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Results for “Medazepam”

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At least 19 recordsLinked to original sources

PubMed1977

Serum medazepam, diazepam, and N-desmethyldiazepam levels after single and multiple oral doses of medazepam.

20 mg of medazepam were taken by mouth by 9 healthy volunteers in an acute absorption study. About a 10-fold variation was found during the first 6 hours after the drug in individual serum medazepam, diazepam, and N-desmethyldiazepam levels. In a subacute study 10 mg of medazepam t.i.d. was given to 10 institutionalized mentally subnormal adults with emotional disorders. After 14 days' treatment serum N-desmethyldiazepam levels were generally above 800 ng/ml, 7 to 8 times higher than the serum medazepam or diazepam levels measured 12 hours after the last dose. No correlation was observed between the serum concentration and efficacy of medazepam.

Administration, Oral↗

PubMed1975

[Treatment of some functional disorders of the digestive system: clinical experimentation with comparison of a medazepam-metoclopramide combination with medazepam-anticholinergic agent combination].

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Adult↗

PubMedDate not supplied

Further studies on medazepam metabolism in the rat.

Previous studies with 9000g supernatant fractions of rat liver revealed that the 1,4-benzodiazepine, medazepam, was converted to N-desmethyldiazepam by a series of reactions including hydroxylation, N-demethylation, and dehydrogenation. The present study was designed to determine if the pathway via diazepam as intermediate, which is one of three possible pathways, is the major route in vivo in the rat for N-desmethyldiazepam formation from medazepam. Measurement of the levels of labeled drug and metabolites in blood, brain, lung, heart, and muscle 5 min after the oral administration of approximately equivalent doses of [14C]medazepam hydrochloride, [14C]diazepam, or N-desmethyl[14C]medazepam revealed that each drug was both rapidly absorbed and oxidatively metabolized in the rat. At 1 hr. the tissue levels of labeled N-desmethyldiazepam were highest after N-desmethyl-[14C]medazepam, intermediate after [14C]medazepam hydrochloride and lowest after [14C]diazepam. These results indicated that in the formation of N-desmethyldiazepam from medazepam in the rat there is a substantial preference for the pathway via N-desmethylmedazepam over that in which diazepam is an intermediate. From consideration of the limited data available, it is suggested that this same preference in pathways may also hold true in humans.

Animals↗

PubMed1979

Plasma concentrations of medazepam and its metabolites after oral administration.

The plasma concentrations of medazepam and its metabolites, diazepam and desmethyldiazepam, were determined in volunteer subjects following the oral administration of medazepam 10 mg. The results indicated that medazepam was absorbed rapidly, that low concentrations of metabolites were present during the 1st h, and that the build-up in the circulation of the major metabolite, desmethyldiazepam, was prolonged and variable. As many of the clinical effects and possible adverse reactions of medazepam appear to be associated with the presence of this major metabolite, the metabolic and pharmacokinetic characteristics of the drug should be considered when using medazepam as an anxiolytic before dentistry or surgery.

Administration, Oral↗

PubMed1976

Residual effects and skills related to driving after a single oral administration of diazepam, medazepam or lorazepam.

Psychomotor skills and visual functions related to driving were measured double-blind cross-over in ten healthy volunteers before, and 1,3,5 and 7 h after a single oral administration of diazepam (10mg), medazepam (15 mg) or lorazepam (2.5 mg). The late effects of lorazepam were tested in seven other subjects 12 and 24 h after the administration. Lorazepam impaired almost all the measured skills more (P less than 0.05 to 0.001) than diazepam, medizepam or the placebo. The lorazepam impairment of reactive skills and flicker fusion discrimination remained statistically significant (P less than 0.05) for as long as 12 h. Medazepam impaired only reactive skills and flicker fusion, the latter remaining impaired (P less than 0.05) for as long a 5 h after the administration. The magnitude and duration of the effects of diazepam were intermediate between those of lorazepam and medazepam. Diazepam impaired perceptual speed and reactive and co-ordinative skills as well as flicker fusion discrimination and visual parameters related to driving. Slight impairments in performance were measurable for up to 5 h after administration but at 7 h the results resembled those measured after the placebo. The lack of alterations in adaptation to darkness, sensitivity to brightness or visual discrimination ability in bright counterlight at a time when flicker fusion discrimination was severely depressed suggests that an impaired ability to discriminate flickering light is of no or little clinical significance to driving ability. It is concluded that patients receiving a 2.5 mg dose of lorazepam should not drive or operate machinery for 24 h after the administration. After diazepam (10 mg) or medazepam (15 mg) patients should refrain from driving or participating inskilled performances for only 5 to 7 hours.

Adult↗

PubMed1976

Changes in excitability of amygdaloid and septal nuclei induced by medazepam hydrochloride.

Electrical stimulations of the central and basolateral part of the amygdaloid complex and of the septum in freely moving cats elicit changes in arterial pressure (i.e., an increase in pressure during stimulation of the central part of the amygdala, and a decrease followed by an increase during stimulation of the basolateral part of the amygdala and of the septum). These changes within the cardiovascular system are followed by rage reactions when the central part of the amygdala is stimulated, defense patterns when the basolateral part of the amygdala is stimulated, and pitiful mewing as a result of septal stimulation. Medazepam hydrochloride in a dose of approximately 15 mg/kg i.v. given over a period of 3 h, in order to maintain constant blood levels of the drug, attenuated slightly the cardiovascular reactions and elevated markedly the thresholds for psychomotoric behavior. The latencies between the onset of electrical stimulation and the beginning of the increase in arterial pressure were only slightly increased, whereas the latencies for spychomotoric behavior were markedly prolonged due to drug application. The data support the view that medazepam hydrochloride exerts depressant effects on the limbic-hypothalamic level with respect to psychomotoric responses. The effect was not identical for all nuclei tested. The basolateral part of the amygdala was significantly less sensitive to medazepam hydrochloride than the central part of the amygdala.

Amygdala↗

PubMedDate not supplied

[Ethological analysis of the action of medazepam and diazepam on the zoosocial behavior of isolated mice].

Tests set up with isolated mice of two groups (aggressive and "fearful") evidenced that diazepam and medazepam weaken the behavioral manifestations of the partner's avoidance, increase sociability in "fearful" mice and help to regain the ability for elementary intraspecies contacts. These drugs have a biphasic action on the behavior of aggressive mice, small doses (medazepam 0.1 mg/kg) facilitating aggression and large one (medazepam, diazepam--5 mg/kg) suppressing it.

Aggression↗

PubMed1977

Medazepam and the driving ability of anxious patients.

A double-blind crossover trial of Medazepam was carried out in 14 anxious hospital patients. The mean self-adjusted dosage was 16.5 mg daily. The active drug was no more effective than placebo in relieving anxiety, which was rated both clinically and by the Middlesex Health Questionnaire (M.H.Q.) (Crown and Crisp, 1970). This may have been because the dose was relatively low for chronically anxious hospital patients. Even this dosage caused significantly higher scores on the M.H.Q. scale for depression. Braking and driving simulator tests were not adversely affected by Medazepam. In real driving conditions those taking the drug made significantly more technical, but not dangerous, errors. Pulse and blood pressure also were not affected.

Adult↗

PubMed1975

Studies of drugs given before anaesthesia XXV: Medazepam, a new benzodiazepine.

Medazepam, a new benzodiazepine, was studied as an oral preanaesthetic medication in adult women in a dose of 10 mg, and the findings compared with those obtained with diazepam 10 mg or a dummy capsule using a double-blind technique. In the doses used medazepam produced less drowsiness than diazepam and was no more anxiolytic than the placebo.

Administration, Oral↗

PubMed1977

Analysis of medazepam, diazepam, and metabolites in plasma by gas-liquid chromatography with electrolytic conductivity detection.

An improved electrolytic conductivity detector allowed the gas-liquid chromatographic analysis of medazepam, diazepam, and major metabolites in 2 ml plasma at concentrations of 20 microgram/l. The detector had a sensitivity limit of less than 1 ng (or 100 pg nitrogen) when operated in the nitrogen-selective mode and a nitrogen/carbon elemental selectivity ratio of greater than 100,000 compared to octadecane and cholesterol. Detector response when operated in various element-selective chemical modes was investigated, and its application to the analysis of the title compounds was compared to electron capture and flame ionization detection systems.

Anti-Anxiety Agents↗

PubMed1977

Actions of iontophoretic phenytoin and medazepam on hippocampal neurons.

In rats anesthetized with methoxyflurane, phenytoin (DPH) and medazepam (MDZ) were administered iontophoretically to pyramidal and granule cells discharging spontaneously or being driven by acetylcholine or glutamic acid. The objectives were to determine if: 1) these anticonvulsant agents exert direct effects on the rates of discharge of hippocampal neurons; 2) similarities exist between responses elicited by DPH and MDZ; and 3) pyramidal and granule cells differ in their responsiveness to the drugs. The firing rates of 38% of spontaneously active neurons were reduced by iontophoretic DPH. The incidence of depression by DPH depended upon the pretest discharge rates of the cells. Only 5% of cells with spontaneous rates less than 12/sec were depressed by DPH, but 80% with rates faster than 12/sec were inhibited. MDZ depressed 79% of spontaneously firing neurons regardless of pretest discharge rate. A majority of neurons whose firing rates were facilitated by either acetylcholine or glutamate were depressed by DPH or MDZ ejected iontophoretically. Pyramidal and granule cells responded similarly to putative transmitters, but differentially to the drugs. MDZ depressed a much greater proportion of spontaneously active granule cells then DPH. Phenytoin and MDZ differed with regard to the incidence of depression of spontaneous discharges, inhibition of slow firing cells, the proportion of granule cells depressed, and the duration of effect. These differences may be due to potency and pharmacokinetic factors or dissimilar mechanisms of action when the compounds are applied directly to single neurons.

Animals↗

PubMed1976