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  • 1
    Electronic Resource
    Electronic Resource
    Buchbesprechungen (1988)
    Springer
    Journal of molecular medicine 66 (1988), S. 1145-1145 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01727852
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  • 2
    Electronic Resource
    Electronic Resource
    Wie viele Beta-Rezeptoren-Blocker braucht der Arzt? (1987)
    Springer
    Journal of molecular medicine 65 (1987), S. 289-295 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01773455
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  • 3
    Electronic Resource
    Electronic Resource
    Hemmung der Monoaminoxydase und Diaminoxydase durch Furazolidon (Furoxon®) (1968)
    Springer
    Journal of molecular medicine 46 (1968), S. 720-728 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Furazolidone, a drug used in the treatment of gastro-intestinal infection, was previously shown to be a potent irreversible and cumulative inhibitor of monoamine oxidase (MAO)in rats, due to its hydrazine structure. 1. Inself-trials, characteristic symptoms of MAO-inhibition were noticed following the oral application of 5 resp. 10 mg/kg per day of furazolidone over a period of 9 resp. 10 days: anorexia, restlessness and disorders of sleep. On the tenth day of treatment (10 mg/kg) orthostatic collaps occurred. 2. Inhibition of MAO was shownindirectly by reduced urinary excretion of 3-methoxy-4-hydroxymandelic acid and 5-hydroxyindoleacetic acid upon loading with serotonin. — The pressor effect after the intravenous injection of tyramine was potentiated 10 to 20 fold. The potentiation declined with the long half life time of 12 days due to the irreversible enzyme inhibition. This value is presumably a measure for the rate of the de novo-synthesis of MAO in sympathetic nerves. 3. Adirect evidence for the inhibition of MAO was given by the complete disappearance of MAO-activity in plasma after 7 resp. 9 days of treatment with furazolidone. Enzyme activity returned to normal within 1 week after the last application of the drug, followed by a rebound effect. 4. Plasma diamine oxidase (DAO) was inhibited up to 90%. Intravenous injection of heparin (15.000 IU) increased the activity of the partially inhibited DAO in plasma to the same degree as prior to the application of furazolidone. Therefore, inhibition of plasma DAO may be taken as a measure for the inhibition of DAO in the organs. It is concluded that the inhibition of DAO is probably caused by a primary metabolite of furazolidone, while that of MAO is due to a secondary metabolite of the drug. 5. Thus, furazolidone isabsorbed from the intestinal tract to a degree sufficient to cause undue side effects — inter alia — by inhibition of MAO and/or DAO.
    Notes: Zusammenfassung Das zur Therapie bakterieller Infektionen des Magen-Darm-Traktes verwendete BacteriostaticumFurazolidon hatte sich in früheren Versuchen auf Grund seiner Hydrazinstruktur anRatten als ein starker irreversibler und daher kumulativ wirkender Hemmstoff der Monoaminoxydase (MAO) erwiesen. 1. ImSelbstversuch traten während einer 9 bzw. 10tägigen oralen Verabfolgung von 5 bzw. 10 mg/kg pro die Furazolidon die für MAO-Hemmstoffe charakteristischensubjektiven Symptome auf: Anorexie, innere Unruhe und Schlafstörungen. Am 10. Tage der Behandlung (10 mg/kg) kam es zu einem orthostatischen Kollaps. 2. Die Hemmung der MAO manifestierte sichindirekt in einer herabgesetzten Ausscheidung von Vanillinmandelsäure und 5-Hydroxy-Indolessigsäure (nach Serotonin-Belastung) in den Harn. — Die blutdrucksteigernde Wirkung von i. v. injiziertem Tyramin war 10–20fach verstärkt. Die Potenzierung klang auf Grund der irreversiblen Fermenthemmung mit der hohen Halbwertzeit von 12 Tagen ab. Diese Halbwertzeit ist möglicherweise ein Maß für die Geschwindigkeit der MAO-Synthese in den sympathischen Nerven. 3. Eindirekter Beweis für die Hemmung der MAO war das völlige Verschwinden der MAO-Aktivität im Plasma nach 7 bzw. 9tägiger Furazolidon-Einnahme. Die Normalisierung der Enzym-Aktivität trat 1 Woche nach Absetzen von Furazolidon ein, gefolgt von einem „rebound effect“. 4. Die Plasma-Diaminoxydase (DAO) war maximal um 90% gehemmt.Heparin (15 000 IE intravenös) steigerte die Aktivität des gehemmten Enzyms um denselben Prozentsatz wie vor der Einnahme von Furazolidon. Eine Hemmung der Plasma-DAO ist somit ein Maß für die Hemmung der DAO in den Organen. — Ursache der DAO-Hemmung ist wahrscheinlich ein primärer, Ursache der MAO-Hemmung ein sekundärer Metabolit des Furazolidon. 5. Furazolidon wird demnach in sohohem Ausmaß resorbiert, daß es — u.a. auf Grund einer Hemmung der MAO und DAO — zum Auftreten unerwünschter Nebenwirkungen kommen kann.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01731161
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  • 4
    Electronic Resource
    Electronic Resource
    Excretion of norephedrine by man after oral administration of oxyfedrine (1975)
    Springer
    European journal of clinical pharmacology 8 (1975), S. 161-166 
    Details
    ISSN: 1432-1041
    Keywords: Oxyfedrine ; norephedrine ; man ; urinary excretion ; sympathomimetic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary After oral administration of oxyfedrine to healthy volunteers, norephedrine was identified in the urine by thin layer chromatography and gas liquid chromatography and mass spectrography. 30 hours after single oral doses of 8, 16 or 24 mg of oxyfedrine, about 4, 8 and 9 mg, respectively, of norephedrine were found in the urine, i.e. on a molar base 75–100% of the dose was excreted as norephedrine. The peak of excretion occurred within 2–4 hours after administration of the drug. No accumulation of oxyfedrine and/or its metabolite was observed after administration of 16 mg of oxyfedrine t.i.d. for three days. It could not be decided whether oxyfedrine was metabolized to norephedrine by liver enzymes, as in rats, or was spontaneously degraded to norephedrine, e.g. in duodenal fluid before absorption. 30–150 min after oral oxyfedrine (24 mg) norephedrine was demonstrable in duodenal fluid. Thus, in addition to the directβ-sympathomimetic effects of oxyfedrine, it may also have indirect sympathomimetic effects because of the noradrenaline-releasing properties of its metabolite norephedrine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00567109
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  • 5
    Electronic Resource
    Electronic Resource
    Congenital muscular dystrophy, brain malformation and ocular problems (muscle, eye and brain disease) in two german families (1984)
    Springer
    European journal of pediatrics 142 (1984), S. 64-68 
    Details
    ISSN: 1432-1076
    Keywords: Congenital muscular dystrophy ; Congenital hypotonia ; Brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report on two brothers and an unrelated girl with congenital muscular dystrophy (CMD), brain malformation and ocular changes (strabismus, myopia, glaucoma, cataracts, retinal dystrophy). Correlations with the inherited autosomal recessive syndromes of CMD, including the Fukuyama-type CMD with CNS malformation, and the Muscle, Eye and Brain Disease published by Santavuori are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442595
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  • 6
    Electronic Resource
    Electronic Resource
    Sympathoneuronal and sympathoadrenal activation during ketamine anesthesia (1979)
    Springer
    European journal of clinical pharmacology 16 (1979), S. 91-95 
    Details
    ISSN: 1432-1041
    Keywords: ketamine ; sympathoneuronal activity ; sympathoadrenal activity ; cardiovascular effects ; plasma catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of ketamine anesthesia (3 mg/kg i.v.) on cardiovascular parameters and noradrenaline, adrenaline and dopamine-β-hydroxylase (DBH) activity in plasma were studied in 12 patients. At 3, 6 and 10 min after induction of anesthesia, a pronounced increase in heart rate (+28%) and in systolic and diastolic blood pressure (+28% and 17% resp.) was observed. Concomitantly noradrenaline and adrenaline concentrations increased significantly from 187 to 415 ng/l and from 97 to 271 ng/l, respectively. DBH-activity in plasma remained almost unchanged. From these results it can be concluded that the well known cardiovascular stimulant effect of ketamine is due to greatly enhanced sympatho-neuronal and sympatho-adrenal activity, presumably brought about by a central mechanism of action of the drug. Furthermore, DBH-activity in plasma appeared not to be a reliable index of sympathetic activity in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00563113
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  • 7
    Electronic Resource
    Electronic Resource
    Standardized mental stress in healthy volunteers induced by delayed auditory feedback (DAF) (1979)
    Springer
    European journal of clinical pharmacology 16 (1979), S. 171-176 
    Details
    ISSN: 1432-1041
    Keywords: mental stress ; sympathetic activation ; delayed auditory feedback ; plasma norepinephrine ; plasma epinephrine ; plasma dopamine-beta-hydroxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Using delayed auditory feedback (delay 0.175 s) a standardized form of mental stress was investigated in 8 healthy male volunteers. After a resting period and a period of undelayed reading, the volunteers were exposed for 5 min to the DAF stress. During the DAF period heart rate increased by 10% and systolic and diastolic blood pressure increased by 9% and 18%, respectively. As a measure of acute sympathetic activation, plasma concentrations of norepinephrine and epinephrine rose by 68% and 49%, respectively. The activity of dopamine-β-hydroxylase in plasma was increased by 25%. From these results it can be concluded that the DAF procedure provides a suitable method for inducing a standardized mental stress in normal subjects, which can be measured as changes in biochemical and cardiovascular variables.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00562057
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  • 8
    Electronic Resource
    Electronic Resource
    Sympathomimetic effects of amezinium on the cardiovascular system and plasma catecholamines in man (1982)
    Springer
    European journal of clinical pharmacology 23 (1982), S. 15-20 
    Details
    ISSN: 1432-1041
    Keywords: amezinium ; sympathomimetic effects ; catecholamines ; echocardiography ; systolic time intervals ; orthostatic stress ; inhibition of noradrenaline uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The cardiovascular effects of the sympathomimetic agent amezinium were investigated in a double-blind, placebo-controlled, randomized trial in six volunteers. Before and 2 h after oral administration of amezinium 30 mg or placebo the cardiovascular responses to orthostatic stress, induced by 80° passive head-up tilt, were assessed by recording blood pressure, systolic time intervals, and echocardiogram. Plasma catecholamines were also determined. After amezinium treatment, the average supine systolic blood pressure was increased by +30 mm Hg and after tilting it remained above both the pre-treatment and placebo values. Compared to placebo, amezinium elicited only minor changes in heart rate and diastolic blood pressure. The effect of amezinium on the pre-ejection period corrected for heart rate (PEPc) and mean velocity of fiber shortening (VCFmean) indicated positive inotropic properties. Its effects were distinctly more pronounced during tilt than with the subjects supine. Plasma concentrations of noradrenaline and adrenaline were not influenced by amezinium during rest or tilt. From these results and previous research it is concluded that amezinium induces its sympathomimetic effects by preferentially inhibiting the re-uptake of noradrenaline which is released by the drug itself, or by sympathetic activation during tilt. This mechanism of action might explain the pronounced sympathomimetic effects of the drug, especially during orthostatic stress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01061371
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  • 9
    Electronic Resource
    Electronic Resource
    Penbutolol: β-Adrenoceptor interaction and the time course of plasma concentrations explain its prolonged duration of action in man (1985)
    Springer
    European journal of clinical pharmacology 29 (1985), S. 293-300 
    Details
    ISSN: 1432-1041
    Keywords: beta-adrenoceptors ; penbutolol ; 4-hydroxy-penbutolol ; plasma concentration kinetics ; plasma protein binding ; effect kinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary β-adrenoceptor binding of (—) penbutolol and its active metabolite 4-hydroxy-penbutolol to rat reticulocyte membranes was shown in the presence of native human plasma. Due to the high plasma protein binding (∼90%) the apparent Ki-values of penbutolol were shifted 100-fold to the right after inclusion of plasma in the assay; the Ki was ∼40–70 ng/ml. That value is comparable to the IC50-values calculated from clinical studies. The interaction of 4-hydroxy-penbutolol with β-adrenoceptors was not affected to the same extent by inclusion of plasma protein binding ∼80%, apparent Ki-value ∼7 ng/ml. Thus, the active metabolite of penbutolol displays higher potency at β-adrenoceptors in vitro due to its lesser degree of plasma protein binding. A prediction procedure for antagonist activity after penbutolol administration using β-adrenoceptor interaction and plasma concentration kinetics suggests that, in addition to a rapid elimination process from human plasma, a slow elimination phase of penbutolol (or an active metabolite) is necessary to explain the long duration of action observed in clinical studies after a single oral dose. Inhibition in vitro of β-adrenoceptor binding by plasma samples obtained after oral administration of 40 mg penbutolol to 3 healthy volunteers indicated a biphasic concentration-time profile of the antagonist in plasma and was in accordance with the time course of the reported reduction in exercise tachycardia. Finally, plasma concentrations of penbutolol equivalents derived from the receptor assay were in the range of penbutolol concentrations detected by physico-chemical methods. It is concluded that the time course of antagonism against β-adrenoceptor-mediated effects after a single oral dose of penbutolol in man can readily be explained by its biphasic elimination kinetics from human plasma together with the properties of the β-adrenoceptor interaction detectable in vitro.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00544083
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  • 10
    Electronic Resource
    Electronic Resource
    Transdermal delivery of bupranolol: Pharmacodynamics and beta-adrenoceptor occupancy (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 419-422 
    Details
    ISSN: 1432-1041
    Keywords: bupranolol ; transdermal delivery system ; beta1- and beta2-adrenoceptor binding ; steady-state concentration ; healthy volunteers ; plasma concentrations ; beta-adrenoceptor antagonism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Bupranolol is a non-selective beta-adrenoceptor antagonist with a Ki-value of 6–15 nmol/l (equivalent to 1.5–4 ng/ml in plasma) at beta1- (rat salivary gland) and beta2-adrenoceptors (rat reticulocytes) in receptor binding studies with3H-CGP 12177 in the presence of human plasma. After oral administration of 200 mg bupranolol to healthy volunteers, the maximal plasma concentration was observed within 1.2 h but it only reached a level close to the Ki-value. Elimination from plasma was rapid (t1/2=2.0 h). Administration of 30 mg bupranolol in a transdermal delivery system (TTS) every 24 h to 6 healthy volunteers for 72 h yielded steady state plasma concentrations 4- to 5-times above the Ki-value as shown by in vitro inhibition of beta-adrenoceptor binding by plasma samples. The pharmacodynamic effect, measured as the reduction in exercise tachycardia, showed a stable inhibitory effect; antagonism of a bolus injection of isoprenaline indicated a 10- to 15-fold right shift of the dose-response curve during the observation period of 72 h. It is concluded that steady-state plasma concentrations and effect of the elsewise rapidly eliminated beta-blocker bupranolol can be achieved by a transdermal delivery system applied each day.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00613517
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