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S L Hansard

Publications and source records attributed to S L Hansard.

At least 19 recordsLinked to original sources

Kinetic model of whole-body vanadium metabolism: studies in sheep.

A compartmental model for vanadium metabolism in sheep has been proposed. The model is consistent with data obtained from sheep fed a control diet (2.6 ppm vanadium) containing 0 or 200 ppm supplemental vanadium. Sheep were administered 48V dioxovanadium either orally or intravenously. Blood, feces, and urine radioactivity were monitored for 6 days postdosing. Several new insights regarding vanadium metabolism are suggested and tested against the data using the model. Some of these include significant absorption of 48V occurs from the upper gastrointestinal tract; an in vivo process is necessary in order for 48V dioxovanadium to be converted into a more biologically reactive species; at steady state the upper and lower gastrointestinal tracts contain at least 10- and 100-fold more mass of vanadium, respectively, than does blood. No statistically significant differences in transport rate constants were found between animals receiving 0 and 200 ppm supplemental dietary vanadium. The availability of a model will enable the refinement of future studies regarding vanadium metabolism in the ruminant.

Administration, Oral↗

Vanadium metabolism in sheep. III. Influence of dietary vanadium on kinetics of 48V administered orally or intravenously and comparison of compartmental and graphical models.

Radiotracer techniques were used to investigate the influence of dietary stable V on the excretion, distribution and blood clearance kinetics of 48V in 14 rams averaging 58 kg body weight. Rams were fed a basal diet with added levels of 0, 50 or 200 mg/kg V as NH4 VO3 for 25 wk before either oral or iv administration of the isotope. A three-compartment model was determined by graphical logarithmic analysis of blood disappearance data from iv-dosed rams and compared with a simultaneous multicompartment model, which made it possible to ascribe physiological processes to the components of the graphical model. The principal route of excretion of 48V administered iv was via urine, whereas the isotope given orally was excreted almost entirely by way of feces, resulting in low tissue and urinary 48V levels. Increasing dietary V increased (P less than .05) the percentage of dose excreted in urine regardless of dosing route, but dietary V had no effect on 48V excreted in feces. Stable dietary V had no effect on blood clearance rates of orally or iv-dosed rams. Dietary V addition decreased 48V concentration in kidney (P less than .01), liver, spleen, testes and muscle (P less than .05) of iv-dosed rams, but had no effect in rams dosed orally. Kidney, bone, liver and spleen retained the highest levels of 48V activity 144 h after dosing. Dietary V appeared to have a minimal effect on V kinetics in rams.

Administration, Oral↗

Vanadium metabolism in sheep. I. Comparative and acute toxicity of vanadium compounds in sheep.

Twelve Florida native wethers were given ammonium metavandate, calcium orthovanadate and calcium pyrovanadate by capsule in a study to examine the toxicity of the compounds. The initial daily dosage of 100 mg elemental vanadium was increased by 50 mg at 2-d intervals for an assessment not only of the toxic effects, but also to determined the amount that caused a decline in feed intake to 25% of that of control animals. The initial decline in feed intake was observed at 400 to 500 mg vanadium/d (9.6 to 12 mg/kg body weight, 310 to 350 ppm); a rapid decline in feed intake was accompanied by diarrhea. One sheep fed 550 mg vanadium as calcium orthovanadate died 3 d after dosing. One animal on each of the other three treatments was killed and necropsied for immediate comparison. Extensive mucosal hemorrhage of the small intestine and diffuse or petechial subcapsular hemorrhages of the kidneys were observed for sheep fed all compounds. The three vanadium compounds appeared to be similar in toxicity, as determined by abrupt declines in feed intake and pathological changes of the intestine and kidney. For a determination of acute toxicosis, three sheep were given 40 mg/kg body weight of vanadium as NH4VO3 in gelatin capsules and two sheep were included as controls. Two of the treated animals died within 80 h after administration and the other three were killed at 96 h. Vanadium content of kidney, liver, bone, spleen, lung and muscle was elevated by treatment.

Acute Disease↗

Vanadium metabolism in sheep. II. Effect of dietary vanadium on performance, vanadium excretion and bone deposition in sheep.

Sixteen ram lambs were fed 0, 50 or 200 ppm supplemental vanadium daily as NH4VO3 for 90 d and coccygeal vertebrae were sampled at 0, 15, 30, 60 and 90 d after the imposition of dietary treatments. Vertebral vanadium content was elevated (P less than .05) after exposure to 200 ppm added vanadium in the diet of 15 d, but nonsignificant increases occurred thereafter. Increasing dietary vanadium increased bone ash vanadium concentration from .4 to 1.7 and 3.8 ppm in sheep fed 0, 50 and 200 ppm supplemental vanadium, respectively. In a balance study, urinary concentrations of the element also were related directly to dietary intake. A trend toward elevated urine volume with increased intake of vanadium was also observed.

Absorption↗

Blood plasma magnesium, potassium, glucose, and immunoreactive insulin changes in cows moved abruptly from barn feeding to early spring pasture.

Cations and immunoreactive insulin in plasma were measured in 35 lactating cows moved abruptly to early spring pasture. After change of cows from grass-clover hay to fescue-bluegrass pasture containing 22 to 31 g potassium/kg dry matter, immunoreactive insulin of 5 Holstein cows increased 30% in 5 days and averaged 45% above prepasture concentrations for 40 days. Magnesium averaged 44% below prepasture content of plasma during this period and was correlated negatively with potassium -.17 and immunoreactive insulin -.37. Thirty Herford cows were changed from corn silage and grass-clover hay to wheat-rye pasture containing 3.06% potassium in the dry matter. Each day on pasture, 10 cows each were fed 2.3 kg cornmeal, 10 were given 30 g magnesium oxide by capsule, and 10 were given no supplement. After unsupplemented cows were moved to pasture, immunoreactive insulin rose 51% in 8 days and plasma magnesium fell 24%. Both supplements reduced immunoreactive insulin, but magnesium was maintained higher by magnesium oxide than by cornmeal. Injection of two Holstein cows with insulin (2 IU/kg body weight) reduced plasma concentrations of both potassium and magnesium 20% below that of two cows injected with only physiological saline. Whether elevated plasma insulin may accelerate development of hypomagnesemia in cattle on spring pasture with relatively high potassium content has not been established.

Animal Husbandry↗

Effect of glucagon infusion on plasma magnesium, glucose, and insulin in bull calves.

Two Holstein bull calves each were infused intravenously with 1 mg glucagon in .9% sodium chloride, and two were given saline alone; 1 wk later treatments were reversed. Glucagon increased concentrations of insulin and glucose but decreased potassium in blood plasma and moderately increased urinary magnesium and calcium losses. When only saline was used, there was no effect. A hypothesis relating elevated glucagon to grass tetany is proposed.

Animals↗

Absorption, excretion, and tissue deposition of titanium in sheep.

Titanium metabolism was measured in three 18 kg lambs each fed 450 g chopped hay daily. Two of the lambs were dosed orally and one intravenously with 3 muCi titanium-44 each. Clearance of the intravenous dose was extremely slow; after oral administration, however, no titanium-44 was detected in blood plasma for 48 h. Over 96% of the oral dose was recovered in feces and digestive tract contents. Titanium-44 absorption, estimated from total carcass recovery and by comparison of concentrations in internal organs of orally and intravenously dosed lambs, was less than .5%. Fecal titanium could be a satisfactory index of soil ingestion by grazing ruminants.

Absorption↗

Magnesium movement in hypothyroid sheep.

We described magnesium transport in hypothyroid and normal sheep with an eight-compartment biomodel fitted by a least-squares technique to data from multiple compartments and routes of entry of 28-Mg. Isotopic equilibrium was not attained during this period of observation in hypothyroid or control sheep. Hypothyroidism reduced transfer coefficients for absorption (P less than 0.01) of 28-Mg from the GI tract but did not change the rate coefficient for endogenous 28-Mg losses to feces (P less than 0.05). Nutritional balance data indicated higher absorption and retention of Mg in hypothyroid sheep, and the observed decrease in rate of passage of digestive residues suggested that mean retention time of GI tract contents had a definite effect on the availability of Mg.

Animals↗