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Biomedical subjects

J Tenczer

Publications and source records attributed to J Tenczer.

90 records · Page 5Linked to original sources
PubMed1978

Double irregular ventricular parasystole: rate-dependent entrance block and "supernormal" exit conduction.

An analysis of electrocardiograms from a patient with spontaneous double irregular ventricular parasystole is presented. Irregularity in one of the two parasystoles was produced by intermittence based on rate-dependent (phase 3) entrance block, and in the other parasystole it was attributed to "supernormal" exist conduction. Critical analysis of electrocardiograms revealed that first degree block, rate-dependent block, and "supernormal" conduction in the exit pathway may account for the alterations in the arrangement and manifestation of the parasystolic beats. An electrocardiographic approach to these properties of the parasystolic structure and demonstration of double ventricular parasystole with irregularity in both parasystoles has not previously been found in the literature.

Arrhythmias, Cardiac↗
PubMed1976

Effect of immunosuppressive therapy on the serum glycoprotein levels in chronic aggressive hepatitis.

The sera of 24 patients with chronic aggressive hepatitis receiving combined immunosuppressive therapy were studied for the concentrations of the carbohydrate components of glycoproteins and the IgG, IgA, IgM, alpha-2-macroglobulin, coeruloplasmin, beta-1-C-globulin and transferrin levels over a period of 2 years. Liver biopsy was performed repeatedly in 50% of the cases. On the evidence of the results, combined immunosuppressive treatment is regarded as apt to normalize the serum concentrations of IgG, IgA, IgM and to reduce those of alpha-2-macroglobulin and coeruloplasmin. Among the carbohydrate components of glycoproteins only the amount of hexose was reduced.

Adult↗
PubMedDate not supplied

Chlormezanone plasma and blood levels in patients after single and repeated oral doses and after suicidal drug overdose.

Chlormezanone plasma concentrations were determined in 5 volunteers (group 1) after a single oral dose of 200 mg of chlormezanone with high performance liquid chromatography. A plasma elimination half-life of 23 +/- 2.3 h was calculated. The mean peak chlormezanone plasma level was 1.86 +/- 0.2 micrograms/ml, 1 h after ingestion. Additionally, chlormezanone plasma levels were determined after repeated oral doses of chlormezanone recommended for treatment of muscular spasms due to degenerative skeletal disease. After 5 days of repeated daily doses of 3 x 200 mg (group 2; 12 patients) or 3 x 400 mg (group 3; 10 patients) of chlormezanone, mean predose chlormezanone plasma levels were 12.0 +/- 2.0 micrograms/ml (group 2) and 22.7 +/- 4.0 micrograms/ml (group 3), respectively. Comparable plasma concentrations were determined after 10 days of repeated doses of 3 x 200 mg or 3 x 400 mg of chlormezanone in 3 patients from each of these 2 groups. In 7 patients of group 3, chlormezanone had to be discontinued on the 5th day due to increasing muscular weakness, ataxia and exercise-inducible tachycardia. After a loading dose of 800 mg and repeated doses of 3 x 200 mg chlormezanone to 5 patients (group 4), plasma levels of 6.5 +/- 2.1 micrograms/ml, 8.9 +/- 2.2 micrograms/ml, 12.7 +/- 2.0 micrograms/ml, and 10.4 +/- 2.4 micrograms/ml were determined after 2, 8, 16, and 36 h, respectively. Trace amounts of a degradation product of the acid-labile chlormezanone could be detected in plasma besides the unchanged drug after administration of repeated oral doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMedDate not supplied

Metabolic disposition of ajmaline.

Urine was collected from six patients receiving a continuous infusion of 20 mg/h ajmaline. Pooled urine was extracted with and without enzymatic conjugate cleavage or hydrolysis with concentrated hydrochloric acid. The extracts were analyzed by gas chromatography/mass spectrometry. Ajmaline and its metabolites in urine were identified in the form of their acetylated derivatives. Twenty two different acetylated derivatives of ajmaline and its metabolites could be detected. Three of these derivatives were artifacts generated by acetylation and/or thermal decomposition. The major metabolic pathways were mono- and di-hydroxylation of the benzene ring with subsequent O-methylation, reduction of the C-21, oxidation of the C-17 and C-21-hydroxyl function, N-oxidation, and a combination of these metabolic steps. Ajmaline and its metabolites were mainly excreted in the form of their conjugates. Furthermore, the interference of sparteine, debrisoquine, quinidine, and nifedipine with ajmaline metabolism was studied with semiquantitative thin-layer chromatography. Ajmaline metabolism was inhibited by co-administration of sparteine or quinidine, but not by debrisoquine or nifedipine. Sparteine most likely competed with ajmaline metabolism. Quinidine probably bound competitively to ajmaline-metabolizing enzymes without being metabolized itself. Additionally, the metabolic ratio of hydroxyajmaline/ajmaline in urine was determined in 9 extensive metabolizers and one poor metabolizer of dextromethorphan. The poor metabolizer had a significantly reduced metabolic ratio of hydroxyajmaline/ajmaline, which indicates that ajmaline metabolism probably co-segregates with polymorphic sparteine/debrisoquine/dextromethorphan metabolism.

Ajmaline↗