Biomedical subjects
Publications and source records attributed to G Seidel.
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A sensitive and specific method for the determination of vincamine in plasma is described. The molecular ion (m/e 426) and the parent peak (m/e 367) of the TMS derivative are assayed simultaneously by selected ion monitoring. Sensitivity is 30 pg ml plasma. The suitability of the method for pharmacokinetic studies is assessed by measuring plasma level profiles in six volunteers receiving 20 mg of vincamine orally.
The general toxic effects of coumarin, as well as coumarin hepatotoxicity were found to be less in DBA/2J mice than in CH3/HeJ mice. These results are discussed in the context of a strain-specific coumarin metabolism and indicate the need for suitable animal models to assess the toxicity of a given substance in man.
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In rats with lymphostatic encephalopathy the duration of harmine tremor was lengthened, and the brain concentrations of harmine decreased more slowly than in sham-operated controls. The tremor began simultaneously in both rat groups at coinciding brain concentrations of harmine. In rats with lymphostatic encephalopathy harmine concentrations in brain at the termination of tremor lay in the same range as in sham-operated controls. The plasma concentrations of harmine were not changed by the disease. It is concluded that during lymphostatic encephalopathy the lymphatic drug elimination from brain is impaired whereas--at least for harmine--the blood-brain barrier functions as normal.
In Wistar rats, combined treatment with ethanol or carbon tetrachloride and a mixture of coumarin and sodium salt of rutin sulphate (Venalot injectable solution) causes slight increases of some liver-specific enzymes in plasma. This effect was not observed in DBA/2 4-mice whose metabolism of coumarin is widely analogous to that of man. The LD50 for coumarin in those mice was twice that in rats. These results are discussed in the light of different metabolic pathways of coumartin in both species.
Treatment of 24 male patients with 3 g/day of xanthinol nicotinate did not change the in vitro measurements of ADP-induced platelet aggregation but produced a marked inhibition of collagen-induced platelet aggregation. This effect may be connected with the drug-induced depression of the ATP level in platelet-rich plasma. Changes in the platelets in the patients' blood or in the lipid composition and the concentration of uric acid in their serum were ruled out as reasons for the decrease of the collagen-induced aggregation. The activity of the three serum enzymes y-GT, GOT, and GPT and the concentration of the blood sugar did not change.
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In rats, pretreatment with caffeine or ethanol shortens the duration of the harmine tremor and decreases the brain concentrations of this alkaloid. Caffeine and ethanol do not influence the plasma concentration of harmine, its plasma protein binding and its cerebral concentration at the termination of the tremor. The findings are regarded as indicative of a reduction by caffeine and ethanol of the blood-brain barrier permeability to harmine.
In rats the hexobarbital metabolism is impaired after different surgical procedures leading to muscle damage. This leads to a prolongation of the hexobarbital action. The prolonged effect of hexobarbital in rats with lymphostatic encephalopathy is considered an unspecific consequence of the tissue damage during lymphectomy.
Injection of Epontol (7 mg/kg i.v.) to male healthy students caused a brief increase in plasma histamine concentration from 0.7 ng/ml to 3.0 ng/ml. Combined injection (7 mg/kg) and infusion of Epontol (21 mg/kg during 15 min) or combined injection of Epontol (7 mg/kg) and suxamethonium (0.5 mg/kg) caused a more prolonged appearance of histamine in plasma without higher maximum concentrations. During anaesthesia with ketamine (Ketanest), halothane or nitrous oxide the histamine concentrations in plasma remained unaltered.
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Injection of the tremorigenic alkaloid harmine into lymphostatic encephalopathic rats leads to a longer duration of tremor and higher brain concentrations than in sham-operated controls. In lymphostatic encephalopathic as well as in normal rats different antiphlogistics shorten the tremor duration and decrease harmine concentration in brain. The antiphlogistics do not influence the plasma concentration of harmine, its protein binding and its tremorend concentration in brain. The effect of antiphlogistics in lymphostatic encephalopathic rats is considered as a consequence of the reduced blood-brain barrier permeability. Obviously in sick animals the blood-brain barrier permeability for harmine is not increased; the prolonged harmine tremor and the increased alkaloid concentration in the brain are consequences of the impaired cerebral lymphatic drainage only.
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