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M Hollmann

Publications and source records attributed to M Hollmann.

65 records · Page 4Linked to original sources
PubMedDate not supplied

The metabolic fate of 2H-labelled propafenone in man.

The metabolism of propafenone was studied in three humans by using 300 mg of the deuterated compound given orally. The excretion of propafenone and its metabolites was assessed by measuring the deuterium content in the excretion products by means of a microwave plasma detector. At selected times the metabolic pattern in plasma, urine, bile and feces was determined. The metabolites were isolated and the structure of the main compounds was characterized. Propafenone is absorbed completely and quantitatively metabolized. Unchanged propafenone is excreted neither in the urine nor in the feces in amounts of more than 1% the dose. The percentage of free unconjugated propafenone of the total deuterium content in the plasma was about 10% 3 and 6 hours after application. Conjugates of hydroxylated derivatives of propafenone are present predominantly in the plasma. The excretion of the metabolites takes place mainly by way of the feces, 53% of the dose is excreted by this route within 48 hours. Urinary elimination accounted for 18.5 and 38% of the dose within 48 hours in two humans. It was possible to elucidate the structure of 11 metabolites, accounting for more than 90% of the dose administered. The major metabolites are conjugates of 5-hydroxypropafenone and hydroxy-methoxy-propafenone with glucuronic and sulphuric acid and propafenone glucuronide. Furthermore, metabolic products of oxydative deamination pathway were identified, i.e. a glycol and a lactic acid derivative. C-C splitting yields a relatively large amount of 3-phenyl-propionic acid, while cleavage of the ether group leads to a phenolic product and is only of minor importance.

Administration, Oral↗
PubMedDate not supplied

Pharmacological differentiation between neuronal and recombinant glutamate receptor channels expressed in Xenopus oocytes.

To determine the molecular components of neuronal glutamate receptors, it is important to identify pharmacological tools that allow differentiation between different glutamate receptor types. Here, we utilized the naphthalene derivative Evans Blue (EB) and a collection of other subtype-specific compounds (polyamine toxins, concanavalin A, cyclothiazide) to compare the pharmacological profile of neuronal and recombinant glutamate receptors GluR1-GluR6 expressed in Xenopus oocytes. Submicromolar concentrations of EB selectively reduced the activity of homomeric glutamate receptors GluR1, GluR2(Q) and GluR4. Applied at concentrations above 100 microM, EB potentiated kainate responses of receptors GluR1, GluR3 and GluR4, while receptors GluR2(Q) and GluR6(Q) were completely blocked. Similar experiments were performed on identified neurones in brain slices and after injection of rat brain RNA in Xenopus oocytes. Neuronal kainate responses were (i) potentiated by 100 microM cyclothiazide, (ii) slightly blocked after preincubation in 10 microM concanavalin A, and (iii) not significantly affected by either low (< 1 microM) or high (> 100 microM) concentrations of EB. Their pharmacological properties were markedly different from those of recombinant glutamate receptor channels GluR1-GluR6 investigated in heterologous expression systems.

Animals↗
PubMedDate not supplied

An evaluation of muscle pathology in idiopathic scoliosis.

This study assessed the degree of longissimus muscle pathology in 15 patients with idiopathic scoliosis. Bilateral muscle biopsy specimens were taken at the apex of the scoliotic curve and from five control subjects and processed histochemically. All biopsy specimens were free of muscle pathology. However, patients had a higher proportion of Type I fibers on the convex than the concave side of the curve (70.2 vs. 59.5%), whereas the controls had no difference. Fiber type imbalance in patients with idiopathic scoliosis is thought to result from compensatory stretching of muscle and not to be the cause of the deformity.

Adolescent↗