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PubMed2000

Influence of volatile and intravenous anesthetics on the threshold of the acoustically evoked stapedius reflex.

The influence of volatile and intravenous anesthetics on the threshold of the acoustically evoked stapedius reflex (SR) was studied prospectively in 45 patients undergoing elective ENT surgical procedures. After premedication with flunitrazepam the patients were randomly assigned to one of nine groups. Group I: 70% nitrous oxide (N2O) in oxygen (O2); Groups II-VII: induction of anesthesia with intravenous thiopental, followed by mask inhalation with 100% O2 and 1.13% halothane (Group II), 2.52% enflurane (Group III) or 1.73% isoflurane (Group IV); or 70% N2O in oxygen, and 0.44% halothane (Group V), 0.86% enflurane (Group VI) or 0.75% isoflurane (Group VII): Group VIII: intravenous midazolam and ketamine; and Group IX: intravenous midazolam and alfentanil. Tympanometry and ipsilateral and contralateral SR measurements were performed when the effects of the anesthetics had achieved a steady state. Flunitrazepam raised the SR threshold only slightly. Substances applied during inhalation anesthesia either markedly increased the threshold contralaterally more than ipsilaterally (thiopental, N2O), or suppressed the reflex completely (thiopental, all volatile anesthetics with or without N2O). Under intravenous anesthesia the reflex was always present. The midazolam-ketamine combination influenced the threshold bilaterally only slightly, while the midazolam-alfentanil combination led to a pronounced, contralaterally significant elevation of the threshold. Based on its minimal influence on the SR threshold, flunitrazepam is especially suitable for sedation and the midazolam-ketamine combination for anesthesia in audiological diagnostic procedures.

Acoustic Impedance Tests↗
PubMed1982

Modulation of benzodiazepine receptor binding: insight into pharmacological efficacy.

The effects of GABA on the binding of analogues of benzodiazepines, triazolopyridazines, beta-carbolines and imidazodiazepines were examined in ligand/[3H] flunitrazepam competition experiments. GABA increased the potency of anxiolytics, like flunitrazepam, whereas the potency of benzodiazepine antagonists, like Ro15-1788, was largely insensitive to the influence of GABA. Several other agents including pyrazolopyridines, barbiturates and etomidate caused a chloride dependent enhancement of [3H] flunitrazepam binding but not an enhancement of [3H] propyl-beta-carboline-3-carboxylate binding.

Animals↗
PubMed1983

Alterations in benzodiazepine and GABA receptor binding in rat brain following systemic injection of kainic acid.

The binding of gamma-aminobutyric acid (GABA) and benzodiazepine to receptors was examined in regions of rat brain at various times after subcutaneous injection of kainic acid (KA, 15 mg/kg). The animals exhibited pronounced convulsions 90 min-4 hr after this treatment. During this period (2 hr after the injection of kainic acid) no alterations in the binding of [3H]-GABA or [3H]flunitrazepam to receptors were detected in the frontal cortex, the hippocampus or the amygdala-pyriform cortex. After recovery from the acute convulsive phase, the rats appeared to be hyperexcitable, hyperactive, and displayed marked aggression and occasional clonic convulsions one to 80 days later. During this period a marked increase (80-200%) in the number of binding sites for GABA in the amygdala-pyriform cortex occurred but this was associated with a slow decrease in the number of binding sites for [3H]flunitrazepam to 70% control value at 3 weeks. Binding of the "peripheral"-type of benzodiazepine ligand, [3H]-Ro5-4864, was increased to 450% of control 3 weeks after injection. In addition, the ability of GABA to stimulate the binding of [3H]flunitrazepam was reduced when measured 3 days after the injection of kainic acid. It is suggested that the long-term behavioural syndrome observed in kainic acid-treated rats, as well as the reduced effectiveness of diazepam in preventing seizures in animals treated with kainic acid, (Czuczwar, Turski, Turski and Kleinrock, 1981) may be explained in part by a reduction in the number of neuronal benzodiazepine receptors and a "desensitization" of the GABA receptors which are coupled to benzodiazepine receptors.

Animals↗
PubMed1992

Effect of sedative drugs upon receptor binding in vivo.

Acute treatment with pentobarbital (PB), ethanol and flunitrazepam significantly decreased 3H-SCH 23390 binding in mouse striatum in a dose dependent manner. In contrast, no significant alterations in 3H-SCH 23390 binding in the cerebral cortex have been observed in mice treated with these sedative and hypnotic drugs. Flumazenil Ro15-1788) reversed the effect of flunitrazepam suggesting the reduction in dopamine D1 receptor binding in the striatum was mediated via GABA-Bz-Cl channel complex. Using kinetic analysis, it was found that such changes in dopamine D1 receptor binding in vivo were mainly due to changes in rates of ligand-receptor binding in vivo. Other non-site-specific drugs such as propanol and butanol also decreased 3H-SCH 23390 binding in vivo, depending on their lipophilicities. These results indicated that micro-environmental factors surrounding receptors, including cell membranes seem to have important roles in receptor binding in vivo. Both PB and flunitrazepam decreased muscarinic acetylcholine receptor binding in mouse cortex, striatum, hippocampus and other regions. Together with the fact that PB also altered 3H-Ro15-1788 binding in vivo, this suggested global changes in microenvironmental factors may occur due to these sedative drugs. In vivo quantitative analysis of neuroreceptors with positron emission tomography (PET) seems to have some potencies to reveal the neurochemical base of benzodiazepine dependence.

Animals↗
PubMed1993

A comparison of Ro 16-6028 with benzodiazepine receptor 'full agonists' on GABAA receptor function.

Ro 16-6028 (bretazenil) has a pharmacological profile characteristic of a partial agonist at the gamma-aminobutyric acidA (GABAA) receptor-linked benzodiazepine site. The present study utilized modulation of [35S]t-butylbicyclophosphorothionate ([35S]TBPS) binding and enhancement of GABA-stimulated 36Cl- uptake to further assess Ro 16-6028's partial agonist profile in vitro. Ro 16-6028 was the most potent benzodiazepine examined, exhibiting an IC50 (concentration at which half-maximal inhibition of specific [35S]TBPS binding occurs) of 6.1 nM, compared to clonazepam (7.9 nM), flunitrazepam (13.6 nM) and diazepam (91.1 nM). The rank order of potency for inhibition of [35S]TBPS binding was identical to that for inhibition of [3H]flunitrazepam binding. However, Ro 16-6028 was less efficacious in that it produced 27% inhibition of specific [35S]TBPS binding, compared to clonazepam (34%), flunitrazepam (41%) or diazepam (49%). Ro 16-6028 antagonized the inhibition of [35S]TBPS binding produced by 10 microM diazepam. Ro 16-6028 was also more potent and less efficacious than diazepam in potentiating GABA-stimulated 36Cl- uptake. These results provide further evidence that Ro 16-6028 is acting as a partial agonist at the benzodiazepine receptor in modulating function of the GABAA receptor complex.

Animals↗
PubMed1992

Benzodiazepines preferentially affect mesolimbic dopamine turnover in rats.

Withdrawal of benzodiazepines in man may induce hallucinatory symptoms and can evoke delusional depressions, which can be treated with dopamine-antagonistic drugs. Withdrawal of benzodiazepines in rats induces a strong hyperactivity during daytime, leaving the nighttime activity relatively undisturbed. This hyperactivity may be related to an enhanced dopaminergic activity in the mesolimbic area, especially in the nucleus accumbens. Mesolimbic dopaminergic activity may be specifically involved in the development of benzodiazepine withdrawal. Acute administration of benzodiazepines in otherwise non-treated rats, has been described not to affect the dopamine-turnover in the nucleus accumbens, measured by synthesis inhibition. However, activation by administration of haloperidol (feedback activation) can be suppressed by benzodiazepines effectively. Five different benzodiazepines viz. desmethyldiazepam (DMD), lorazepam (LRZ), brotizolam (BTZ), triazolam (TRZ) and flunitrazepam (FNZ) have been compared with respect to their acute effects. Using a 3-fold increase in dopamine turnover (determined by measuring the DOPAC-concentration), benzodiazepines were capable to reduce this increase maximally for 70-80% in the nucleus accumbens. The results point to a selective effect of benzodiazepines in the nucleus accumbens. The increase induced by haloperidol in the corpus striatum was found to be much less sensitive to benzodiazepines. In contrast to the other compounds lorazepam appeared to have no effect on haloperidol-induced increase in DOPAC concentration. Flunitrazepam and brotizolam did affect not only the haloperidol-induced DOPAC increase but also the basal DOPAC concentrations. Linear dose-response curves could not be obtained for the compounds, but minimal effective doses could be assessed. Flunitrazepam and triazolam appeared to be the most active compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

The effect of benzodiazepines and beta-carbolines on GABA-stimulated chloride influx by membrane vesicles from the rat cerebral cortex.

Benzodiazepine agonists such as diazepam, flunitrazepam and clonazepam enhanced GABA (30 microM)-stimulated 36Cl- uptake in membrane vesicles from the rat cerebral cortex. The rank order of potencies was flunitrazepam greater than diazepam = clonazepam. beta-Carboline-3-carboxylate esters beta-CCM, beta-CCE and DMCM inhibited GABA-stimulated 36Cl- uptake. The rank order of inhibitory potencies was DMCM greater than beta-CCM greater than beta-CCE. The benzodiazepine antagonist Ro15-1788 antagonized the enhancement of flunitrazepam and the inhibition of DMCM on GABA-stimulated 36Cl- uptake in a competitive inhibitory manner. These results suggest that benzodiazepine receptors regulate GABA-stimulated 36Cl- uptake and there is a functional coupling between the GABA and benzodiazepine receptors, and chloride channels in membrane vesicles from the rat cerebral cortex.

Animals↗
PubMed1998

Pharmacological properties of the GABA(A) receptor complex from brain regions of (hypoemotional) Roman high- and (hyperemotional) low-avoidance rats.

The pharmacological properties of benzodiazepine binding sites of the gamma-aminobutyric acid (GABA)A receptor complex from cortical, hippocampal and cerebellar membranes of Roman high-avoidance (RHA/Verh) and Roman low-avoidance (RLH/Verh) rats were investigated. No major differences between the two lines were found in the binding parameters of [3H]flunitrazepam (a non-selective agonist). [3 H]zolpidem (a Type I selective agonist) or [3 H]ethyl 8-azido-6-dihydro-5-methyl-6-oxo-4H-imidazol[1,5-a]-[1,4]benzodiazepine- 3-carboxylate (Ro15-4513) (a partial inverse agonist). Neither the Kd values nor the Bmax for these ligands differed between RHA/Verh and RLA/Verh rats in any of the brain regions studied. As a result, the proportion of Type I binding sites in cortical and hippocampal membranes of RHA/Verh and RLA/Verh rats or the 'diazepam-sensitive' and the 'diazepam-insensitive' binding sites in cerebellar membranes, calculated from the [3H]flunitrazepam and [3H]zolpidem maximal binding sites or from [3H]Ro15-4513 binding (in the absence or in presence of diazepam), respectively, was also similar. Furthermore, there were no differences between the two rat lines in the allosteric interactions between GABA and the benzodiazepine binding sites (labeled with [3H]flunitrazepam) in all three areas tested or the Type I binding sites (labeled with [3H]zolpidem) in the hippocampus. In contrast, RLA/Verh rats showed a significant reduction in the allosteric interactions between GABA and [3H]zolpidem binding sites in the cortex. As a whole, these results indicate the absence of generalized between-line differences in the GABA(A) receptor complex showing, at the same time, the existence of some specific differences in allosterism within the GABA(A) complex. These differences may contribute to the divergent emotional responses which characterize the RHA/Verh and RLA/Verh rat lines.

Animals↗
PubMed2001

Lack of allosteric modulation of striatal GABA(A) receptor binding and function after cocaine sensitization.

GABA(A) receptor binding after repeated cocaine has been shown to be either increased as indicated by benzodiazepine binding or decreased as indicated by convulsant-site binding. We measured the GABA binding site with [3H]-muscimol binding to GABA(A) receptors and found no differences between saline- and cocaine-sensitized rats. Allosteric modulation of [3H]-muscimol binding with flunitrazepam was also unchanged after cocaine sensitization. In addition, [3H]-flunitrazepam binding and allosteric modulation of [3H]-flunitrazepam binding with GABA was unchanged after 1 day withdrawal from repeated cocaine. GABA(A) receptor function and allosteric modulation of GABA(A) receptor function measured by GABA-stimulated Cl(-) uptake was also unchanged after withdrawal from repeated cocaine. Finally, in vitro cocaine reduced GABA(A) receptor function in striatal microsacs of saline- and cocaine-treated rats. In conclusion, repeated cocaine did not change the coupling of the GABA(A) receptor between the GABA and benzodiazepine (BZD) binding site after 1 day withdrawal.

Allosteric Regulation↗
PubMed1997

Alterations in acetylcholine, NMDA, benzodiazepine receptors and protein kinase C in the brain of the senescence-accelerated mouse: an animal model useful for studies on cognitive enhancers.

The senescence-accelerated mouse (SAMP8) is a useful murine model of accelerated aging and learning deficiency. We examined bindings of [3H]pirenzepine, [3H]dizocilpine (MK-801), [3H]flunitrazepam, [3H]8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) and [3H]phorbol 12,13-dibutylate (PDBu) in SAMP8 brains, and compared them to those of SAMR1 (control). In the hippocampus of SAMP8 at 12 months, bindings of [3H]pirenzepine, [3H]MK-801, [3H]flunitrazepam, [3H]8-OH-DPAT and [3H]PDBu were significantly lower than those in SAMR1. In the cerebral cortex, bindings of [3H]pirenzepine, [3H]flunitrazepam and [3H]8-OH-DPAT were higher in SAMP8 than in SAMR1 at 12 months. [3H]PDBu binding was decreased in both the fractions of the membrane and cytosol in the hippocampus of SAMP8. The neurochemical findings presented here support behavioral and pharmacological findings that SAMP8 is a useful model of learning dysfunction and anxiety-deficiency. The usefulness of SAMP8 in studies on cognitive enhancers is also discussed.

Aging↗
PubMed1991

[Effect of peroperative analgesia on immediate postoperative oxygen consumption].

Oxygen consumption in the immediate postoperative period was assessed in a series of twelve patients undergoing maxillofacial surgery, randomly assigned to two groups (n = 6 for each). The anaesthetic protocol was the same in all patients: premedication with flunitrazepam 30 micrograms.kg-1, induction with flunitrazepam 20 micrograms.kg-1, fentanyl 5 micrograms.kg-1, thiopentone 5 mg.kg-1, pancuronium bromide 80 micrograms.kg-1, and maintenance during the first three hours with flunitrazepam 10 micrograms.kg-1.h-1 and pancuronium 0.03 micrograms.kg-1.h-1. All the patients were given a continuous infusion of fentanyl during the whole length of the surgery: in Group I (GI), 3 micrograms.kg-1.h-1 and in Group II (GII), 1 microgram.kg-1.h-1. The patients in Group II were also given enflurane 1.2 +/- 0.3 vol %. During the immediate postoperative period, the parameters studied were measured by means of an Engström Metabolism Calculator at the 15th, 30th, 45th, 60th, 120th and 240th minutes, and at the time of extubation. In GII, postoperative heart rate and lactic acid levels were higher than in GI (p less than 0.05). Both groups had oxygen consumption values greater than theoretical resting levels. However, postoperative oxygen consumption was greatly increased in GII with respect to GI during the first 4 hours (p less than 0.01). The respiratory quotient was greater in GI than in GII at the end of the study (p less than 0.05). These data indicate that the intraoperative analgesic technique influences postoperative oxygen consumption. A dose of fentanyl of 3 micrograms.kg-1.h-1 is more efficient than one of 1 microgram.kg-1.h-1 associated with enflurane.

Adult↗
PubMed1987

[Propofol versus propanidid for the conduction of suspension laryngoscopy].

Forty patients who where to undergo suspension laryngoscopy were randomly assigned to two groups, the first receiving 1 microgram . kg-1 fentanyl and a bolus of 2.5 mg . kg-1 propofol followed by 5 to 10 mg . kg-1 . h-1 propofol infusion, and the second 1 microgram . kg-1 fentanyl and 0.2 mg . kg-1 flunitrazepam with 8 mg . kg-1 propanidid in a bolus followed by 40 to 50 mg . kg-1 propanidid infusion. The following parameters were studied: length of apnoea, quality of anaesthesia, the time between stopping giving the anaesthetic and the moment when the patient opens the eyes, gives his name and date of birth, the heart rate, the systolic, diastolic and mean blood pressures, blood gases, before induction, during suspension and at stopping the infusion. Anaesthetic quality was the same for both protocols, and the variations of the haemodynamic parameters were very similar for both groups. Apnoea lasted twice as long with propofol as with the flunitrazepam-propanidid association (p less than 0.001), whereas recovery was twice as quick (p less than 0.001). This seemed to confirm that propofol is better indicated for this type of surgery than the previously used flunitrazepam-propanidid association.

Adult↗
PubMed1983

Kinetics of five benzodiazepine hypnotics in healthy subjects.

Kinetics of five benzodiazepine hypnotics (15 mg flurazepam, 1 mg flunitrazepam, 5 mg nitrazepam, 10 mg temazepam, and 0.5 mg triazolam) were compared in the same group of 12 healthy subjects. Plasma concentrations of parent drugs were determined by capillary gas chromatography with electron-capture detection. For flurazepam, the N-desalkyl metabolite (DAF) was measured. Flunitrazepam, nitrazepam, temazepam, and triazolam were rapidly absorbed, although there was considerable variability; mean peak times (ranges) were: 1.3 (0.3 to 3) hr, 1.8 (0.7 to 6) hr, 1.2 (0.3 to 4) hr, and 1.1 (0.7 to 2) hr. Plasma concentrations of DAF increased rather slowly and reached their maximum between 3 and 48 hr after flurazepam. There were considerable differences in elimination t1/2s, with means of 35 (15 to 66) hr for flunitrazepam, 28 (22 to 33) hr for nitrazepam, 12 (8 to 22) hr for temazepam, 2.4 (1.4 to 3.9) hr for triazolam, and 84 (40 to 114) hr for DAF. Sex differences in elimination t1/2 were only observed for DAF: 99 hr in women and 69 hr in men. Our results show that there are considerable differences in the kinetics of the diazepines.

Adult↗
PubMed2000

Cyclic AMP-mediated regulation of GABA(A) receptor subunit expression in mature rat cerebellar granule cells: evidence for transcriptional and translational control.

Exposure of rat cerebellar granule cells cultured to maturity in vitro to forskolin, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2cAMP), and 3-isobutyl-1-methylxanthine (IBMX) down-regulated GABA(A) receptor alpha6 and beta3 subunits but up-regulated alpha1 and beta2 subunits with respect to vehicle-treated controls. Dideoxyforskolin had no effect on subunit expression. Protein kinase A inhibitors, H-89 and Rp-adenosine 3',5'cyclic monophosphothioate, prevented these effects on alpha1 but not alpha6 subunit expression. Flunitrazepam-sensitive [3H]Ro 15-4513 binding sites were increased by 144 +/- 20% following forskolin treatment. [3H]Ro 15-4513 photoaffinity labelling showed that the GABA(A) receptor alpha1 subunit was the principal locus of the increased flunitrazepam-sensitive [3H]Ro 15-4513 binding. Forskolin decreased flunitrazepam-insensitive [3H]Ro 15-4513 binding sites by 25 +/- 8% and resulted in a 20% decrease in the irreversible incorporation of radioactivity in the alpha6 subunit. Steady-state levels of GABA(A) receptor subunit mRNAs were determined by semiquantitative RT-PCR in forskolin-treated cultures. Forskolin, Bt2cAMP, and IBMX down-regulated GABA(A) receptor alpha6 subunit mRNA expression; alpha1 and beta3 mRNA levels were unaffected, whereas beta2 subunit mRNA was up-regulated. Dideoxyforskolin had no significant effect on alpha1, alpha6, beta2, and beta3 mRNA levels. Thus, in mature cerebellar granule cells, GABA(A) receptor expression can be regulated by intracellular cyclic AMP levels. This occurs at the level of gene transcription and/or translation by mechanisms that are only partially governed by protein kinase A.

Affinity Labels↗
PubMed1991

Stoichiometry of muscimol and benzodiazepine binding sites in developing mouse cerebellum.

The ontogeny of high affinity GABAA and central benzodiazepine receptors in the mouse cerebellum was investigated by measuring [3H]muscimol and [3H]flunitrazepam binding to membrane preparations during postnatal development. In the P2 fraction, [3H]muscimol binding was much more abundant than [3H]flunitrazepam binding at all ages. [3H]muscimol Bmax exhibited a peak around postnatal day 25 while [3H]flunitrazepam binding did not follow a parallel course. These results can be explained by the preferential presence in cerebellum of certain variants of the different subunits of the GABAA receptor complex and with different topographical distributions of the different receptor subtypes. Development dependent changes of organelle distribution during subcellular fractionation also contributed to the described developmental pattern.

Animals↗
PubMed1982

A radioreceptor assay to study the affinity of benzodiazepines and their receptor binding activity in human plasma including their active metabolites.

1 A radioreceptor assay has been established to measure the receptor affinities of numerous benzodiazepines in clinical use. 2 The time course of receptor binding activity was studied by this method in the plasma of eight healthy subjects randomly treated with 1 mg lormetazepam (Noctamid, 2 mg flunitrazepam (Rohypnol, and 10 mg diazepam (Valium, and placebo on a cross-over basis. Blood samples were collected up to 154 h after treatment. 3 Receptor affinities of numerous benzodiazepines on vitro show good correlation with therapeutic human doses (r = 0.96) and may be predictive of drug potency in man. 4 Mean peak plasma levels of lormetazepam binding equivalents were 4.8 +/- 1 ng/ml at 2 h after lormetazepam, 7.2 +/- 1.8 ng/ml at 8 h after flunitrazepam, and 17.9 +/- 2.7 ng/ml at 15 h after diazepam. Plasma elimination half-lives of benzodiazepine binding equivalents were 9.3, 23 and 63 h, respectively. 5 Slow elimination of benzodiazepine binding equivalents following flunitrazepam and diazepam may be due to persistent active metabolites.

Adult↗
PubMed1983

Peroral diazepam compared with parenteral morphine/scopolamine with regard to gastric content.

In a prospective study, 62 adult patients were studied with respect to the volume and pH of their gastric contents after receiving randomly one of three different premedications. One group received flunitrazepam 2 mg perorally on the night before operation and diazepam 0.2 mg per kg body weight perorally at 7.00 a.m. on the day of operation. The patients in the second group were given flunitrazepam 2 mg perorally the night before operation and morphine/scopolamine i.m. 1 h prior to operation. In the third group no flunitrazepam was given on the night before operation, and the patients were premedicated with morphine/scopolamine i.m. 1 h preoperatively. No statistically significant difference was found between the groups with respect to the volume and pH of gastric contents after induction of anaesthesia.

Adult↗
PubMed1993

Propofol induces bronchodilation in mechanically ventilated chronic obstructive pulmonary disease (COPD) patients.

The aim of this study was to evaluate the effects of propofol administration (2 mg.kg-1 i.v.) on the airways resistances and respiratory mechanics of patients affected by COPD exacerbation, requiring mechanical ventilation. Twenty patients required anaesthesia for diagnostic or therapeutic procedures. Fourteen consecutive patients were divided at random into two groups: Group P received propofol and Group C (control) received only Intralipid 10%; an additional group of six patients received i.v. flunitrazepam (0.03 mg.kg-1). Lung mechanics (dynamic and static compliance, peak inspiratory pressure, intrinsic positive and expiratory pressure, minimal and maximal resistances of the respiratory system) were evaluated in basal conditions and 3 and 6 min after propofol, Intralipid or flunitrazepam administration. We did not observe significant variations of the evaluated variables after Intralipid or flunitrazepam (Groups C and F), while in patients who received propofol (Group P), we observed the following modifications: dynamic compliance increased from 2.3 +/- 0.3 to 2.8 +/- 0.4 ml.kPa-1 (P < 0.05), peak inspiratory pressure decreased from 3.3 +/- 0.7 to 2.8 +/- 0.4 kPa (P < 0.05), minimal resistances of the respiratory system (that mainly reflect airways resistances) decreased from 1 +/- 0.2 to 0.7 +/- 0.2 kPa.l-1 x s-1 (P < 0.01). Our results suggest that propofol induces bronchodilation in mechanically ventilated COPD patients, and that this effect is not related specifically to the induction of general anesthesia.

Aged↗