a succinimide (0.4 or 1.0 mmol kg-1) or vehicle, and the renal function was monitored for 48 h. Only N-(3,5-dichlorophenyl)succinimide (0.4 or 1.0 mmol kg-1) induced marked changes in renal function. Urine volume, BUN concentration and proteinuria were increased following N-(3,5-dinitrophenyl)succinimide (1.0 mmol kg-1) treatment but other renal parameters and renal morphology were unchanged in this treatment group. These results indicate that the presence of halogen atoms at the 3- and 5-positions of the phenyl ring in N-phenylsuccinimides is more important for nephrotoxic potential than the presence of non-halogen substituents. The reason why halogen substitution is an important determinant for N-phenylsuccinimide nephrotoxicity is unknown.

Animals↗

PubMed1992

Role of para-hydroxylation in phensuximide-induced urotoxicity in the Fischer 344 rat.

Phensuximide (PSX) is an antiepileptic agent which has been shown to induce hemorrhagic cystitis and mild nephrotoxicity following repeated administration in man or rats or when acutely administered to phenobarbital-pretreated rats. The purpose of this study was to explore the role of para-hydroxylation of the phenyl group of PSX in PSX-induced urotoxicity. Two PSX derivatives, 2-(4-fluorophenyl)-N-methylsuccinimide (FMPS) and N-methyl-2-(4-methylphenyl)succinimide (MMPS), were synthesized and evaluated for urotoxic potential. Male Fischer 344 rats (four rats/group) were administered intraperitoneally (i.p.) a succinimide (0.4 or 1.0 mmol/kg) or vehicle and renal function monitored for 48 h. In a separate experiment, rats were pretreated with phenobarbital (75 mg/kg/day; 3 days, i.p.) prior to succinimide or succinimide vehicle. In non-phenobarbital pretreated rats, acute FMPS or MMPS treatment had little effect on renal function or morphology at the doses tested. Hematuria (+) was noted in the FMPS (1.0 mmol/kg) group on post-treatment day 2. However, in the phenobarbital-pretreated rats, FMPS (0.4 or 1.0 mmol/kg) induced marked hematuria (++) and increased proteinuria while having little or no effect on other renal functional parameters or renal morphology. At killing, bladders of treated rats were distended with bloody urine and exhibited hemorrhagic areas within the bladder wall. In phenobarbital-pretreated rats, MMPS administration had little effect on any renal functional parameter measured or urological morphology. These results suggest that para-hydroxylation does not contribute to the hemorrhagic cystitis induced by PSX.

Animals↗

PubMed1992

Aflatoxin and glutathione in domestic fowl (Gallus domesticus)--II. Effects on hepatic blood flow.

1. The effect of aflatoxin on plasma aspartate aminotransferase (AST), protein, and hepatic glutathione (GSH) and hepatic blood flow (perfusion), were determined in 3-week-old male chickens. 2. Daily aflatoxin gavage (2 mg/kg body wt, in corn oil) for 5 and 10 days elevated plasma AST and hepatic GSH, and depressed plasma protein and hepatic perfusion. Also, renal GSH was elevated after 10 days of aflatoxin treatment. 3. Birds given aflatoxin for 10 days followed by a 10-day recovery period exhibited tissue GSH, plasma AST and protein levels that were not different from control, but hepatic perfusion remained depressed.

Aflatoxins↗

PubMed1992

Aflatoxin and glutathione in domestic fowl (Gallus domesticus)--I. Glutathione elevation and attenuation by high dietary methionine.

1. Changes in hepatic and renal glutathione (GSH) and plasma aspartate aminotransferase (AST) following single or daily oral doses of aflatoxin B1 (AFB1, 2 mg/kg BW) or corn oil vehicle (1 ml/kg BW) were determined in male chickens (14-21-day-old). 2. Plasma AST and hepatic GSH increased 2 and 8 hr, respectively, following a single AFB1 dose. 3. Hepatic GSH continued to increase through 5 daily doses of AFB1, but there were no differences in AST levels on days 1-5. Feeding a diet containing 150% of NRC requirement for methionine attenuated the AFB1-induced increase in hepatic GSH. Renal GSH was unaffected by AFB1 or dietary treatment.

Aflatoxin B1↗

PubMed1991

Effect of glutathione manipulation on prostaglandin synthesis in renal medullary homogenates.

1. The effect of glutathione (GSH) manipulation on arachidonic acid (AA) metabolism in renal medullary (RM) homogenates was investigated. 2. Diethyl maleate (DEM) depleted GSH initially by 50% (P less than 0.05) and produced a general suppression (P less than 0.05) of all PGs with the exception of TXB2. GSH was further depleted during homogenization and a 30-min incubation period (P less than 0.01). 3. Adding glutathione monoethyl ester (GSH-MEE) (0, 0.8, 1.6 or 3.2 mmol/ml) to RM homogenates increased GSH (P less than 0.01) and decreased RM homogenates' PGs-synthesizing capability (P less than 0.05), with the exception of PGE2 and TXB2 at the highest concentration. 4. The results indicate that homogenization has a significant impact (P less than 0.05) on GSH concentration of the media and alterations in GSH concentration affect the profile and quantity of AA metabolites in renal medullary homogenates.

Animals↗

PubMed1991

Aflatoxicosis alters avian renal function, calcium, and vitamin D metabolism.

Experiments were designed to determine the effects of aflatoxicosis on avian renal function, calcium (CA), inorganic phosphorous (Pi), and vitamin D metabolism, and to determine if the effects of aflatoxin are reversible upon discontinuation of toxin administration. Three-week-old male broiler chickens (n = 12 per treatment) received aflatoxin (AF; 2 mg/kg po) or an equal volume of corn oil, the AF carrier vehicle, for 10 consecutive days. After 10 d of treatment, half of the birds from each treatment group were anesthetized and prepared for renal function analysis, which included a 2-h phosphate loading period. Ten days after discontinuation of AF treatment, the remaining birds in each treatment group were anesthetized and prepared for renal function analysis. AF decreased plasma 25-hydroxy vitamin D [25(OH)D] and 1,25-dihydroxy vitamin D [1,25(OH)2D] levels after 5 d of treatment. After 10 d of treatment, urine flow rate (V), fractional sodium excretion (FENa), and fractional potassium excretion (FEK) were lower in AF-treated birds. In addition, total plasma Ca tended to be lower (p = .10) and fractional Ca excretion (FECa) tended to be higher (p = .10) in the AF-treated birds. Intravenous phosphate loading produced a sharp increase in urine hydrogen ion concentration ([H+]) in the AF-treated birds. Glomerular filtration rate (GFR) was reduced and plasma osmolality was increased in AF-treated birds 10 d after discontinuation of toxin administration. The results indicate that AF directly or indirectly affects Ca and Pi metabolism in avians. At the present time, the effects may be related to altered vitamin D and parathyroid hormone (PTH) metabolism. Aflatoxicosis may decrease endogenous PTH synthesis and the renal sensitivity to PTH. The AF-related increase in urine [H+] during phosphate loading is probably due to increased Na+/H+ counterport, suggesting that AF stimulates sodium reabsorption. Also, the decrease in GFR exhibited 10 d after toxin removal indicates that AF may cause prolonged alteration in renal function.

Aflatoxins↗

PubMed1990

Altered renal function in broilers during aflatoxicosis.

Experiments were conducted to determine the effects of aflatoxicosis on acid-base balance, urine flow rate (V), glomerular filtration rate (GFR), clearance of para-aminohippuric acid (CPAH), plasma osmolality, and the renal handling of Na, K, Ca, and P. Three-week-old broilers were gavaged with aflatoxin at a dose of 2 mg/kg of BW per day for 10 consecutive days. Control birds received an equal volume of corn oil, the aflatoxin carrier vehicle. On the eleventh day, the birds were anesthetized and prepared for renal function analysis. A solution containing inulin, para-aminohippuric acid, and mannitol was infused at a low infusion rate (.1 mL/kg of BW per min) and a high infusion rate (.4 mL/kg of BW per min) to determine if aflatoxin affects the renal response to an acute volume load. Aflatoxicosis decreased the fractional excretion of phosphorous (FEP) and plasma Ca concentration but did not significantly alter any other renal function or acid-base variables. The decrease in FEP and plasma Ca may be a direct result of renal tubular damage, decreased Ca absorption from the gut, or a result of altered circulating levels of parathyroid hormone (PTH), and possibly decreased renal sensitivity to PTH.

Animals↗

PubMed1989

Physiological responses of heat-stressed broilers fed nicarbazin.

Two experiments were conducted to determine physiological responses in heat-stressed broilers fed a control diet or one containing 125 ppm Nicarbazin. Male birds were surgically implanted with a carotid catheter and fitted with a chest movement transducer and rectal probe. In Experiment 1, birds were exposed to an abrupt change from thermoneutral (22.5 C, 70% relative humidity [RH]) to heat stress (37 C and 40 to 50% RH) conditions within 10 min and maintained in this environment for 120 min. In Experiment 2, birds were exposed to a gradual change from thermoneutral to heat stress (38 C, 68% RH) conditions over 4 h and maintained in this environment for an additional 1 h. Heart rate (HR), respiration rate (RR), and body temperature (Tb) were monitored throughout each experiment, and arterial samples were obtained for determination of acid-base balance and lactate. Birds fed Nicarbazin had higher (P less than .05) Tb and lower (P less than .05) blood PCO2 and bicarbonate during heat stress than controls in both experiments. Thermal polypnea was observed in both experiments, but, although there were no treatment differences in Experiment 1, RR was lower (P less than .05) in the last hour of heat stress for Nicarbazin-fed birds in Experiment 2. In the second experiment, birds fed Nicarbazin exhibited higher (P less than .05) HR and blood lactate during heat stress than control-fed birds. The results of this study indicate that Nicarbazin, by an as yet unidentified mechanism, increases Tb in heat-stressed birds, which results in greater deviations in blood acid-base balance, blood lactate, and HR than in control-fed birds.

Acid-Base Equilibrium↗

PubMed1988

Effects of supplemental Bermuda grass hay or corn on intake, digestion and performance of cattle consuming endophyte-infected fescue.

Effects of supplemental Bermuda grass hay (BG) or ground corn on intake, digestion and performance of cattle consuming endophyte-infected fescue (I) were studied. In Exp. 1, a Latin square study, five growing Holstein steers (158.1 kg) consumed I ad libitum and were offered 0, .3, .6, .9 or 1.2% body weight (BW) of BG daily. Total dry matter (DM) intake rose linearly (P less than .05) with increasing BG, although intake was numerically similar with .6, .9 and 1.2% BW of BG. Digestibility was constant with diet (P greater than .10). Six growing Holstein steers used in Exp. 2, a Latin square with a 2 x 3 factorial arrangement of treatments, ingested I or noninfected (NI) fescue hay ad libitum with 0, .5 or 1.0% BW of ground corn. Total DM intake increased linearly as the level of corn rose (P less than .05). Total intake with I increased more with the first than with the second addition of corn, and the opposite occurred with NI (interaction between fescue infection and the quadratic effect of corn level, P less than .10). Organic matter digested (g/d) was greater for NI than for I and rose linearly with increasing corn ingestion (P less than .05). Ninety-six crossbred beef heifers and steers (184.2 kg avg initial live weight) were used in a 77-d fall grazing experiment (Exp. 3) with a 2 x 3 factorial treatment arrangement. Cattle grazed I or NI paddocks and were given no supplement or .34% BW of BG or .65% BW of ground corn on a daily basis (DM).(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

PubMed1988

Effects of frequency of offering and type of supplemental forage on intake and digestion in calves consuming endophyte-infected fescue hay.

Two experiments were conducted to determine the effects of frequency of offering and type of supplemental forage on intake and digestion in calves consuming endophyte-infected fescue hay (I). In Exp. 1, five Holstein steers, averaging 128 kg body weight (BW), were used in a 5 X 5 Latin square experiment. All steers were given free access to I in the afternoon. Morning meals consisted of 1) ad libitum access to I daily (control), 2) .5% BW of Bermuda-grass hay (BG) daily, 3) 1.0% BW of BG every 2nd d, 4) 1.5% BW of BG every 3rd d and 5) 2.0% BW of BG every 4th d. Steers receiving BG consumed less (P less than .01) I and more (P less than .01) total dry matter (DM) than did steers given I alone. Within treatment, I intake was similar (P greater than .10) among days of the feeding cycle without BG. Organic matter (OM) digestion was lower (P less than .05) with than without BG. In Exp. 2, 12 beef calves (Angus and Hereford X Angus; 6 mo of age, 155 kg initial BW) were used in a completely randomized-design experiment. Calves were given ad libitum access to I daily (control) or to BG or wheat hay (WH) on d 1 and I the following 3 d. Hay (I, BG or WH) intake d 1 of the feeding cycle was higher for BG and WH than for the control treatment (16 and 45%, respectively) and higher for WH than BG (25%; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗