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J Harmeyer

Publications and source records attributed to J Harmeyer.

At least 37 records · Page 2Linked to original sources
PubMed1986

[The quantitative determination of vitamin D3 and its metabolites in plasma].

A method is described which enables determination of vitamin D3 and its physiologically most important metabolites, i.e. 25-OHD3, 24,25-(OH)2D3, 25,26-(OH)2D3 and 1,25-(OH)2D3 in a plasma sample of about 2 to 4 ml. The whole procedure involves two preparative and one analytical steps: Extraction with methanol/methylene chloride (2:1), chromatographic separation on Lipidex 5000 using a stepwise gradient of n-hexane and chloroform and finally HPLC separation on Zorbax-Sil columns with n-hexane isopropanol mixtures and subsequently reversed phase separation on RP 18-columns and mixtures of methanol and water. Except for 1,25-(OH)2D3 all D compounds were quantified by UV-detection with 1.4 ng of substance being the lowest detectable amount. 1,25-(OH)2D3 was measured by radioimmunoassay. Prior to HPLC analysis the extract was separated into three fractions on Lipidex 5000 which contained 1) vitamin D3, 2) 25-OHD3 and 3) the dihydroxy metabolites. The three fractions were separated by HPLC using different mixtures of isopropanol/n-hexane and methanol/water, respectively. Retention times of the individual D-components longer than 10 min appeared to be essential to separate these compounds from accompanying material. Overall recoveries of the individual metabolites were for vitamin D3 48.9%, for 25-OHD3 54.2%, for 24,25-(OH)2D3 50.9% and for 1,25-(OH)2D3 52.5%. Application of the methods to plasma samples from pigs with pseudovitamin D deficiency rickets, typ I, revealed a reduced concentration of 1,25-(OH)2D3 and 24,25-(OH)2D3 and an elevated level of 25-OHD3 in these animals. The results obtained by this method contributed substantially to a better understanding of the aetiological factors associated with this disease.

Biotransformation↗
PubMed1980

Glucocorticoid levels in blood plasma of normal and preketotic cows.

Twenty pregnant cows were kept in two feeding groups. Feeding regimens were designed to induce high milk production (16 kg milk/day) in group I and low production (2 kg/day) in group II. Milk weights were corrected for fat content. After onset of lactation, each cow was fed according to actual production level. Four cows from group I and two from group II developed clinical ketosis during the first few weeks of lactation. Blood taken weekly from all animals from about 2 weeks before until an average of 7 weeks after parturition was assayed for glucocorticoids, glucose and ketone bodies. Average plasma cortisol concentration for both groups was 4.5 +/- 2.6 ng/ml (range from 0 to 13 ng/ml). Plasma cortisol levels in cows which later developed clinical ketosis were not different from those in cows that remained healthy. There was, however, a positive correlation between blood glucose and plasma cortisol, and a negative correlation between blood ketone bodies and plasma cortisol. The findings suggest that adrenal cortical activity is interrelated with onset of ketosis although plasma cortisol levels appear unsuitable for identifying ketotic cows prior to clinical manifestation of the disorder.

Acidosis↗
PubMed1980

Thiamin balance in the gastrointestinal tract of sheep.

Six 5- to 6-month-old sheep fitted with rumen fistulas and reentrant cannulas in the duodenum and in the ileum were adapted to two dies low in thiamin and containing different percentages of urea nitrogen. The sheep were subjected to seven thiamin balance experiments, with continuous feeding and total collection of duodenal and ideal contents and feces for periods of 6 day each. Thiamin and dry matter were determined in aliquots of collected digesta and feces. Daily thiamin intake was always less than .3 mg, but average daily flow of thiamin into the duodenum was between 1.53 and 3.46 milligrams. Microbial net synthesis of thiamin in the forestomach system was between 1.44 and 3.23 mg/day, so 90 to 96% of thiamin entering the duodenum was of microbial origin. Disappearance of thiamin from the small intestines approximately equaled thiamin net synthesis in the forestomachs, indicating high absorption of microbially produced thiamin. In five experiments, thiamin balance in the large intestines was positive, but no measurements were made of thiamin breakdown within, and absorption from, the large intestines.

Animals↗
PubMed1980

Aspects of urea metabolism in ruminants with reference to the goat.

In goats and other ruminants, urea functions as a source of nitrogen for protein biosynthesis in the digestive tract. Ammonia can be absorbed in the digestive system when formed in excessive quantitites and enhance formation of urea, or it can be derived from urea of blood plasma when its formation from feed sources is small. Entry rates of urea into plasma may vary from 4 to 80 mumol/min per kg.75 body weight depending on dietary conditions. Urea formation is related to nitrogen intake of which approximately 70% passes into the urea pool of plasma. Irreversible losses of urea of plasma into the digestive tract vary between 10 and 90% depending on the protein to energy ratios of the diet. Entry of urea from plasma into the rumen appears to be a passive process which is sensitive to short-term changes of urea concentrations in plasma. Permeability of ruminal epithelium to urea may be altered by fermentation products of rumen (ammonia, carbon dioxide, volatile fatty acids). The influx of nitrogen into the rumen is related to needs for nitrogen of microbial populations and is associated with changes of renal excretion and tubular reabsorption of urea. Combined gastrointestinal and renal responses exert a synergistic effect on improved utilization of urea of plasma when uptake of dietary nitrogen is limited in goats and other ruminants.

Animals↗
PubMed1979

Effect of hyperammonaemia on blood glucose and plasma insulin levels in sheep.

The effects of continuous intravenous infusions (6 h) of ammonium chloride (5.6; 11.2; and 16.8 mumol.kg-1.min) on plasma glucose and immunoreactive insulin (I.R.I.) levels were studied in three adult sheep. Infusions of 5.6 and 11.2 mumol.kg-1.min elevated ammonia levels in circulating blood from 100 to 150 and 300 microgram.100 ml-1, respectively, but showed no appreciable effect on plasma glucose and I.R.I. concentrations. Infusion of 16.8 mumol.kg-1.min-1 resulted in a blood ammonia concentration of about 400 microgram.100 ml-1 after six hours of infusion. Blood ammonia returned to normal 1 to 2 hours after the end of infusion. Plasma glucose concentration tended to increase slightly from 65 to 75 mg . 100 ml-1 when 16.8 mumol of NH4Cl were infused kg-1.min-1 and remained at the elevated level at least for two additional hours when ammonia infusions were stopped. Plasma I.R.I. tended to decrease from 48 to 38 microunits . ml-1 during the time of the NH4Cl infusion and increased continually to 82 microunits . ml-1 when NH4Cl infusions were stopped. It is concluded from the time courses of plasma glucose and plasma I.R.I. that the effect of ammonia infusion of these parameters cannot entirely be explained by a regulatory release of adrenaline.

Ammonium Chloride↗
PubMed1979

Regulatory hyperparathyroidism in a pig breed with vitamin D dependency rickets.

A radioimmunoassay for porcine parathyroid hormone has been developed and applied to measure immunoreactive parathyroid hormone (PTH) in plasma of pigs with hereditary vitamin D dependency rickets (VDDR) (pseudovitamin D deficiency rickets). Levels of 25-hydroxycholecalciferol (25-(OH)-D3) in plasma were measured by a protein binding assay. Both plasma concentrations of PTH and 25-(OH)-D3 showed an approximately 4-fold increase compared to normal pigs. PTH levels increased with duration of the disease. Daily dosing of the animals with 1--4 micrograms of 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) reduced PTH concentrations and resulted in clinical healing. Iv administration of 10 micrograms of 25-(OH)-D3/day did not alter PTH concentrations nor the clinical symptoms. The results suggest that these animals suffer from regulatory hyperparathyroidism. The metabolic defect could be due to a failure of the kidney to convert 25-(OH)-D3 to 1,25-(OH)2-D3.

Animals↗