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PubMed2000

Effect of diazepam on the immune response of rats exposed to acute and chronic swim stress.

To examine the effect of the anti-stress agent diazepam on the immune response, rats were exposed either to acute swim stress, i.e., swimming once only for 30 minutes (non-trained swimmers), or to chronic stress with gradual progressive training for 6 weeks (trained swimmers). Both groups of animals were divided into subgroups treated before swimming with and without diazepam, 1 mg/kg, administered i.m. The phagocytic capacity and superoxide anion generation of the peritoneal macrophages was examined. In addition, the proliferative response of the splenic cells (splenocytes) to concanavalin A (Con A) and phytohemagglutinin (PHA), as well as the serum corticosterone levels were investigated. Diazepam abolished increased superoxide anion production in both non-trained and trained swimmers. In non-trained swimmers, the number of latex particles internalized by each cell was decreased and further reduced by the drug. In trained rats treated with diazepam, the percentage of phagocytosing cells remained reduced compared to controls, whereas the drug prevented a decrease in the engulfing capacity of individual cells. Diazepam lowered the suppressed proliferative response of the splenocytes to PHA found in non-trained swimmers. It is concluded that diazepam modifies the immune response of rats exposed to acute and chronic swim stress.

Animals↗
PubMed1999

The effects of flumazenil on two way active avoidance and locomotor activity in diazepam-treated rats.

The present study was undertaken to determine the effects of chronic flumazenil treatment alone and simultaneously with diazepam on acquisition performance in an active-avoidance task and on locomotor activity in rats. Flumazenil (5, 10 and 20 mg/kg) and diazepam (0,5, 1.0 and 2.0 mg/kg) were administered intraperitoneally to rats before each daily training session for 5 days. The baseline of avoidance performance was set to approximately 50% and responses were expressed as acquisition rate. Locomotor activity of the rats was simultaneously recorded but only following the first training session. Diazepam decreased acquisition rate between the dose range used. Flumazenil had no effect on the acquisition rate of naive rats but reversed low dose diazepam-induced learning and memory impairment. Diazepam induced locomotor depression within the same dose range that decreased acquisition rate. Flumazenil had no effect on locomotor activity, but reversed the locomotor depressant effect of diazepam. The striking contradiction with previous data that flumazenil has no effect on learning-memory processing is discussed.

Animals↗
PubMed2003

Diazepam or midazolam for external DC cardioversion (the DORM Study).

AIMS: To compare the clinical efficacy and tolerability of two intravenous sedatives for physician-led DC cardioversion of atrial arrhythmias. METHODS AND RESULTS: One hundred and forty-one patients attending for elective DC cardioversion of atrial arrhythmias were randomized to intravenous midazolam or diazepam. Sedation was administered using titration protocols. Procedure times, operator satisfaction scores and adverse events were documented. The patients immediate, 24- and 48-h recall and awareness of after-effects were obtained from questionnaires. Seventy-one patients received midazolam (mean 12.5 mg) and 70 patients received diazepam (mean 28.1 mg). There were 16 minor adverse events with midazolam (20% hypotension, 3% oxygen desaturation) and nine with diazepam (7% hypotension, 6% required additional analgesia), P = 0.14. There were no major adverse events. Sedation time was 5.0 +/- 3.4 min for midazolam and 6.5 +/- 3.4 min for diazepam (P = 0.0016). Patients awoke 77 +/- 46 min post-sedation with midazolam and 39 +/- 24 min with diazepam (P < 0.0001). There was no recall of the procedure at 48 h and no difference in awareness of after-effects between the two groups at 24 or 48 h, P = ns. CONCLUSION: Physician-led cardioversion of atrial arrhythmias using intravenous sedation is effective and well tolerated. Sedation with diazepam was associated with fewer minor adverse events and a quicker recovery time than midazolam.

Atrial Fibrillation↗
PubMed1999

Respiratory depression in children receiving diazepam for acute seizures: a prospective study.

The aim of this study was to determine the incidence of respiratory depression following the use of diazepam in children presenting with seizures. All children presenting with seizures to a children's A & E department over a period of 9 months were studied prospectively. Respiratory depression was defined as a fall in respiratory rate or oxygen saturation, or apnoea resulting in ventilation or resuscitation with bag-and-mask oxygen. There were 130 patient episodes involving 97 children who received treatment for their seizures before admission and/or in the A & E department. Administration of diazepam resulted in 122 patient episodes. The route of administration was rectal in 91 episodes, intravenous in 12 episodes, and both rectal and intravenous in 19 episodes. Eleven children had respiratory depression in relation to diazepam administration. Eight of these children required ventilation. The overall incidence of respiratory depression following the use of diazepam was 9%. The incidence of respiratory depression following diazepam given intravenously or rectally is high. The use of diazepam as first-line therapy for children with acute seizures needs to be reviewed.

Acute Disease↗
PubMed1992

Studies on the excretion of diazepam and nordazepam into milk for the prediction of milk-to-plasma drug concentration ratios.

The influence of varying protein and fat content in milk of New Zealand White rabbits on the milk-to-plasma drug concentration (M/P) ratio of diazepam was studied. At various time points after littering, a bolus dose (1.5 mg/kg) followed by a 26-hr infusion (1.8 mg/h) of diazepam was administered to freely moving rabbits via a jugular vein catheter. Milk and blood samples were collected to allow characterization of milk composition and quantitative determination of diazepam and nordazepam in milk and plasma. At steady state diazepam showed M/P ratios between 3.7 and 9.5, whereas nordazepam showed ratios between 2.1 and 4.3, respectively. The relative importance of milk protein binding and milk-fat partitioning for the excretion of a drug into milk depended on the drug's affinity to milk fat. A stepwise multiple regression analysis suggested that observed M/P ratios of diazepam could be explained by considering the fat content of milk alone. Nordazepam with a lower solubility in milk fat showed M/P ratios which could be best explained by considering protein and fat concentrations together. Using the data from the infusion studies, two recently published diffusional models to predict M/P ratios were evaluated. Neither model could accurately predict the M/P ratios of diazepam and nordazepam observed in rabbits. However, after extending the model described by Atkinson and Begg to take the actually measured partitioning between skim milk and milk fat into account, a great improvement in the predictive power for observed M/P ratios occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effect of omeprazole on diazepam disposition in the rat: in vitro and in vivo studies.

PURPOSE: The inhibitory effects of omeprazole on diazepam metabolism in vitro and in vivo are compared in the rat. METHODS: 3-hydroxylation and N-demethylation of diazepam was investigated in the presence of a range of omeprazole concentrations (2-500 microM) in hepatic microsomes and hepatocytes. Zero order infusions together with matched bolus doses of omeprazole were used to achieve a range of steady state plasma concentrations (10-50mg/L) and to study the diazepam-omeprazole interaction in vivo. RESULTS: The 3-hydroxlation pathway was more prone to inhibition (KIs 108 +/- 30 and 28 +/- 11 microM in microsomes and hepatocytes, respectively) than the demethylation pathway (KIs of 226 +/- 76 and 59 +/- 27 microM in microsomes and hepatocytes, respectively). In both in vitro systems, the mechanism of inhibition was competitive with Km/KI ratios larger than 1 for the 3HDZ pathway and smaller than 1 for the NDZ pathway. There was an omeprazole concentration dependent decrease in diazepam clearance in vivo which could be modelled using a simple inhibition equation with a KI of 57 microM (19.8mg/L). In contrast there was no statistically significant change in the steady state volume of distribution for diazepam in the presence of omeprazole. CONCLUSIONS: The in vivo KI for the omeprazole: diazepam inhibition interaction shows closer agreement with the KI values obtained in hepatocytes than with those observed in microsomes.

Animals↗
PubMed2000

Local transfer of diazepam, but not of cocaine, from the nasal cavities to the brain arterial blood in rats.

Nasal administration to rats of small molecules (tritiated water, tyrosine, and propanol) results in a higher concentration in the brain arterial blood than in other arteries. The preferential distribution is based on a counter current transfer, which takes place between nasal vein blood and brain arterial blood in the cavernous sinus-carotid artery complex. The present experiments attempt to document that drugs may also be transferred by this system. Groups of 10 large male rats were anaesthetised and intubated. Two catheters were inserted into the same carotid artery, one tip pointing towards the head, the other towards the heart. Parallel blood samples were obtained every 30 sec. for 10 min. after nasal administration of radioactively labelled diazepam or cocaine, and the plasma radioactivity measured. Control groups received the drugs intravenously. The uptake of diazepam was rapid, while cocaine uptake was slow. The average ratio between the radioactivity of parallel samples (R: "Head" plasma/"Heart" plasma) in rats treated with nasal diazepam was 1.12+/-0.04, 181 (average+/-S.E.M., n) for the whole 10 min. period and 1.20+/-0.05, 96 for the second half of the sampling period. The increase of 12 and 20% is highly significant. The intravenous ratio for diazepam and both R's for the cocaine groups were not significantly different from 1.00. The present experiments show that nasal administration of diazepam induces a relatively higher concentration in the brain arterial blood than in parallel samples obtained from another artery. A preferential, first-pass distribution to the brain after nasal administration of diazepam may thus exist.

Animals↗
PubMed1980

Intravenous diazepam and oral ethanol interaction.

The mechanism of the interaction between ethanol and diazepam is not known. Six healthy male subjects (aged 21 to 32 yr) were randomly assigned in a balanced crossover study to each of two treatments, 28 days apart: (1) diazepam 10 mg intravenously over 20 min, preceded by 60 min with ethanol 0.7 gm/kg (diluted to 20% v/v) orally over 15 min and followed for 8 hr by ethanol 0.15 gm/kg/hr to maintain the blood alcohol concentrations between 800 to 1,000 mg/l; (2) diazepam 10 mg intravenously over 20 min. The area under the curve (AUC) for total diazepam increased in all subjects (30.1 +/- 10.7%, mean = SD, p < 0.02) after ethanol. Since AUCfree diazepam also rose in all (mean - 26.5 +/- 17.3%) and AUC of the metabolite N-desmethyldiazepam fell (mean = 50.5 +/- 11.7%, p < 0.01) there had been inhibition of hepatic intrinsic clearance of free drug. The susceptibility of individuals to inhibition of N-desmethylation by ethanol is qualitatively determined by total drug concentrations. Estimation of free diazepam concentration coupled with measurement of metabolite affords a qualitative and quantitative evaluation of the mechanism of this interaction.

Administration, Oral↗
PubMed1980

Diazepam disposition determinants.

Factors influencing diazepam kinetics were assessed in 4 equal groups (n = 11) of young male and female (aged 21 to 37 yr) and elderly male and female (aged 61 to 84 yr) subjects, all of whom were healthy. In all 44, plasma diazepam concentrations were determined by electron-capture gas-liquid chromatography in multiple samples drawn for as long as 9 days after a single 5- to 10-mg intravenous dose. Based upon total (bound + free) diazepam concentrations, volume of distribution (Vd) ranged from 0.7 to 4.7 l/kg, and became larger both with increasing age and with female sex. Clearances of total (bound + free) diazepam in young and elderly females were nearly identical (0.51 and 0.48 ml/min/kg), but clearance was higher in young than elderly males (0.39 and 0.24 ml/min/kg, p less than 0.01). The unbound fraction of diazepam in plasma (range, 0.9% to 2.7%) did not depend on sex, but was greater in the elderly than in the young. In part this related to lower plasma albumin concentrations in the elderly. After correction of kinetic data for individual differences in free fraction, Vd was larger in the females than in the males, but the effect of age was small. Clearance of unbound diazepam (intrinsic clearance) tended to be higher in the females than in the males of both age groups, and was higher in the young than in the elderly of both sexes (male: 29.9 and 14.9 ml/min/kg, p less than 0.005; female: 43.6 and 28.0 ml/min/kg, p less than 0.05). Smoking was associated with higher clearance values, particularly among young subjects.

Adult↗
PubMed1984

Ketamine kinetics in unmedicated and diazepam-premedicated subjects.

Plasma ketamine concentrations after diazepam and placebo pretreatment were examined in a double-blind, randomized, cross-over study. Eight healthy male subjects received either diazepam or a 0.9% NaCl placebo before ketamine and received the alternate combination 5 to 24 days later. Ten minutes before ketamine dosing, diazepam, 0.3 mg/kg, or placebo in equal volume was injected intravenously at a rate not exceeding 5 mg/min. Ketamine, 2.2 mg/kg iv, was injected over 1 min. For the clinically relevant period for anesthesia (1 to 30 min), diazepam-ketamine treatment resulted in higher plasma levels at most time points, but diazepam pretreatment did not alter plasma levels of metabolite KI and pseudometabolite KII nor the 24-hr urinary excretion of ketamine, KI, and KII. Ketamine kinetics followed a three-term exponential decline under both treatment conditions. After placebo-ketamine dosing, plasma t 1/2s were as follows: distribution (pi t 1/2) = 24.1 sec, redistribution (alpha t 1/2) = 4.68 min, and elimination (beta t 1/2) = 2.17 hr. After diazepam-ketamine dosing, t 1/2s were: pi t 1/2 = 25.0 sec, alpha t 1/2 6.37 min, and beta t 1/2 = 2.32 hr.

Adult↗
PubMed1989

Pharmacokinetic and electroencephalographic study of intravenous diazepam, midazolam, and placebo.

Eleven healthy volunteers received a single intravenous dose of diazepam (0.15 mg/kg), midazolam (0.1 mg/kg), and placebo by 1-minute infusion in a double-blind, three-way crossover study. Plasma concentrations were measured during 24 hours after dosage, and the electroencephalographic (EEG) power spectrum was simultaneously computed by fast-Fourier transform to determine the percentage of total EEG amplitude occurring in the 13 to 30 Hz range. Both diazepam and midazolam had large volumes of distribution (1.2 and 2.3 L/kg, respectively), but diazepam's half-life was considerably longer (33 versus 2.8 hours) and its metabolic clearance lower (0.5 versus 11.0 ml/min kg) than those of midazolam. EEG changes were maximal at the end of the diazepam infusion and 5 to 10 minutes after midazolam infusion. Percent 13 to 30 Hz activity remained significantly above baseline until 5 hours for diazepam but only until 2 hours for midazolam. For both drugs, EEG effects were indistinguishable from baseline by 6 to 8 hours, suggesting that distribution contributes importantly to terminating pharmacodynamic action. The relationship of EEG change to plasma drug concentration indicated an apparent EC50 value of 269 ng/ml for diazepam as opposed to 35 ng/ml for midazolam. However, Emax values were similar for both drugs (+19.4% and +21.3%, respectively).

Adult↗
PubMed1991

Differing effects of the anxiolytic agents buspirone and diazepam on control of breathing.

We compared ventilatory effects of the nonsedating anxiolytic buspirone with those of the sedating anxiolytic diazepam in nine normal men. Resting ventilatory parameters and ventilatory responses to CO2 rebreathing and inspiratory threshold loading were measured before and after placebo, diazepam, and buspirone. Placebo had no ventilatory effects. Diazepam had no effect on resting ventilation but depressed response to CO2. Buspirone had no effect on resting ventilation or CO2 response. During loading, buspirone did not alter the augmentation of mouth pressure; diazepam produced a trend toward less augmentation. Both anxiolytics altered the load compensation response for the group; in particular, an increase in ventilation during loading (seen in three of nine subjects) was suppressed by drug administration. Diazepam also markedly depressed one subject's loaded ventilation below unloaded ventilation. In summary, buspirone did not cause the depression of respiratory center chemosensitivity that was seen with diazepam and produced less depression of load compensation in normal subjects. This suggests that it may be a safer anxiolytic in patients with lung disease.

Administration, Oral↗
PubMed1982

Clinical effects and metabolism of diazepam in patients with chronic liver disease.

1. After a fixed weight-related dose given intravenously, plasma diazepam concentrations were significantly lower in 11 cirrhotic patients than in controls matched for age and sex, in the 4 h after diazepam administration but not thereafter. 2. When measured at a single fixed time point, a greater proportion of the drug was in the unbound from in the plasma of cirrhotic patients, but non-bound diazepam concentrations were not significantly different in the two groups. 3. Several psychomotor tests showed that cirrhotic patients, although having significantly impaired liver function, did not as a group have increased sensitivity to diazepam compared with their matched controls. 4. Only those cirrhotic patients who at the time of drug administration had impaired cerebral function, as judged by baseline performance of psychomotor tests, showed increased sensitivity to the effects of intravenous diazepam. 5. Psychomotor tests, particularly the Reitan trail test, seem more useful than tests of liver function or drug metabolism for identifying those patients with liver cirrhosis at risk of excessive sedation after diazepam administration.

Adult↗
PubMed1996

Pharmacokinetic and pharmacodynamic interactions of bretazenil and diazepam with alcohol.

1. Interaction between alcohol and bretazenil (a benzodiazepine partial agonist in animals) was studied with diazepam as a comparator in a randomized, double-blind, placebo controlled six-way cross over experiment in 12 healthy volunteers, aged 19-26 years. 2. Bretazenil (0.5 mg), diazepam (10 mg) and matching placebos were given as single oral doses after intravenous infusion of alcohol to a steady target-blood concentration of 0.5 g l-1 or a control infusion of 5% w/v glucose at 1 week intervals. 3. CNS effects were evaluated between 0 and 3.5 h after drug administration by smooth pursuit and saccadic eye movements, adaptive tracking, body sway, digit symbol substitution test and visual analogue scales. 4. Compared with placebo all treatments caused significant decrements in performance. Overall, the following sequence was found for the magnitude of treatment effects: bretazenil+alcohol > diazepam+alcohol > or = bretazenil > diazepam > alcohol > placebo. 5. There were no consistent indications for synergistic, supra-additive pharmacodynamic interactions between alcohol and bretazenil or diazepam. 6. Bretazenil with or without alcohol, and diazepam+alcohol had marked effects. Because subjects were often too sedated to perform the adaptive tracking test and the eye movement tests adequately, ceiling effects may have affected the outcome of these tests. 7. No significant pharmacokinetic interactions were found. 8. Contrary to the results in animals, there were no indications for a dissociation of the sedative and anxiolytic effects of bretazenil in man.

Administration, Oral↗
PubMed1998

Diazepam potentiates the positive inotropic effects of histamine and forskolin in guinea-pig papillary muscles.

There have been diverse reports on the effects of diazepam on cardiac contractility. The purpose of this study was to examine whether diazepam modifies the inotropic response elicited by histamine on an isolated guinea-pig papillary muscle. The responses of electrically driven papillary muscle to histamine and cyclic AMP-related inotropic agents were recorded in the absence and in the presence of diazepam. Histamine and forskolin, which directly stimulate adenylate cyclase, significantly increased the contractile force in the papillary muscle in a concentration-dependent manner. A histaminergic H2-receptor antagonist, cimetidine, but not a H1-receptor antagonist, diphenhydramine, at 10 microM produced a rightward shift in the concentration-response curve for histamine. Diazepam (10 microM) shifted the concentration-response curve for histamine and forskolin to the left by 1.8 and 1.6 times, respectively. Neither a central type (fulmazenil) nor a peripheral type (PK11195) of benzodiazepine receptor antagonist modified the effect of diazepam on the histaminergic-evoked contraction. Phosphodiesterase blockade by 3-isobutyl-1-methylxanthine shifted the concentration-dependent curve for histamine to the left. A combination of 3-isobutyl-1-methylxanthine also produced a leftward shift of the curve. However, there was no significant difference between the 3-isobutyl-1-methylxanthine only group and the combination group. These results indicate that diazepam potentiates the positive inotropic effect produced by histamine, probably mediated via an increase in cyclic AMP levels induced by histamine.

Anesthetics, Intravenous↗
PubMed2002

Controlling seizures in the prehospital setting: diazepam or midazolam?

OBJECTIVE: To determine which is the most effective and safe treatment for controlling seizures in children out-of-hospital: diazepam or midazolam. METHODS: A retrospective review of the medical records of children presenting to the Emergency Department of the Children's Hospital at Westmead (CHW-ED) with seizures requiring treatment in the field by paramedics was carried out over a 4-year period (April 1996 to March 2000). In New South Wales, children with seizures in the prehospital setting received 0.5 mg/kg per rectum (p.r.) or 0.1 mg/kg i.v. diazepam until March 1998 and from March 1997 onwards they received 0.15 mg/kg i.m. or 0.1 mg/kg i.v. midazolam. The main outcome measured was cessation of seizure in the prehospital setting. Secondary outcomes were time taken to initiate treatment and the frequency of cardiorespiratory compromise. RESULTS: Over the 4-year period, 2566 children presented to CHW-ED with a seizure; 107 children were eligible for entry into the present study. Of these 107 patients, 62 received diazepam and 45 received midazolam. Thirty-one (50.0%) in the diazepam group and 15 (33.3%) in the midazolam group were febrile seizures. Both groups were similar in terms of demographics and seizure type. A comparison of diazepam with midazolam showed that both drugs were effective in stopping seizures within 5 min of drug administration (37.1% cf. 51.1%). Fewer patients in the midazolam group suffered apnoea (20.0% cf. 29.0%; P < 0.05). CONCLUSION: Midazolam controls seizures as effectively as diazepam in the prehospital setting. Furthermore, midazolam potentially reduces respiratory depression and time to treatment.

Anticonvulsants↗
PubMed2003

alpha2-gamma-Aminobutyric acid (GABA)A receptors are the molecular substrates mediating precipitation of narcosis but not of sedation by the combined use of diazepam and alcohol in vivo.

Classical benzodiazepines such as diazepam are widely used tranquillisers and hypnotics in various neuropsychiatric diseases including alcohol-related disorders. One of the major drawbacks of benzodiazepine therapy, however, is an exacerbation of the sedative and hypnotic effects associated with alcohol intake, even at low doses. Even though the gamma-aminobutyric acid (GABA)A receptor complex is a common target for the actions of both classes of drugs, the molecular mechanisms underlying the enhanced pharmacological properties of the combined use of benzodiazepines and alcohol remain to be identified. The present experiments aimed at clarifying which of the GABAA receptor subtypes mediate the augmented hypnotic-like and sedative effects of combined diazepam and alcohol using the righting reflex and motor activity assays, respectively, in histidine-to-arginine point mutated mice that possess diazepam-insensitive alpha1-, alpha2-, alpha3- or alpha5-GABAA receptors. The combination of diazepam (2 or 3 mg/kg) and ethanol (3 g/kg) induced loss of righting reflex with a significantly dose-dependent increase of the latency to its full recovery in wild-type, alpha1(H101R), alpha3(H126R) and alpha5(H105R) but not in alpha2(H101R) mice. A combined treatment with diazepam (1 mg/kg) and ethanol (2.5 g/kg) precipitated motor inhibition similarly in wild-type and alpha2(H101R) mice. Responsiveness of the alpha2(H101R) mice to ethanol alone was similar to that of wild-type mice. These results demonstrate that induction of loss of righting reflex by combined diazepam and alcohol is closely dependent on the activation of the alpha2-GABAA receptors by the benzodiazepine whereas precipitation of sedation involves GABAA receptors other than the alpha2-GABAA receptors.

Anesthesia↗
PubMed2000

Diazepam promotes ATP recovery and prevents cytochrome c release in hippocampal slices after in vitro ischemia.

Benzodiazepines protect hippocampal neurons when administered within the first few hours after transient cerebral ischemia. Here, we examined the ability of diazepam to prevent early signals of cell injury (before cell death) after in vitro ischemia. Ischemia in vitro or in vivo causes a rapid depletion of ATP and the generation of cell death signals, such as the release of cytochrome c from mitochondria. Hippocampal slices from adult rats were subjected to 7 min of oxygen-glucose deprivation (OGD) and assessed histologically 3 h after reoxygenation. At this time, area CA1 neurons appeared viable, although slight abnormalities in structure were evident. Immediately following OGD, ATP levels in hippocampus were decreased by 70%, and they recovered partially over the next 3 h of reoxygenation. When diazepam was included in the reoxygenation buffer, ATP levels recovered completely by 3 h after OGD. The effects of diazepam were blocked by picrotoxin, indicating that the protection was mediated by an influx of Cl(-) through the GABA(A) receptor. It is interesting that the benzodiazepine antagonist flumazenil did not prevent the action of diazepam, as has been shown in other studies using the hippocampus. Two hours after OGD, the partial recovery of ATP levels occurred simultaneously with an increase of cytochrome c (approximately 400%) in the cytosol. When diazepam was included in the reoxygenation buffer, it completely prevented the increase in cytosolic cytochrome c. Thus, complete recovery of ATP and prevention of cytochrome c release from mitochondria can be achieved when diazepam is given after the loss of ATP induced by OGD.

Adenosine Triphosphate↗