Search

Your search keyword '"Freundt, K. J."' showing total 174 results
Start Over Author "Freundt, K. J."
174 results on '"Freundt, K. J."'

11. Referate

Author

Lochner, W., Aubert, X., Bachmann, G. W., Bauereisen, E., Baumann, Christian, Baust, W., Wittke, G., Behmann, F. W., Behrenbeck, D., Hensel, H., Betz, E., Bogenschütz, Standfuss, K., Boroffka, I., Braasch, D., Braasch, W., Braun, M., Müller-Limmroth, W., Brechmann, W., Brendel, W., Bromm, B., Brück, K., ten Bruggencate, H. G., Meves, H., Creutzfeldt, O., Deetjen, P., Deüticke, B., Döring, H. J., Doutheil, U., Düdel, J., Dunker, E., Eberlein, H. J., Eckert, P., Ehrenberger, K., Ehrenstein, W., Engel, H. -J., Fabel, H., Fredrickson, J. M., Kornhuber, H. H., Freundt, K. J., Gärtner, Walter, Gercken, G., Gerlach, E., Gertz, K. -H., Haas, H. G., Golenhofen, K., Grubel, G., Grüsser, O. -J., Haab, P., Haas, H. G., Haberich, F. J., Hahn, N., Haedegg, Wolfgang, Harth, O., Hauck, G., Heerd, E., Henatsch, H. -D., Hille H., Hlrche, H. J., Hirsch, H., Holzbauer, M., Iravani, J., Jacob, R., Jageneau, A. H. M., Pringle, J. W. S., Josenhans, W. T., Kanzow, E., Kaufmann, R., Kenner, Th., Waldhäusl, W., Kessler, M., König, Annemarie, Koepchen, H. P., Kornhuber, H. H., Kossow, K. -D., Kübler, W., Langhorst, P., Sharman, D. F., Leder, O., Leenders, H. J., Leeche, E., Llemann, F., Llndemann, B., Locker, A., Lübbers, D. W., Lutz, J., Creutzfeldt, O. D., Meissner, H. P., Messmer, K., Meurer, K. -A., Monnier, M., Dodt, E., Müller-Mohnssen, H., Nagel, W., Nlesel, W., Noell, W. K., Nowacki, P. E., Oelert, H., Ohnesorge, F. K., Pabst, H., Pavlović, V., Peiper, Ulrich, Peper, K., Pierau, F. -K., Piiper, J., Pohl, H., Popp, C., Poetzehl, H. P., Postma, N., Potthoff, P. C., Hensel, H., Witt, I., Raths, P., Reulen, H. -J., Röskenbleck, H., Rüegg, J. C., Schaper, W. K. A., Schildberg, F. W., Schirmer, R. H., Schmidt, G., Schmidt, H., Schmier, J., Schmidt, K., Schmidt, R. F., Schmidt, S. S., Schollmeyer, P., Scheorder, W., v. Skramlik, E., Spreng, M., Stange, G., Steinhausen, M., Stoboy, H., Straschill, M., Strauer, B. E., Thurau, K., Thürm, U., Trincker, D., Ulbricht, W., Varjú, D., Vatter, O., Vogel, G., Vogel, H. R., Wachsmuth, D., Waldeck, F., Creutzfeldt, O., Weichert, Weidinger, Wenzel, H. G., Westphal, W., Wetterer, E., Kenner, Th., Wiederholt, M., Wolff, G., and Zerbst, E.

Published
1964
Full Text
View/download PDF

37. Energy potential and hepatic function in rats under acute exposure to carbon disulphide

Author

Freundt, K. J. and Kürzinger, R.

Abstract

In adult female rats 8-hr exposure to 400 ppm CS2 did not produce a change in conventional liver function tests (SGOT, SGPT, and SLDH activities; BSP clearance in the bile). This would seem to imply that the severe inhibition of the hepatic mixed-function oxidases observed in earlier experiments after the same dose of CS2 is not attributable to generalized cell damage, but should rather be taken to represent a selective lesion. Eight-hr exposures of the experimental animals to graded CS2 concentrations ranging from 20 to 400 ppm triggered a rapidly reversible substantial depletion of the hepatic glycogen. A concurrent increase of the lactate and inorganic phosphate levels and also of the oxygen consumption was demonstrated, in conjunction with an increased respiratory uptake of oxygen by the exposed animals, a fall in body temperature, and a decrease of the serum potassium and calcium levels. These changes may be interpreted as an extensive defect in the energy supply in the liver cell. The concomitant slight decrease of the liver weight is largely explained by the disappearance of glycogen; a possible reduction of the water content could be excluded. The small increase in total liver protein, which was another finding, is attributable to a nonspecific stimulation of protein synthesis. The observed quantitative changes in the liver substance required balancing of the food ingested: following 8-hr inhalation of 100 or 400 ppm there was a marked reduction in body weight, intake of standard food and water, and fecal excretion, whereas slight increases were observed after 20 ppm over 8 hrs. These alterations are probably due to a disturbance of the diencephalic controlling mechanisms.

Published
1975
Full Text
View/download PDF

47. Inhaled tert-butyl acetate and its metabolite tert-butyl alcohol accumulate in the blood during exposure.

Author

Groth G and Freundt KJ

Subjects
Acetates blood, Administration, Inhalation, Animals, Female, Rats, Rats, Sprague-Dawley, tert-Butyl Alcohol, Acetates metabolism, Butanols blood, Solvents metabolism
Abstract

1. A continuous 5 h-exposure to approximately 440 ppm tert-butyl acetate in air (via a tracheal canule) resulted in continuously increasing concentrations of tert-butyl acetate and tert-butyl alcohol (metabolite of tert-butyl acetate) in the blood of rats. 2. This accumulation of tert-butyl acetate and tert-butyl alcohol was reproduced during a continuous exposure to about 900 ppm tert-butyl acetate in air over a period of 4 h and 15 min. After the inhalation approximately 50% of the blood level of tert-butyl acetate decreased within 45 min, but that of tert-butyl alcohol remained unchanged at a high level. 3. The accumulation of tert-butyl acetate and tert-butyl alcohol should be relevant for the health risk assessment at the workside.

Published
1994
Full Text
View/download PDF

48. The karyotype of the zebrafish (Brachydanio rerio).

Author

Schreeb KH, Groth G, Sachsse W, and Freundt KJ

Subjects
Animals, Karyotyping, Zebrafish genetics
Abstract

Fertilized eggs of the age of 24 hr from the zebrafish (Brachydanio rerio) were examined. The number of chromosomes is 2n = 50. The size of a metaphase chromosome is 1.5-2 microns. The karyogram of the zebrafish is characterized by metacentric and submetacentric, but only few acrocentric chromosomes.

Published
1993

49. [Blood alcohol in relation to the presence of n-butyl acetate].

Author

Groth G and Freundt KJ

Subjects
Animals, Female, Metabolic Clearance Rate physiology, Rats, Rats, Inbred Strains, Acetates pharmacokinetics, Alcoholic Intoxication blood, Ethanol pharmacokinetics
Abstract

Adult female SPF rats (strain: Sprague-Dawley) were treated with 790 mg ethanol/kg body weight by intraperitoneal injection 30 minutes after the beginning of a 5-hr-inhalation of about 1,000 ppm n-butyl acetate in air via a tracheotomy tube (under urethane anesthesia). The elimination of the ethanol from blood which was increased to about 24 mmol/l (1.1%, g/v) was not delayed during the initial linear phase as compared to control (ethanol treatment without inhalation of n-butyl acetate). During inhalation approximately 24 mumol n-butyl acetate/l were measured in blood without ethanol treatment and approximately 52 mumol n-butanol/l as a metabolite of n-butyl acetate. The n-butanol content in blood was doubled under ethanol treatment. This increase is explained by substrate competition of both alcohols at the alcohol dehydrogenase with ethanol excess.

Published
1991

50. Ferrous sulfate combined with ascorbic acid does not significantly reduce acetaldehyde accumulation in the blood of alcoholized rats treated with disulfiram or betalactam antibiotics.

Author

Freundt KJ, Heiler C, and Schreiner E

Subjects
Animals, Anti-Bacterial Agents adverse effects, Ascorbic Acid therapeutic use, Disulfiram adverse effects, Drug Interactions, Ethanol adverse effects, Female, Ferrous Compounds therapeutic use, Lactams, Rats, Rats, Inbred Strains, Acetaldehyde blood, Anti-Bacterial Agents pharmacology, Ascorbic Acid pharmacology, Disulfiram pharmacology, Ethanol pharmacology, Ferrous Compounds pharmacology
Abstract

Adult female SPF Sprague-Dawley rats treated orally by gavage with disulfiram (1 g/kg b.wt.) or betalactam antibiotics (3.38 mmol/kg b.wt.) with a 1-methyltetrazole-5-thiol side chain (cefmenoxime, latamoxef, cefotetan, cefoperazone, cefamandole) produced a marked, statistically significant rise of acetaldehyde in the blood 1 and 3 hr following IP administration of ethanol [2 g/kg b.wt., 20% (g/v) solution]. This accumulation of blood acetaldehyde remained unchanged or was reduced only very slightly by a mixture of iron sulfate [Fe(II)SO4.7H2O, 2.64 mg/kg b.wt.] and ascorbic acid (6.67 mg/kg b.wt.) injected intravenously. This slight decrease is considered to be due to a formation of a complex between ferrous sulfate and agents (disulfiram and the betalactam antibiotics as well as their metabolites) producing acetaldehyde by inhibition of acetaldehyde metabolizing enzymes. A possible coaction of ascorbic acid cannot be explained satisfactorily; ascorbic acid may support cellular redox potentials. The combination of ferrous sulfate and ascorbic acid was used for examination since both chemicals are recommended to reduce adverse symptoms of an ethanol incompatibility reaction in the course of a therapy with the mentioned antibiotics or disulfiram. Since acetaldehyde augmentation in the blood is regarded as a cause of complaints and because the acetaldehyde rise was not depressed significantly by ferrous sulfate and ascorbic acid it can be concluded that these two agents are not potent enough for a rational therapy of ethanol incompatibility symptoms initiated by the investigated drugs.

Published
1990
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results