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Biomedical subjects

J Tenczer

Publications and source records attributed to J Tenczer.

At least 37 records · Page 2Linked to original sources
PubMed1987

Urinary metabolism of chlorphenoxamine in man.

After an oral dose of 40 mg of 4-chlorophenyl-methylbenzyloxy-N,N-dimethyl-ethylamine(chlorphe noxamine, Systral) urinary metabolism was studied by gas chromatography/mass spectrometry. Besides the unchanged drug, 8 metabolites and 7 artifacts and derivates could be identified. Metabolism is similar to that of the structurally related antihistaminic drugs diphenhydramine and doxylamine. The main metabolic pathways are: 1. N-demethylation, 2. oxidative desamination and formation of an alcohol and a carbonic acid derivative, 3. cleavage of the ether bond, and 4. hydroxylation of the phenyl ring. For determination of chlorphenoxamine in plasma an assay using gas chromatography was developed. Chlorphenoxamine plasma levels were beyond the limit of detection (10 ng/ml) 30, 60, 120, 240, 480, and 1200 min after oral intake.

Ethylamines↗
PubMed1987

Urinary metabolism of dextromethorphan in man.

After an oral dose of 50 mg of (+)-3-methoxy-N-methylmorphinan (dextromethorphan) to volunteers, urinary metabolism was studied by gas chromatography/mass spectrometry. A total of 15 previously unknown metabolites and derivatives of dextromethorphan could be identified by mass spectrometric techniques. The main metabolic pathways were: O,N-demethylation, O,N-acetylation, hydroxylation of the phenyl ring and the saturated ring system with subsequent further oxidation.

Acetylation↗
PubMed1987

Urinary metabolism of chloroquine.

For reinvestigation of the metabolism of 7-chloro-4-(4-diethylamino-1-methylbutylamino)quinoline (chloroquine, Resochin), urine samples from patients and volunteers with single or repeated chloroquine doses were collected and analyzed by gas chromatography, thin-layer chromatography, and gas chromatography/mass spectrometry. Furthermore, urine samples from two cases of chloroquine overdose were included in the study. Three previously unknown metabolites could be identified in nearly all samples, although they amounted to less than 2% of the concentration of unchanged chloroquine in the urine. However, in those samples with failure of detection, the chloroquine urine levels were already so low that metabolite concentrations were beyond the limit of detection of the analytical method. Altogether, the study gave no evidence for a dose-dependent formation of the three previously unknown metabolites. Besides the new metabolites, an artifact generated from chloroquine-N-oxide could be characterized by gas chromatography/mass spectrometry. However, the formation of a further chloroquine metabolite with an alcohol function which has been described in the literature could not be confirmed.

Adult↗
PubMed1986

Rate-dependent patterns of modulated ventricular parasystole.

The effects of ventricular pacing on the arrangement of ventricular parasystolic beats were studied in 14 patients. By analyzing the effects of various pacing rates and modalities, it was found that both rate and pattern of manifest parasystolic beats were intimately related to the rate and coupling interval of the paced rhythm. Our findings indicate that fixed coupling of ectopic beats is not incompatible with parasystole; modulated parasystole may manifest as fixed rate classic parasystole; a parasystolic pacemaker can be entrained by a wide range of driving rates both above and below the intrinsic rate of the parasystole; and with different driving rates, these rate-dependent patterns can be observed in the same patient. Our observations suggest that spontaneous or drug-induced changes in the heart rate can lead to major alterations in the frequency and patterns of ventricular parasystole.

Electrocardiography↗
PubMed1986

Failure of idioventricular suppression in man by overdrive pacing as well as lidocaine: the role of abnormal automaticity.

Five patients with third-degree atrioventricular block and an idioventricular escape rhythm who showed unusual responses to overdrive ventricular pacing and lidocaine are presented. In four cases, the idioventricular rhythm was not suppressed by overdrive; in one, the recovery time of the escape rhythm was shorter than the escape cycle length. Lidocaine did not affect the cycle lengths and recovery times of the idioventricular rhythms. These responses are characteristic of abnormal automaticity. The role of abnormal automaticity in human idioventricular escape rhythms has not been previously supported by these characteristic responses to overdrive pacing and lidocaine.

Aged↗
PubMed1986

Metabolism of chlormezanone in man.

The metabolism of chlormezanone (Muskel Trancopal) in man was studied by the aid of gas chromatography/mass spectrometry and high performance liquid chromatography after an oral dose of 400 mg. Six metabolites and/or degradation products were identified in the urine. Some of the metabolites are formed at least partially by nonenzymatic hydrolysis in the stomach. In contrast to previous publications, no unchanged drug was detected in plasma and urine. The main metabolite in plasma is generated by cleavage of the amide bond in the six-membered heterocyclic ring. This derivative is easily formed by in vitro hydrolysis at pH 1, too. It structurally resembles baclofene. About 40% of the dose is excreted with the urine. The major metabolite in urine is 4-chlorohippuric acid. Additionally, 4-chloro-benzoyl-N-methylamide, 4-chlorobenzoic acid, N-methylimino-4-chlorobenzaldehyde, 4-chlorobenzaldehyde, and "hydrolized" chlormezanone were identified.

Biotransformation↗
PubMed1986

Simple approach to an apparently chaotic arrhythmia.

Deciphering complex arrhythmias requires a strict, systematic approach. In a step-by-step analysis of an electrocardiogram recorded from a patient with severe metabolic disturbances, we present a few simple suggestions that may often be helpful in electrocardiographic interpretation.

Arrhythmias, Cardiac↗
PubMed1985

A revision of the metabolic disposition of amantadine.

Amantadine is one of the most commonly used drugs for the control of tremor in Parkinson's disease. Additionally, it has an antiviral action in the prevention of type A influenza. It has been previously reported that amantadine is nearly completely eliminated in the urine. No metabolites have been detected. Surprisingly, in a case of amantadine overdose, several metabolites could be identified by gas chromatography/mas spectrometry. This finding prompted us to re-investigate the metabolism of amantadine under a therapeutic dosing regimen. The bulk of the dose was eliminated unchanged. However, eight metabolites could be identified. Besides N-acetylation which is the major metabolic pathway, several rather unusual metabolic pathways were observed: N-methylation, formation of Schiff bases and N-formiates. No metabolites with a hydroxylated adamantane ring system could be detected.

Acetylation↗
PubMed1985

Electrophysiologic study of tachycardia-dependent paroxysmal His bundle block in man.

Electrophysiologic study was performed in a patient with tachycardia-dependent paroxysmal atrioventricular block. The site of block was within the His bundle. The effective refractory period of the His bundle was markedly prolonged and it was comparable to the critical atrial cycle length producing type II His bundle block. The most likely mechanism of paroxysmal atrioventricular block was repetitive concealed penetration of the blocking zone by nonconducted impulses that reached the proximal His bundle. Enhancing the blocking ratio at the atrioventricular nodal level resulted in improvement of overall atrioventricular conduction.

Atrioventricular Node↗
PubMed1985

The effects of overdrive pacing and lidocaine on atrioventricular junctional rhythm in man: the role of abnormal automaticity.

The effects of overdrive pacing and lidocaine were studied in 22 patients with atrioventricular (AV) junctional rhythms. Based on the responses to cardiac pacing and lidocaine, patients were divided into two groups. AV junctional rhythms in group I (17 patients) were suppressed by overdrive pacing, and their rates were decreased by lidocaine. Lidocaine also prolonged the junctional recovery time in these patients. AV junctional rhythms in group II (five patients) were not suppressed by overdrive pacing. In contrast, the rate increased after overdrive pacing. Lidocaine did not alter the basic cycle lengths or the recovery times of the AV junctional rhythms in this group of patients. The data suggest that AV junctional rhythms in group I were caused by normal automaticity, while those in group II were probably due to abnormal automaticity.

Adult↗
PubMed1985

Underdrive suppression of the sinus rhythm in man.

This report demonstrates unusual responses of the sinus rhythm to atrial pacing. The sinus rhythm failed to become manifest when the heart was driven at a rate slower than the inherent sinus rate. Sinus rhythm returned only after termination of underdrive pacing with the recovery time longer than twice the cycle length of the control sinus rhythm. The largest difference between underdrive and sinus cycle lengths measured 600 msec. To the best of our knowledge, underdrive suppression of the sinus rhythm has not been previously reported in man.

Aged↗
PubMed1985

Problems of differential diagnosis in a case of bone lesions caused by myelosclerosis associated with hyperparathyroidism.

The authors present a report on the case of a female patient with myelofibrosis where X-ray examinations of the bone skeleton predominantly showed such osteolytic changes which are no typical of myelosclerosis. Morphological criteria rather would have corresponded to osteitis fibrosa cystica generalisata. Laboratory examinations partially indicated primary hyperparathyroidism, this assumption could not be confirmed by other examinations. Also histological findings of repeated bone biopsies did not lead to a uniform diagnosis. Autopsy confirmed the presence of both diseases. The authors consider the synergistic effect of both diseases to be the cause for the development of those bone changes mentioned above.

Bone Resorption↗
PubMed1985

The metabolism of tromantadine.

The metabolism of the antiviral drug tromantadine (1-adamantyl-2-(2-dimethylaminoethoxy)acetamide) was studied after an oral dose of 120 mg tromantadine hydrochloride using capillary gas chromatography/mass spectrometry. Most of the dose was excreted unchanged with the urine. Six metabolites could be identified. The main metabolic products were 1-aminoadamantane (amantadine) and 1-adamantyl-(2-hydroxy)acetamide. Further metabolic pathways were demethylation of the dimethylamino function and oxidative desamination to an unstable aldehyde which is oxidized to a carbonic acid or reduced to an alcohol.

Acetylation↗
PubMed1985

Metabolism of benzydamine.

After an oral dose of 50 mg benzydamine to three volunteers, urinary metabolites were identified by mass spectrometric techniques. 50-65% of the dose was excreted unchanged with the urine. The main metabolic pathways were elimination of the dimethylaminopropyl group, elimination of the benzyl group, desmethylation, N-oxidation, and hydroxylation of the benzene ring. Didesmethylbenzydamine and hydroxybenzydamine were excreted in form of their corresponding glucuronides.

Benzydamine↗