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Biomedical subjects

D W Hamar

Publications and source records attributed to D W Hamar.

At least 19 recordsLinked to original sources

Sulphide-induced polioencephalomalacia in lambs.

Polioencephalomalacia (PEM) was induced in four of 10 lambs by the administration of a sulphide solution into the oesophagus at 20 min intervals for a period of 40 to 120 min. Signs of neurological dysfunction occurred in all 10 lambs during that time and included stupor, visual impairment and seizures. Gross autofluorescent and microscopic lesions in cerebrocortical grey matter were present as soon as 20 h after sulphide administration and were indistinguishable from lesions in naturally occurring disease. These findings, when considered together with an earlier study that revealed an association between high ruminal concentrations of sulphide and PEM, indicate that this disease can result from sulphide toxicosis, independent of the metabolic status of thiamine.

Administration, Oral

Effect of dietary phosphoric acid supplementation on acid-base balance and mineral and bone metabolism in adult cats.

Experimental evidence indicates that maintenance of urinary pH < or = 6.4 is the single most effective means of preventing feline struvite crystalluria or urolithiasis of noninfectious causes. This may be accomplished by dietary acidification, but must be moderated to avoid potential adverse effects of excessive acidification, including bone demineralization, negative calcium balance, potassium depletion, and renal disease. Effects of chronic dietary phosphoric acid supplementation on acid-base balance and on mineral and bone metabolism were investigated in adult, domestic cats. One group of 6 cats was fed a basal, naturally acidifying diet without added acidifiers, and another group of 6 cats was fed 1.7% dietary phosphoric acid. Changes observed during 12 months of study included development of noncompensated metabolic acidosis, increased urinary calcium excretion, and lower but positive calcium balance in cats of both groups. Urinary pH decreased in cats of both groups, but was significantly (P < 0.05) and consistently maintained < or = 6.4 in cats given dietary phosphoric acid. Urinary phosphorus excretion increased in cats of both groups, but was significantly (P < 0.05) greater in phosphoric acid-supplemented cats, leading to lower overall phosphorus balance as well. Potassium balance decreased in cats of both groups, but was only transiently negative in the phosphoric acid-supplemented cats midway through the study, and normalized at positive values thereafter. Plasma taurine concentration was not affected by dietary acidification, and remained well within the acceptable reference range for taurine metabolism. Double labeling of bone in vivo with fluorescent markers was followed by bone biopsy and histomorphometric measurement of several static and dynamic variables of bone formation. Overall indices of bone formation decreased in cats of both groups with age and confinement, but were not affected by dietary phosphoric acid supplementation. Dietary supplementation with phosphoric acid used as the principal inorganic P source to achieve moderate and stable degree of urinary acidification, did not appear over the course of 1 year, to have induced adverse effects on mineral, bone, or taurine balance in these adult domestic cats.

Acid-Base Equilibrium

Taurine depletion and cardiovascular disease in adult cats fed a potassium-depleted acidified diet.

Although low plasma taurine concentrations have been associated with congestive cardiomyopathy in cats, the cause of taurine depletion in cats consuming adequate quantities of taurine is unknown. Taurine depletion and cardiovascular disease (cardiomyopathy and thromboembolism) developed unexpectedly in 3 of 6 healthy adult cats during a potassium-depletion study. Plasma taurine concentration decreased significantly (P less than 0.05) and rapidly over an 8-week period (from 98 to 36 nmol/ml) in 6 cats that consumed a potassium-deficient diet (0.20% potassium, dry matter basis) that was acidified with 0.8% ammonium chloride, despite containing dietary taurine concentrations (0.12% dry matter basis) in excess of amounts currently recommended. Taurine concentrations were significantly lower in cats fed the acidified diet than in 6 cats fed a potassium-deficient diet that was not acidified (36 nmol/ml vs 75 nmol/ml) after 8 weeks. In addition, plasma taurine concentrations did not decrease over a 6-month period in 8 cats that were fed a potassium-replete diet with acidifier. Plasma taurine concentrations were lowest in 3 cats that died of cardiovascular disease in the group receiving potassium-deficient, acidified diets. These data indicated an association between taurine and potassium balance in cats and suggested that development of taurine depletion and cardiovascular disease may be linked to concurrent potassium depletion.

Ammonium Chloride

Bioelectrical impedance and zoometry for body composition analysis in domestic cats.

Zoometric measurements and bioelectrical impedance analysis were evaluated as methods of body composition determination in healthy cats. Zoometric and impedance measurements were taken on 22 anesthetized adult cats of various ages, genders, breeds, and body weights. The cats were then euthanatized. The bodies were processed through a tissue homogenizer and free-catch specimens were taken, freeze-dried, and analyzed for total body water, protein, fat, potassium, and ash content. Stepwise regression analysis was implemented to identify statistically significant relationships between the chemically determined dependent variables (total body water, protein, potassium, fat-free mass, fat mass, and percent body fat) and the zoometric measurements, with or without bioelectrical impedance analysis. Statistical analysis revealed high correlations between the dependent variables and the corresponding predicted values of those variables. Body weight alone was a poor predictor of body composition in these cats. On the basis of these findings, we suggest that zoometric and bioelectrical impedance measurements may serve as practical, noninvasive, simple, and accurate methods for estimating body composition in domestic cats.

Animals

Screening of anionic salts for palatability, effects on acid-base status, and urinary calcium excretion in dairy cows.

Six anionic salts [MgCl2.6H2O, MgSO4.7H2O, CaCl2.2H2O, CaSO4.2H2O, NH4Cl, and (NH4)2SO4] were evaluated for their effects on dietary DM intake, systemic acid-base balance, and urinary excretion of Ca. Each of the six salts was fed to 12 nonlactating, nonpregnant Holstein cows for 1-wk periods in two replicates of a 6 x 6 Latin square design. All salts were fed at the rate of two equivalents cow-1 d-1. Anionic salt treatments did not decrease DM intake compared with the control diet fed without salts. Blood pH was not affected by any of the salt treatments; however, mild, compensated metabolic acidosis was evidenced by decreased blood bicarbonate concentrations and decreased blood base excess when any of the salts was fed. Urinary pH and urinary base excess also were lowered by all of the salts. Fractional excretion of urinary Ca was increased by all salt treatments. All six anionic salts tested were of similar value in their acidifying effects and in their ability to increase urinary excretion of Ca.

Acid-Base Equilibrium

High sulfide concentrations in rumen fluid associated with nutritionally induced polioencephalomalacia in calves.

Nine 115- to 180-kg, hay-adapted, Holstein steers were fed an experimental diet with added sodium sulfate that induces polioencephalomalacia (PEM). Five calves developed the disease. Thiamine concentrations in blood, CSF, brain, and liver were not indicative of thiamine deficiency. The odor of hydrogen sulfide in eructated rumen gas was associated with the onset of PEM. Sulfide concentrations in rumen fluid were measured 1 or 2 times a week by 2 techniques. Sulfide concentrations progressively increased in all 9 calves after the feeding of the PEM-inducing diet commenced. The highest concentrations coincided with the onset of clinical signs of PEM and were significantly higher in the calves that developed PEM than in those that did not. This suggests that PEM can result from sulfide toxicosis following excess production of sulfide in the rumen.

Animals

Effects of dietary acidification and potassium depletion on acid-base balance, mineral metabolism and renal function in adult cats.

Effects of dietary potassium restriction, with or without dietary acidification, on acid-base balance, mineral metabolism and renal function were evaluated in 12 adult cats. Six cats were fed a potassium-restricted diet (0.2% potassium) for 8 wk, and six cats were fed the same potassium-restricted diet plus a dietary acidifier (0.8% NH4Cl) for 8 wk. Both groups of cats were then fed the same diet supplemented with potassium gluconate (0.7% dietary potassium) for an additional 4 wk. Renal function was evaluated before treatment and again at 8 and 12 wk. Serum potassium concentration declined in all cats by wk 1 and was also lower in NH4Cl-treated cats at 2, 3, 6 and 8 wk than in control cats. Metabolic acidosis developed in both groups of cats. Dietary balance studies indicated negative potassium balance in NH4Cl-treated cats. Glomerular filtration rate declined significantly in NH4Cl-treated cats after 8 wk but was unchanged in control cats. From the results of this study, we conclude that adding a dietary acidifier to a potassium-restricted diet worsens hypokalemia, possibly by affecting gastrointestinal potassium handling, and induces severe metabolic acidosis and renal dysfunction in adult cats.

Acidosis, Renal Tubular

Clinical and biochemical alterations in calves with nutritionally induced polioencephalomalacia.

Polioencephalomalacia (PEM) was induced in calves by feeding a semipurified, low-roughage diet of variable copper and molybdenum composition. Two formulations resulting in Cu-insufficient and Cu-sufficient forms of the diet were fed (n = 10 and 4 calves, respectively); both diets induced PEM. Clinical signs of disease developed as early as 15 days after transition to the experimental diets and included impaired vision, decreased response to external stimuli, and abnormal gait. Grossly evident cerebrocortical lesions consisted of laminar areas of cavitation and/or autofluorescence seen under UV illumination. Hepatic Cu concentration was decreased in calves fed the Cu-insufficient diet, but not below normal range. During the course of feeding either diet, rumen pH decreased, rumen volatile fatty acid concentrations increased, rumen and blood lactic acid concentrations increased, and rumen and plasma thiamine concentrations increased. The thiamine pyrophosphate effect on erythrocyte transketolase activity was unaltered in calves of either diet group. This nutritionally induced form of PEM does not appear to be related to Cu deficiency or reduction in plasma or rumen thiamine concentration.

Animals

Method comparison for calcium determination by flame atomic absorption spectrophotometry in the presence of phosphate.

We investigated the suppressive effects of phosphate on calcium determinations with lanthanum-air/acetylene and potassium-nitrous oxide/acetylene methods, and we evaluated the ability of these methods to meet the suggested analytical goals for urine samples. The 20 g/L La-air/acetylene method was the most nearly accurate for predicting the actual calcium concentrations (t-test value = -0.042), followed by the 2 g/L K-nitrous oxide/acetylene method (t-test value = 0.450), 10 g/L La-air/acetylene (t-test value = -0.733), and finally 5 g/L La-air/acetylene (t-test value = -2.446). The dilution used significantly influences the apparent calcium concentration measured with the La-air/acetylene methods.

Animals

4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs.

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.

Animals

The effect of chronic dietary acidification using ammonium chloride on acid-base and mineral metabolism in the adult cat.

Adult cats with normal renal function were fed a nutritionally balanced, vitamin A-replete, experimental dry diet with or without ammonium chloride (NH4Cl) for 6 mo to study the effects of chronic dietary acidification on acid-base parameters and the metabolism of selected minerals. Dietary balance studies were performed monthly. Blood and urine samples were collected monthly to evaluate acid-base parameters, plasma parathyroid hormone (PTH) and 1.25-dihydroxycholecalciferol levels. Ammonium chloride-treated cats had significantly lower blood and urinary pH, and lower blood bicarbonate concentrations. Treated cats also had higher blood ionized calcium concentrations, hypercalciuria and lower intestinal calcium absorption relative to baseline (prior to feeding the experimental diet) and to control cats. This resulted in the development of lower calcium balance in the first several months. PTH levels were unaffected by dietary acidification; however, 1.25-dihydroxycholecalciferol levels were significantly decreased in treated cats. Treated cats had negative potassium balance during 5 mo of dietary acidification. Magnesium, sodium, and phosphorus balances were lower, but positive, in treated cats compared to control cats. Cats consuming the NH4Cl-supplemented diet had increased chloride balance. Thus, chronic dietary acidification with 1.5% NH4Cl produced chronic metabolic acidosis and lower or negative, calcium and potassium balance.

Acid-Base Equilibrium

Comparative effects of captopril and enalapril on the progression of chronic renal disease in partially nephrectomized rats.

Comparative effects of the angiotensin converting enzyme inhibitors captopril and enalapril on progression of chronic renal disease was studied in 3/4 nephrectomized rats. Rats were divided into sham and nephrectomized groups, and treated with plain water or water containing captopril (150 mg/liter) or enalapril (50 mg/liter). Evaluations were made 4 weeks before and 0, 4, 8, and 10 weeks after nephrectomy. Endogenous creatinine clearance decreased in drug-treated, nephrectomized rats to values less than sham controls, but remained greater than water-treated rats. Significant (P less than 0.05) proteinuria developed 4 weeks post-nephrectomy in water-treated rats, 8 weeks post-nephrectomy in captopril-treated rats, but did not develop in enalapril treated rats. Regression analysis of carbamylated plasma protein values vs plasma creatinine revealed significant (P less than 0.05) relationships only in the water-treated, nephrectomized rats from weeks 0 through 8, but were otherwise unaffected by treatment. Both drugs resulted in significantly (P less than 0.05) improved scores for renal histologic lesions as compared to water treatment. Modifications of proteinuria in captopril and enalapril-treated rats occurred prior to onset of changes in systolic blood pressure, which was significantly elevated only in water-treated, nephrectomized rats at weeks 8 and 10. We conclude that angiotensin converting enzyme inhibitors may ameliorate progression of experimental renal disease through intrarenal effects, independent of modulation of systemic blood pressure, and that enalapril may be superior to captopril in some regards.

Animals

Kochia scoparia oxalate content.

Kochia scoparia was collected periodically during the growing seasons of 1984, 1985 and 1986. The 10, 16 and 16 samples, respectively, from these years were air dried, hammer milled and analyzed at a later date for soluble and total oxalates. An additional 6 samples from New Mexico were analyzed from the 1987 growing season. A maximum of 4.7% soluble oxalates and 11.4% total oxalates were present in 1986 Colorado kochia following heavy rainfall. This concentration of soluble oxalate could cause chronic oxalate poisoning (alkalosis) in cattle.

Oxalates

Potassium depletion in cats: renal and dietary influences.

Excessive urinary potassium loss was diagnosed in 7 cats with persistent hypokalemia and high serum creatinine concentrations. Renal tubular acidosis (proximal or distal) was not evident in the affected cats. Plasma aldosterone concentrations and plasma renin activities in affected cats were not significantly different from control values. Potassium depletion and hypokalemia were attributed to the combined effects of decreased dietary potassium intake and excessive urinary potassium losses. It was concluded that increased urinary potassium excretion may represent a basic response to renal dysfunction in cats. Data suggested that dietary potassium supplementation improved renal function in most cats in this study.

Acidosis, Renal Tubular

Cecal short-chain fatty acids in experimental rabbit mucoid enteropathy.

Short-chain fatty acid concentrations were measured in the cecal contents of 9 healthy rabbits and 20 rabbits with experimentally induced mucoid enteropathy. In control rabbits, cecal concentration of acetate was the most abundant, followed by that of butyrate and propionate--a feature distinguishing rabbits from most other mammals. In mucoid enteropathy, cecal acetate and butyrate concentrations were lower, whereas propionate, isobutyrate, valerate, and isovalerate were increased. The results indicated that there were abnormal fermentation and cecal maldigestion in rabbits with mucoid enteropathy.

Acetates

Brain enzyme and clinical alterations induced in rats and mice by nitroaliphatic toxicants.

The effects of a single subcutaneous (s.c.) injection of the nitroaliphatic toxicants 3-nitropropanol (NPOH) and 3-nitropropionic acid (NPA) dissolved in physiological saline solution were studied in mice and rats, respectively. Clinical signs observed in both NPOH-treated mice and NPA-treated rats included depression, abnormal motor activity, and recumbency. Succinate dehydrogenase (SDH) activity, demonstrated histochemically in frozen brain sections, was markedly reduced in intoxicated mice and rats. The SDH activity of mitochondrial preparations from brains of intoxicated mice and rats was diminished to 18-24% of control values, although the activity of another mitochondrial flavoprotein enzyme, alpha-glycerophosphate dehydrogenase (alpha-GPDH), was not altered.

1-Propanol

A comparative study of ketone body metabolism between the camel (Camelus dromedarius) and the sheep (Ovis aries).

1. Plasma levels of beta-hydroxybutyrate (BHB), and acetoacetate (AcAc) have been measured in camels (Camelus dromedarius) and sheep (Ovis aries). The activity of beta-hydroxybutyrate dehydrogenase (BHB-deH2) (E.C. 1.1.1.30) was studied in the rumen epithelium and the liver of these animals. 2. Concentrations of plasma BHB and AcAc in the camel were in respective order 33 and 4 times lower than that of the sheep. The ratios of BHB to AcAc were 0.61 and 4.8 for the camel and sheep, respectively. 3. The activity of BHB-deH2 in the rumen epithelium of the camel and sheep were 7.15 and 66 mumol/hr/g wet wt tissue, respectively. The activity in both species was higher in the rumen epithelium than in the liver.

Acetoacetates