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Biomedical subjects

B Schulze

Publications and source records attributed to B Schulze.

At least 127 records · Page 7Linked to original sources

[Biochemical investigations of cancer cachexia. II. Depletion of glycogenolysis and stimulation of gluconeogenesis in Walker carcinoma 256 bearing rats (author's transl)].

150-200 g heavy, Walker-carcinoma bearing, male Sprague-Dawley-rats showed rapid, tumour weight dependent, loss of liver glycogen until complete depletion in tumour groups heavier than 40 g/animal. Simultaneously the glycogen mobilization after massive glucagon stimulation, was successivly diminished and finally abolished in different groups with increasing tumor weight. Concomitantly the spontaneous and stimulated activity of liver phosphorylase a was found markedly reduced in advanced tumour cachexia, the extent of stimulation of liver phosphorylase a activity by intracardial injections of epinephrine not being altered. Tumour induced inhibition of glycogen mobilization thus appears to have been excluded. To account for the relative late pronounced hypoglycemia in peripherial rat blood in face of the early loss of liver glycogen, accelerated gluconeogenesis has been postulated. In accord with this spontaneous rise in liver tyrosine amino transferase was found in tumour bearing rats along with a doubled maximal stimulation value after medrol injection as compared to control groups. This behavior could not be shown for liver alanine aminotransferase and liver fructose 1,6-di-phosphatase. The former showed no differences between control and tumour groups neither of spontaneous nor of stimulated activity. The latter showed only a very reluctant rise after massive stimulation by triamcinolone for 3 days in the control groups, the tumour bearing groups showing no deviation from spontaneous control values.

Alanine Transaminase↗

[The effect of tri-iodinated contrast media on acetylcholinesterase of human erythrocytes (author's transl)].

The side effects of water soluble iodinated contrast media often mimic the clinical picture of acetylcholine intoxication. This prompted us to determine the amount of inhibition of human acetylcholinesterase by the following contrast media in vivo and in vitro: methyl glucamineiodipamide (Biligrafin forte), methylglucamine iothalamate (Conray 60), sodium-iothalamate (Conray 80). In vivo no correlation could be found between clinically manifest adverse reaction and enzyme inhibition after contrast media application. The in vitro values for 50% inhibition of erythrocyte acetylcholinesterase are: methylglucamine-iodipamide: 0.036 M, methylglucamine-iothalamate: 0.158 M, sodium-iothalamate: 0.3 M. Since in vitro, the maximal inhibitory effect of a given dose of contrast media can only be registered after a time interval when most of the contrast media in vivo has already been excreted by the kidneys or extracted by the liver, it seems very improbable that the enzyme inhibition seen in vitro should have any consequence whatsoever under clinical conditions. The in vitro inhibition of acetylcholinesterase is quickly reversible, with nearly all the activity regained 15 min after the removal of the contrast media.

Acetylcholinesterase↗