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Biomedical subjects

R F Wideman

Publications and source records attributed to R F Wideman.

At least 127 records · Page 7Linked to original sources

Urolithiasis in pullets and laying hens: role of dietary calcium and phosphorus.

A study was conducted to test the independent and combined effects of high dietary calcium and low available phosphorus on the incidence of urolithiasis in pullets and laying hens. One thousand Single Comb White Leghorn pullets were divided into four diet treatment groups beginning at 50 days of age. A normal calcium (1%), normal available phosphorus (.6%) diet (NCNP) was fed to control pullets. Other pullet groups were fed a high calcium (3.25%), normal available phosphorus (.6%) diet (HCNP), a normal calcium (1%), low available phosphorus (.4%) diet (NCLP), or a high calcium (3.25%), low available phosphorus (.4%) diet (HCLP). At 18 weeks of age, 368 pullets were necropsied. One percent of the HCNP group and 14% of the HCLP group developed urolithiasis. Urolithiasis was not found in pullets raised on the NCNP and NCLP diets. The remaining pullets were transferred to laying cages and were fed a commercial layer ration until they were 51 weeks old. None of the hens raised on the NCNP diet, 12% of the hens raised on the HCNP diet, 2% of the hens raised on the NCLP diet, and 14% of the hens raised on the HCLP diet had urolithiasis. Renal function studies were performed on 18-week-old pullets and 51-week-old hens. Pullets raised on the HCLP diet had significantly higher urine pH, significantly lower fractional inorganic phosphate excretion, and significantly higher fractional calcium excretion when compared with pullets raised on the other diet treatments. The profound effect of the HCLP diet on renal calcium and phosphorus excretion in pullets was not retained in the hens.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Organic phosphate probes of the avian renal phosphate secretory mechanism.

Parathyroid hormone (PTH) stimulates net renal inorganic phosphate (Pi) secretion in domestic fowl (Gallus domesticus). Recent evidence indicates that secreted Pi is derived from a highly sequestered, presumably organic, phosphate pool. A modified Sperber technique was used to survey the response of domestic fowl to unilateral renal portal infusions of organic phosphate compounds that had been implicated in previous studies of Pi secretion. None of the organic phosphate compounds produced a significant unilateral Pi secretory effect. It is concluded that these compounds neither directly stimulate Pi secretion in normal or parathyroidectomized birds, nor are they rate-limiting for the Pi secretory mechanism in birds infused with PTH.

Animals↗

Parathyroid hormone-induced phosphate excretion following preequilibration with 32P.

Parathyroid hormone (PTH) stimulates a secretory component of avian renal inorganic phosphate (Pi) transport, but the secreted Pi does not appear to be derived directly from peritubular (plasma) Pi. In the present study, experiments were conducted to determine whether differences in parathyroid status during 32P infusion influenced entry of the isotope into the Pi secretory pool. Fractional excretion values for Pi (FEPi) and 32P (FE32P) were compared in normal and parathyroidectomized (PTX) anesthetized birds that had been preinfused with 32P for 0, 90, and 240 min before PTH infusion. The results demonstrate that in the absence of exogenous PTH, FEPi is identical to FE32P in normal and PTX birds, reflecting full equilibration of 32P with excreted Pi under these conditions; and, regardless of the duration of 32P preequilibration or the parathyroid status of the experimental animals, exogenous PTH always causes FEPi to exceed FE32P. It is concluded that the Pi secretory pool is inaccessible to 32P under conditions that should markedly alter cellular Pi influx and efflux.

Animals↗

Blood ionic calcium response to hypocalcemia in the chicken induced by ethyleneglycol-bis-(B-aminoethylether) -N,N'-tetraacetic acid: role of the parathyroids.

Eight groups of cockerels were used to test an ethyleneglycol-bis-(B-aminoethylether)-N,N'-tetraacetic acid (EGTA) challenge as a possible means for estimating parathyroid function and responsiveness in birds. Intravenous injections of EGTA significantly depressed blood ionic calcium concentrations (hypocalcemia), and the recovery from this hypocalcemia was dependent upon the presence of parathyroid hormone (PTH). However, it also was demonstrated that a surge of PTH is not necessary for recovery from the EGTA-induced hypocalcemia. Therefore, in the bird, the EGTA challenge is a test of the ability of PTH target tissues (bone or soft tissues) to buffer ionic calcium in the blood. The EGTA challenge is not a quantitative means of testing parathyroid gland function or responsiveness.

Animals↗

Blood ionic calcium responses of hens from thick-shell and thin-shell lines to ethyleneglycol-bis-(B-aminoethylether)-N,N'-tetraacetic acid injections.

Experiments were conducted on laying and nonlaying hens from genetically selected lines that produce thick (TK) or thin (TN) eggshells. At 44 weeks of age, TK layers exhibited significantly higher total plasma calcium concentrations than TN layers. Total plasma calcium concentrations were not significantly different between TK and TN layers at 80 weeks of age, reflecting an effect of aging on total plasma calcium. Intravenous injections of ethyleneglycol-bis-(B-aminoethylether-N,N'-tetraacetic acid (EGTA) were administered to TK and TN layers at 44 weeks of age and to TK and TN layers and nonlayers at 80 weeks of age. EGTA is a calcium chelating agent that creates hypocalcemia when injected intravenously. Laying hens of both lines and at both ages exhibited a similar degree of hypocalcemia during EGTA injections, and a similar rate of recovery to normocalcemia was noted after cessation of EGTA administration. Nonlayers were unable to recover from the EGTA-induced hypocalcemia. Because the pattern of calcium depression and recovery during and after the EGTA challenge has been shown to be associated with the capacity of parathyroid hormone-sensitive target tissues to buffer blood ionized calcium, it was concluded that the capacity to buffer ionized calcium by these target tissues is similar in TK and TN layers. However, nonlayers have a restricted capacity to buffer blood ionic calcium.

Animals↗

Effect of parathyroid hormone on total phosphate and inorganic phosphate in blood, plasma, and urine of domestic fowl.

Previous work has shown that parathyroid hormone causes the kidneys of domestic fowl to secrete inorganic phosphate (Pi) into the urine. Secreted Pi is not derived directly from plasma Pi. The objective of the present study was to determine if direct or indirect correlations exist between the urinary Pi excretion rate and the concentration of phosphate in plasma or whole blood. Parathyroid hormone dissolved in gelatin carrier vehicle was injected into immature domestic fowl to cause net renal Pi secretion. Control birds were injected with carrier vehicle alone, resulting in net Pi reabsorption. Urine, plasma, and whole blood samples obtained during net Pi secretion were compared with samples obtained during net Pi reabsorption. Each sample was assayed for total and inorganic phosphate. Neither time course nor point by point comparisons of individual samples provided any evidence that secreted Pi is derived from organic phosphate in plasma or whole blood. These experiments suggest that phosphate pools within the kidneys may serve as a source for the Pi that is secreted in response to parathyroid hormone.

Animals↗

Hypothyroidism and antibody production in immature male chickens.

This study was conducted to determine if hypothyroidism has an effect on humoral immunity in immature male chickens. Two week old Single Comb White Leghorn male chicks were used as experimental animals. Two experiments were conducted using different methods to induce hypothyroidism. In Experiment 1, birds were surgically thyroidectomized (Tx group) and in Experiment 2, hypothyroidism was induced by supplementing the feed throughout the experiment with 0.1% propylthiouracil (PTU group). Antibody production against sheep red blood cells (SRBC) (thymus-dependent antigen) and Brucella abortus (BA) (thymus-independent antigen) was tested at 4 weeks of age. Serum concentrations of T4 and T3 were measured in birds from each treatment group at 5 and 9 weeks of age. Body weights were recorded and birds were then autopsied and thyroid gland weights were measured. Hypothyroidism was successfully induced in both Tx and PTU birds, as reflected by significant reduction in body weights in both groups, enlargement of thyroid glands in PTU birds and absence of thyroid glands in Tx birds. Though T4 and T3 were reduced in sera of treated birds, considerable amounts of these hormones were detected. Hypothyroidism did not seem to have profound or consistent effects on antibody production against SRBC or BA. The possibility that thyroid hormones play a role in antibody production was not ruled out. However, it was suggested that within the physiological range of thyroid gland activity, thyroid hormones may not significantly regulate antibody production.

Animals↗

Kidney function of pullets and laying hens during outbreaks of urolithiasis.

Renal function evaluations were conducted on pullets and laying hens during outbreaks of urolithiasis. The following parameters were measured: kidney weights; hematocrits; plasma concentrations of uric acid, calcium, inorganic phosphate, magnesium, sodium, and potassium; urine flow rates; glomerular filtration rates; renal plasma flow rates; urine pH; and relative clearances of inorganic phosphate, calcium, magnesium, sodium, potassium, and para-amino hippuric acid. The adequacy of renal portal perfusion was estimated by timed phenol red extraction. Considerable interindividual variability was noted, presumably due to differences in age and reproductive status. Intraindividual left versus right kidney comparisons also were made, since urolithiasis often is associated with macroscopic lesions of one kidney but not the other. The results indicate that even when gross lesions of only one kidney were present, specific tubular transport processes were similar in both kidneys. Urolithiasis did cause significant alterations in urine flow rates, glomerular filtration rates and renal plasma flow rates. it was concluded that the changes associated with urolithiasis reflect the expected compensatory hypertrophic responses of surviving kidney tissue to a reduction of renal mass. The physiological impact of this form of kidney damage appears to arise from reduced renal mass rather than from inappropriate renal handling of minerals or electrolytes.

Animals↗

Stimulation of avian renal phosphate secretion by parathyroid hormone.

Phosphate buffers (ammonium, sodium, potassium, and calcium phosphate, pH 5.5, 7.2, 8.5) and 32P were infused unilaterally into the renal portal systems of intact, parathyroidectomized (PTX), and parathyroid hormone-infused (PTH) domestic fowl to study the secretory flux for inorganic phosphate (Pi). Urine samples were collected simultaneously from both kidneys, with the uninfused kidney serving as a control for the portal-perfused kidney (modified Sperber technique). No consistent unilateral excess of Pi or 32P excretion occurred for any of the experimental groups. For intact birds, fractional 32P excretion by both kidneys (FE32p) was identical to fractional Pi excretion (FEpi) (determined by chemical analysis) and reflected net reabsorption (0.64). However, during PTH infusion, FE32p was 0.82 (net reabsorption) while FEPi was 1.21 (net secretion). These results indicate that a) the peritubular-to-lumen flux for Pi and 32P is a minor component of net tubular transport, regardless of the parathyroid status, counterion availability, or peritubular Pi concentration; b) plasma Pi and 32P enter the tubule lumen predominantly by filtration; c) PTH stimulates tubular Pi secretion; and d) the secreted Pi is derived from an organic or inorganic pool that does not readily equilibrate with infused 32P (or presumably peritubular Pi).

Animals↗

Innervation of the parathyroid in the European starling (Sturnus vulgaris).

Anatomical studies were conducted to characterize the source, type, and distribution of parathyroid gland innervation in European starlings. Denervation experiments demonstrated that the parathyroid glands and adjacent carotid bodies are innervated by nerve fibers originating in the nodose ganglion of the vagus nerve. In the parathyroid parenchyma, these fibers terminate adjacent to chief cells or near vascular smooth muscle. Vagal fibers also form synapses with catecholamine-containing glomus cells of the carotid body. Blood parenchyma. These observations suggest that vagal innervation may influence parenchyma. These observations suggest that vagal innervation may influence parathyroid function in starlings either through direct chief cell innervation or through alteration of vascular perfusion. A neurohemal relationship also may exist between the carotid body and parathyroids.

Adrenergic Fibers↗

Calcitonin stimulation of urine flow and sodium excretion in the starling.

Renal effects of synthetic salmon calcitonin (CT) were examined in normal and parathyroidectomized (PTX) starlings, Sturnus vulgaris. Standard clearance studies were performed. Anesthetized birds were infused with [14C]-inulin in 2.5% mannitol containing either 0.25% gelatin alone as a control, or gelatin plus CT (2 IU CT/h; Armour). In intact starlings, CT significantly increased urine flow and relative clearance of sodium (CNa/CIn). CCa/CIn was significantly elevated only 40 min after start of hormone infusion. No significant change occurred in CK/CIn, CPO4/CIn or in serum levels of Na, K, Ca, or PO4. In PTX starlings, CT induced significantly higher CNa/CIn. Urine flow was significantly higher at 40 and 60 min, whereas CK/CIn increased significantly only 20 min following start of CT infusion. Serum calcium decreased significantly 1 h after hormone administration and was accompanied by increased incidence of tetany. Serum phosphate levels were significantly lower than those of corresponding PTX controls 1 h post-CT, indicating that CT prevented the expected hyperphosphatemia. Higher CT dose (20 IU/h) in PTX birds substantially enhanced urine flow, CNa/CIn, CK/CIn, and occurrence of tetany.

Animals↗

Effects of phosphate loading and parathyroid hormone on starling renal phosphate excretion.

The effects of phosphate loading were examined in intact, parathyroidectomized (PTX), and PTX starlings infused with parathyroid extract (PTX +/- PTE). In intact starlings, there was no correlation between the filtered phosphate load and the quantity of phosphate excreted. Net secretion predominated at lower filtered loads (2.5-20 mu mol . kg-1 . min-1) but net reabsorption occurred at filtered loads between 20 and 35 mu mol . kg-1 . min-1. Phosphate-loaded PTX starlings reabsorb phosphate over a wide range of filtered loads (5-45 mu mol . kg-1 . min-1). Excretion was significantly correlated with the filtered load in PTX birds (r = 0.943). Phosphate loaded PTX + PTE starlings secreted phosphate when filtered loads ranged from 2.5 to 30 mu mol . kg-1 . min-1. Excretion also was significantly correlated with the filtered load in this group (r = 0.972). The results of these experiments indicate that a) variations in endogenous PTH release in intact starlings result in wide variations in the renal pattern of phosphate excretion during phosphate loading; b) net phosphate secretion rarely occurs during phosphate loading in PTX starlings, but always occurs in PTX + PTE starlings; and c) both phosphate secretion and phosphate reabsorption are limited by maximal tubular transport capacities. Additional evidence indicates that PTH inhibits tubular phosphate reabsorption in starlings.

Animals↗

Renal excretion of phosphate and calcium in parathyroidectomized starlings.

Renal excretion patterns of calcium, phosphate, sodium, and potassium were studied in parathyroidectomized (PTX) and parathyroid extract (PTE)-injected PTX starlings. Sturnus vulgaris. Anesthetized birds (Equi-Thesin or Dial) were infused intravenously with 2.5% mannitol containing [14C]inulin. PTX caused significant hypocalcemia, hyperphosphatemia, increased relative calcium clearance (CCa/CIn), and decreased relative clearances of phosphate and potassium, but did not change the clearance of sodium. Glomerular filtration rate (GFR=CIn) and urine flow remained unchanged up to 2 h after PTX. PTE administration 3 h after PTX returned serum calcium and phosphate values to control levels and caused a transient (10-min) increase in GFR. Following PTE, the relative clearances of phosphate, sodium- and potassium increased, while that of calcium decreased significantly relative to the PTX levels. PTE caused net tubular secretion of phosphate, decreased tubular reabsorption of sodium and potassium (sometimes potassium secretion), and a return of excretion of calcium to control levels. These studies indicate that the parathyroid role in calcium and phosphate homeostasis in starlings is predominantly on the kidney.

Animals↗

Parathyroid hormone and renal excretion of phosphate and calcium in normal starlings.

The renal handling of calcium, phosphate, sodium, and potassium was studied in normal and parathyroid extract (PTE)-injected starlings, Sturnus vulgaris. The birds were anesthetized with Equi-Thesin and infused intravenously with 2.5% mannitol containing [14C]inulin. Normal starlings actively reabsorb all four of these substances. After intravenous administration of 50 IU PTE/100 g body wt, the relative phosphate clearance (CPO4/CIn) as well as tubular transfer of phosphate (TPO4) increased significantly. Phosphate secretion occurred and usually persisted longer than 2 h. The relative calcium clearance also rose after PTE, but the TCa did not shift. This probably indicates that the tubular transport maximum (Tm) for calcium had been exceeded. The relative clearances of sodium and potassium also increased after PTE; however, only the rise in CNa/CIn was significantly different from the controls. The glomerular filtration rate (CIn) also increased significantly after PTE, but this effect was transient and cannot explain the longer lasting effects of PTE on excretion of phosphate, calcium, or sodium.

Animals↗

Use of a hypobaric chamber as a model system for investigating ascites in broilers.

In a series of experiments, broilers were reared at simulated altitudes of 3000, 3500, and 5000 meters utilizing a hypobaric chamber. The purpose was to evaluate the chamber as a model for ascites syndrome and to further study the pathophysiology of this disease. Results show that this model can effectively reproduce the disease as it is seen in the field. Birds reared at the simulated altitude of 5000 meters had a statistically significant increase in EKG amplitude, packed cell volume, and heart-to-body-weight and lung-to-body-weight ratios when compared with controls reared at 366 meters. Additionally, there was a trend for birds dying of ascites to have larger-amplitude EKGs than survivors when reared at 5000 meters.

Altitude↗

An infectious bronchitis virus isolated from chickens experiencing a urolithiasis outbreak. I. In vitro characterization studies.

An infectious bronchitis virus (IBV) strain isolated from commercial layers experiencing urolithiasis was 50-100 nm in size and possessed widely spaced, club-shaped surface projections. It was sensitive to lipid solvents and exhibited responses characteristic of IBV when exposed to heat, divalent cations, and trypsin. Reciprocal virus-neutralization tests demonstrated it to be closely related to Gray, JMK, Delaware 2868, and Delaware 2897 strains of IBV.

Animals↗

An outbreak of avian urolithiasis on a large commercial egg farm.

A significant outbreak of avian urolithiasis was observed on a large commercial egg farm. From the initial outbreak site (a single laying house), the incidence of urolithiasis slowly spread in the ensuing months to numerous other laying houses. Increasing mortality associated with urolithiasis commenced during late growout to early lay and then leveled off when egg production peaked. At the height of the outbreak, mortality was typically 0.5% per week; 75% of this mortality was due to urolithiasis. The clinical and pathologic features of this condition are described. Both infectious bronchitis virus (IBV) and fowl adenoviruses were isolated from organ homogenates of sampled birds. A clone of the IBV strain was found to induce nephritis in specific-pathogen-free white leghorns.

Animals↗