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Biomedical subjects

J Meier

Publications and source records attributed to J Meier.

At least 127 records · Page 7Linked to original sources
PubMed1981

[Ultrasonic findings in renal diseases with hypertension (author's transl)].

Ultrasound investigations of the kidney were performed in a prospective study in 51 patients with hypertension. It was shown by means of characteristic changes that renovascular and renal parenchymatous diseases can be differentiated. The case of renal atrophy could be demonstrated in 14 out of 20 cases with renovascular changes and in 15 out of 18 cases wtih primary renal parenchymatous disease. There were false positive results in two out of 13 cases of essential hypertension. The importance of intrarenal cysts in the aetiology of hypertension requires further investigation.

False Positive Reactions↗
PubMed1981

[Sonography in the evaluation of reduced function of kidney transplants (author's transl)].

Sonography of 58 kidney transplants has been performed in 56 patients and morphological alterations have been registrated. These results have been compared with clinical examination, blood samples and histological evaluation whenever possible. It is our opinion that certain sonographical phenomena exist, which make the rejection of kidney transplants most probable and even allow for differentiation of different degrees. We found a correlation of right results between sonography and final pathological diagnosis in more than 80% of our patients. Moreover sonography permits the diagnosis of ureteral obstruction or leakage.

Adolescent↗
PubMed1981

Pindolol: disposition and metabolism in rhesus monkeys after chronic treatment.

1. The absorption, distribution, excretion and metabolism of pindolol were studied in rhesus monkeys after a single oral dose of 2.5 mg/kg or 25 mg/kg and after a chronic treatment of 5 years at the same daily dosage. 2. The pharmacokinetic parameters were the same for animals which received pindolol for the first time, and animals which underwent the 5 years' chronic treatment. An elimination half-life of 1.5 to 1.9 h was estimated in plasma for unchanged pindolol. 3. The distribution pattern of unchanged pindolol determined fluorimetrically, as well as total 14C in the tissues, following administration of [14C]pindolol showed no difference between a single dose and 5 years of chronic treatment. No accumulation of pindolol or metabolites was detected in the tissues of chronically treated animals. A mean elimination half-life of 10h was evaluated in 21 organs. 4. Acutely dosed and chronically treated rhesus monkeys showed the same metabolic pattern in urine. There was no evidence for induction or inhibition of the metabolism of pindolol.

Animals↗
PubMed1981

An automated fluorimetric method for the determination of fluproquazone in plasma and urine.

A rapid and sensitive fluorimetric assay was developed for the quantitative determination of 4-(p-fluorophenyl)-1-isopropyl-7-methyl-2(1H)-quinazolinone(fluproquazone) in plasma and urine. The unchanged drug was extracted from alkalinized plasma or urine into n-heptane containing 0--1.5% isoamyl alcohol followed by a back extraction into 5 N HCl. After oxidation with potassium persulfate the fluorescence measurements were taken at 326 nm excitation and 520 nm emission. Detection limits were about 15 ng/ml plasma and 6 ng/ml urine, using 1 ml plasma and 2 ml urine, respectively. The automated assay had a five times higher sample capacity and better reproducibility (+/- 3%) than the manual assay (+/- 5%). The method was applied to animal studies including assays in milk and proved to be suitable in human studies after oral doses in the therapeutical range.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1979

Mutagenicity and metabolism of dimethylnitrosamine and benzo[alpha]pyrene in tissue homogenates from inbred Syrian hamsters treated with phenobarbital, 3-methylcholanthrene or polychlorinated biphenyls.

There are significant differences between mice and hamsters in polycyclic hydrocarbon and nitrosamine metabolism. Homogenates of liver, lung and intestinal mucosa from 6 strains of Syrian golden hamster were compared for their ability to metabolize benzo[alpha]pyrene (BP) and dimethylnitrosamine (DMN) to mutagens. Females of strains MHA/SSLak, LSH/SlLak, CB/SsLak, PD4/Lak LHC/Lak and Lak:LVG (SYR) were either untreated or received phenobarbital (PB), 3-methylcholanthrene (MC) or polychlorinated biphenyls (AR) to induce drug-metabolizing enzymes. Salmonella typhimurium TA92 and TA98 were used as indicators of the formation of mutagans. Dimethylnitrosamine demethylase (DMND) was assayed using 1 mM DMN as substrate. Aryl hydrocarbon hydroxylase (AHH) was measured using benzo[alpha]pyrene as substrate. MC does not induced AHH activity in hamster liver, but is an excellent inducer of enzymes converting BP to mutagens. This lack of correlation between increased AHH activity and increased metabolism of BP to mutagen in liver is in marked contrast to correlations seen in mice. MC induces AHH in hamster lung and intestinal mucosa. AR induces AHH in liver, lung and intestinal mucosa. Activity of DMND in liver is not affected by treatment of hamsters with BP or AR, but is repressed approx. 30% by treatment with MC. Activity of DMND and conversion of DMN to mutagen are correlated (r = 0.59) in hamster liver. Microsomes of hamster liver are more effective than those from mouse in converting DMN to mutagen, despite similar DMND activities in livers from the two species.

Animals↗
PubMed1979

Comparison of the in vitro mutagenicity and metabolism of dimethylnitrosamine and benzo[a]pyrene in tissues from inbred mice treated with phenobarbital, 3-methylcholanthrene or polychlorinated biphenyls.

Homogenates of liver, lung, kidney, stomach, small intestine and colon from 8 strains of mice were compared for their ability to metabolize benzo[a]pyrene (BP) and dimethylnitrosamine (DMN) to mutagens. Females of strains CF1, AKR/J, AU/SsJ, DBA/2J, SWR/J, A/J, C3H/HeJ, and C57BL/6J were either untreated or received phenobarbital (PB), 3-methylcholanthrene (MC) or polychlorinated biphenyls (AR) to induce drug-metabolizing enzymes. The effects of these drugs on organ weight and on the amounts of DNA, S-10 protein, and microsomal protein per unit weight of tissue are reported. Salmonella typhimurium TA92 and TA98 were used as indicators of the formation of mutagens. For each organ there was an optimal balance between amount of tissue homogenate and concentration of test compound for maximal yield of revertants. A sensitive radiometric assay of DMN demethylase (DMND) is described which permits measurement of the enzyme in liver, lung and kidney. DMN at 1 mM is used as substrate. Aryl hydrocarbon hydroxylase (AHH) was measured in all tissue using BP as substrate. AR and MC are very good inducers of AHH activity in livers of mice classified as aromatic hydrocarbon responsive, but not in those classified as hydrocarbon nonresponsive. Responsiveness is strain-specific and genetically regulated. Metabolism of BP to mutagens by liver homogenates was correlated with extent of AHH induction. This dimorphism of response of AHH to inducers was present, but less pronounced, in non-hepatic tissues. Basal activities of AHH and DMND were correlated in livers and lungs from untreated mice. DMND activities were increased less than 2-fold by PB, MC or AR treatments. Metabolism of DMN to mutagens was not closely correlated with DMND activities. Strain of mouse, type of tissue and test substance are important variables in assessing the potential effect of microsomal enzyme-inducing agents on the metabolism of mutagenic substances.

Animals↗
PubMed1979

Effect of acute alcohol intoxication on the metabolism and plasma kinetics of chlordiazepoxide.

1. The metabolism and plasma kinetics of chlordiazepoxide have been determined in a group of volunteers and in a group of patients with acute alcohol intoxication. 2. Using the SAAM 26 non-linear least squares fitting programme, all chlordiazepoxide plasma concentration v time data following oral administration could be analysed in terms of a one-compartment open model with metabolic conversion of chlordiazepoxide to desmethylchlordiazepoxide. 3. Acutely intoxicated patients showed a prolonged elimination of chlordiazepoxide and a reduced clearance when compared with alcohol-free volunteers. The elimination of desmethylchlordiazepoxide, on the other hand, appeared to be faster in the alcoholics. 4. Alcohol exerts significant effects on the metabolism of chlordiazepoxide in acutely intoxicated patients.

Adult↗
PubMed1978

[Permeability of hydrogel plastics (PHEMA) to different substances of corneal metabolism (author's transl)].

With a new two-chamber apparatus for diffusion measurements, the permeability of Poly (2-hydroxy-ethyl-methacrylate) (PHEMA) is determined for metabolites of the corneal metabolism. Except for ATP, all substances tested, including several amino acids, penetrated the PHEMA material. Compared to the corneal stroma, the permeability of PHEMA is relatively low. Therefore, intracorneal implants of this hydrogel should be as thin as possible.

Acrylates↗
PubMed1978

The application of HPLC to the determination of some 1,4 benzodiazepines and their metabolites in plasma.

1 A high pressure liquid chromatographic (HPLC) assay has been developed for the measurement of chlordiazepoxide and its metabolites, N-desmethylchlordiazepoxide and demoxepam in microgram concentrations in human plasma. 2 Another metabolite was detected in appreciable amounts in the plasma from patients receiving high doses of chlordiazepoxide after the first 3 days of treatment. 3 Preliminary studies would indicate that this metabolite is N-desmethyldiazepam. 4 A modified HPLC system, using a microparticulate column was developed to separate N-desmethyldiazepam from chlordiazepoxide and its other metabolites in plasma.

Benzodiazepines↗
PubMed1978

The distribution of proquazone and three of its metabolites in serum and synovial fluid.

In 13 patients with hydrarthrosis of the knee, samples of synovial fluid and blood were drawn at regular intervals, following a single oral dose of 600 mg proquazone. The concentrations of the unchanged drug were measured fluorimetrically and those of its three principal, active metabolites by high pressure liquid chromatography. The absorption and distribution of proquazone and its metabolites were rapid. Measurable--in some cases considerable--concentrations were to be found in both the synovial fluid and serum as early as 30 minutes after intake. High concentrations were still present up to 7 hours after intake. Considerable variations were observed, both between patients and over time for each patient, so that only qualitative rather than quantitative kinetic conclusions could be drawn from the results. The concentrations were generally lower in the synovial fluid than in the serum, which may be ascribed to the drug's high protein binding.

Administration, Oral↗