Disease relevance of R(+)-Secobarbital

• In a hypothesis-generating study looking for possible carcinogenic effects of drugs in humans, each of three barbiturates (pentobarbital sodium, phenobarbital, and secobarbital sodium) showed a statistically significant association with the subsequent development of lung cancer, with relative risks ranging from 1.5 to 2 [1].
• To determine the time course of efferent sympathetic denervation after transmural myocardial infarction (TMI) and of efferent vagal denervation after transmural or nontransmural myocardial infarction (NTMI), we measured effective refractory periods (ERP) basal and apical to TMI or NTMI in secobarbital-anesthetized, open-chest dogs [2].
• There was a reduction of the hypoprothrombinemia of the pseuoracemate during the secobarbital regimen over that on warfarin alone (p < 0.001) [3].
• N-Methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionate, and kainate toxicities were attenuated in a concentration-dependent fashion by high concentrations of secobarbital or thiopental [4].
• Radiosensitization of Staphylococcus aureus by secobarbital sodium and other barbiturates [5].

Psychiatry related information on R(+)-Secobarbital

• In both studies, the effect of secobarbital in inducing and maintaining sleep was evaluated, as well as the effects of the drug on sleep stages [6].
• With short-term administration, secobarbital induced a slight decrease in rapid eye movement (REM) and slow-wave sleep and a significant increase in stage 2 sleep [6].
• In combination, marihuana and secobarbital had an additive effect on subjective responses and impairment in certain psychomotor performance tests [7].
• Mean reaction times obtained in a Sternberg memory-scanning task were examined for the effects of secobarbital at two doses (1.47 mg/kg and 2.94 mg/kg) spanning the dose range commonly used in clinical practice [8].
• Effect of d-amphetamine, secobarbital, and marijuana on choice behavior: social versus nonsocial options [9].

High impact information on R(+)-Secobarbital

• Influence of secobarbital and alpha-chloralose, and of vagal and sympathetic interruption, on left ventricular activation after acute coronary artery occlusion in the dog [10].
• Secobarbital-mediated inactivation of cytochrome P450 2B1 and its active site mutants. Partitioning between heme and protein alkylation and epoxidation [11].
• We report the intriguing finding that peroxisome proliferators, a major class of epigenetic carcinogen, are also extremely potent inducers of this enzyme being up to 50-fold more potent than one of the most effective barbiturates, secobarbital [12].
• Furthermore, although phenylbutazone and secobarbital altered the pharmacokinetics of warfarin, these compounds do not appear to influence its pharmacodynamics [13].
• They were experienced but nondependent users of central nervous system depressants who had the ability to reliably distinguish 150 mg secobarbital from placebo and to report positive subjective effects [14].

Chemical compound and disease context of R(+)-Secobarbital

• Flurazepam and secobarbital produced withdrawal symptoms during the post-treatment week, while tryptophan and placebo did not [15].
• In a double-blind parallel study in which a placebo phase preceded and followed the double-blind verum phase, midazolam 15 mg and Vesparax (150 mg secobarbital, 50 mg brallobarbital, 50 mg hydroxyzine) were administered to 30 female patients aged 20-76 years, suffering from insomnia secondary to neuromuscular disease [16].
• Spontaneously hypertensive rats (n = 22) and normotensive Wistar-Kyoto rats (WKY) (n = 23) 4-5 weeks of age were anesthetized with secobarbital sodium (50 mg/kg) intraperitoneally and acute hypertension was produced by an intravenous injection of norepinephrine (75 micrograms) [17].
• Self-assessments of drowsiness, anxiety and performance on a perceptual-motor task were similar in the melatonin and secobarbital patients [18].
• Patients from a polydrug abuse treatment program were titrated with either secobarbital or methaqualone, their primary drug of abuse, to a state of mild intoxication, consisting of lateral and vertical nystagmus, ataxia, slurred speech, and drownsiness [19].

Biological context of R(+)-Secobarbital

• To further characterize heterotropic allosteric regulation of ligand binding in general, and of ethidium binding in particular, to the Torpedo receptor, we measured the effects of three liquid anesthetics (diethyl ether, halothane, and butanol), two barbiturates (secobarbital and thiamylal), and urethane [20].
• Identification of the heme adduct and an active site peptide modified during mechanism-based inactivation of rat liver cytochrome P450 2B1 by secobarbital [21].
• In repeated testing of a single subject, 130 mg of secobarbital disrupted smooth-pursuit movements at least until 24 hrs after ingestion [22].
• Gas chromatographic assay utilized secobarbital as an internal standard and employed on-column methylation of the barbiturates to improve peak resolution [23].
• Post mortem kinetics of secobarbital [24].

Anatomical context of R(+)-Secobarbital

• Secobarbital caused a slight contraction only in the cerebral artery [25].
• The following drugs have been demonstrated to be secreted by the parotid glands of rats and human beings: amobarbital, chlorpromazine, codeine, glutethimide, meprobamate, pentobarbital, phenobarbital, and secobarbital [26].
• More than 90% of amorbarbital, phenobarbital, and secobarbital were removed within 10 min by the liquid membranes [27].
• Cyclobarbital, pentobarbital, and secobarbital also induced CYP1A2 mRNA in primary culture hepatocytes from C57BL/6 mice [28].
• Fast and slow skeletal muscles: effect of secobarbital on contractility of muscles from mice [29].

Associations of R(+)-Secobarbital with other chemical compounds

• To drug-free urine specimens, we added the following drugs of abuse to give concentrations twice the cutoff value for positive test results: 11-nor-9-carboxy-delta-9-tetrahydrocannabinol (9-carboxy-THC), oxazepam, secobarbital, morphine, benzoylecgonine, amphetamine, or phencyclidine (PCP) [30].
• EEG correlates of impaired attention performance under secobarbital and chlorpromazine in the monkey [31].
• Effects of phencyclidine, secobarbital and diazepam on eye tracking in rhesus monkeys [32].
• SR 41378 and secobarbital increased the power of the middle-frequencies (8-16 Hz) of the EEG, reduced that of 4-8 Hz (theta) activities and did not affect 1-4 Hz (delta) activities [33].
• To monitor their presence and fate in the aquatic environment, a method based on gas chromatography-mass spectrometry (GC-MS) has been developed to quantify butalbital, secobarbital, hexobarbital, aprobarbital, phenobarbital, and pentobarbital, all with a limit of detection (LOD) down to 1 ng/L [34].

Gene context of R(+)-Secobarbital

• Modulation of the biphasic effect of muscimol on prolactin secretion by benzodiazepines and secobarbital was investigated, using an in vitro superfusion system [35].
• Within-run and between-run precision were determined using three control samples (35, 100, and 250 ng/mL PCP; 0.4, 0.6, and 1.0 mg/L secobarbital) tested over a two-week period [36].
• Secobarbital did not influence P300 amplitude [37].
• Resting Cai was altered by all barbiturates tested except secobarbital and barbital, but not in a consistent manner, suggesting that the effect of barbiturates on resting Cai is not related either to their effects on NMDA receptor responses or to their behavioral effects [38].
• The glutathione peroxidase activity decreased significantly on PCB administration and the secobarbital further decreased the activity [39].

Analytical, diagnostic and therapeutic context of R(+)-Secobarbital

• Secobarbital, 100 mg, was evaluated in two separate sleep laboratory drug evaluation studies, each with 4 insomniac patients [6].
• Secobarbital attenuates excitotoxicity but potentiates oxygen-glucose deprivation neuronal injury in cortical cell culture [4].
• Effect of secobarbital and morphine on arterial blood gases in healthy human volunteers [40].
• The children received premedication with secobarbital, 6 mg.kg-1, pentazocine, 0.5 mg.kg-1, and atropine, 0.01 mg.kg-1 im [41].
• Samples were spiked with THC acid metabolite, benzoylecgonine, morphine, secobarbital, PCP, amphetamine, and lysergic acid diethylamide (LSD) then tested by Roche OnLine and Microgenics CEDIA immunoassay reagents [42].

References