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PubMed1994

Comparison of sedative recovery time after midazolam versus diazepam administration.

OBJECTIVE: To compare the sedative recovery rate pharmacology of intravenous midazolam vs. diazepam when used for short-term sedation. DATA SOURCES: English-language articles were identified through a search of the MEDLINE and InPharma databases. Bibliographies of retrieved articles were examined for relevant articles. STUDY SELECTION: Twenty-eight studies were identified based on a priori inclusion criteria. Eight trials had enough information to combine results for sedative recovery rate. DATA EXTRACTION: The difference in mean time to sedative recovery, weighted by sample size, was determined. DATA SYNTHESIS: Of the 28 trials, eight reported a significantly faster sedation recovery rate from diazepam vs. midazolam, whereas 19 trials reported no difference in sedative recovery time, and a single trial reported that midazolam offered significantly faster recovery from sedation than diazepam. A commonly defined time to sedative recovery event was available for only eight trials. The median dosing ratio for these eight trials was 2.1:1 for diazepam over midazolam. The weighted mean time difference was 4 mins 16 secs in favor of diazepam as the agent from which patients recover more quickly. CONCLUSIONS: These results firmly underscore the understanding that elimination half-lives of benzodiazepines do not necessarily correspond with their sedative pharmacodynamic effects, and we conclude that there are no clinically important sedative recovery rate differences between midazolam and diazepam, while midazolam is a more expensive agent.

Diazepam↗
PubMed2002

Short-term effects of intravenous benzodiazepines on autonomic neurocardiac regulation in humans: a comparison between midazolam, diazepam, and lorazepam.

OBJECTIVES: To evaluate the effects of intravenously applied diazepam, lorazepam, and midazolam on autonomic neurocardiac regulation assessed by standardized measurements of heart rate variability. DESIGN: Prospective, randomized clinical study. SETTING: University teaching hospital. PATIENTS: Forty-five patients, who underwent a gastroscopy, were randomly assigned to intravenous premedication with midazolam (5 mg), diazepam (10 mg), or lorazepam (4 mg). Six subjects refused an injection and served as nonpremedicated controls. INTERVENTIONS: Serial recordings of the 5-min resting heart rate variability were obtained before and 15 and 30 mins after premedication. Seven benzodiazepine-treated patients received intravenous flumazenil (0.5 mg). MEASUREMENTS AND MAIN RESULTS: The average doses applied were 0.07 mg/kg for midazolam, 0.13 mg/kg for diazepam, and 0.06 mg/kg for lorazepam. Fifteen minutes after intravenous benzodiazepines were administered, we found an increase in resting heart rate and a reduction of vagal tone compared with baseline in all three benzodiazepine-treated subgroups. Multivariate analysis (covariate age) of the changes in heart rate variability indices over the experimental course revealed a significant reduction in absolute high-frequency power with midazolam or diazepam compared with nonpremedicated subjects. Moreover, midazolam-treated subjects showed a significantly larger reduction in relative high-frequency power not only compared with nontreated subjects, but also compared with lorazepam- or diazepam-treated subjects. Vagal tone remained reduced compared with baseline even 30 mins after benzodiazepine application, however, the resting heart rate decreased toward baseline levels. After flumazenil administration, there was a linear correlation between an increase in high-frequency power and a corresponding decrease in resting heart rate. CONCLUSIONS: Benzodiazepines can influence autonomic neurocardiac regulation in man, probably through their interaction with the gamma-aminobutyric acidA-receptor chloride ion channel complex. The pattern of findings suggests that intravenous midazolam, diazepam, and lorazepam influence human autonomic neurocardiac regulation in a biphasic way. First, they cause a reduction of central vagal tone, and second, they may decrease the cardiac pacemaker directly. Flumazenil completely abolished the autonomic neurocardiac regulation effects of benzodiazepines.

Adult↗
PubMed1997

Gepirone and diazepam in generalized anxiety disorder: a placebo-controlled trial.

This randomized, double-blind clinical trial involving 198 generalized anxiety disorder (GAD) patients was conducted to more clearly define gepirone's role for the treatment of anxiety in daily dosages of 10 to 45 mg compared with diazepam and placebo. A secondary goal was to test for possible discontinuation symptoms after abrupt discontinuation of therapy. After a 1-week washout period, patients were treated for 8 weeks and then abruptly shifted under single-blind conditions for 2 weeks on placebo. The highest attrition rate occurred with patients on gepirone (58%) and the lowest on diazepam (34%). Medication intake for week 4 was 19.5 +/- 12.5 mg/day diazepam and 19.0 +/- 11.5 mg/day gepirone and was similar at week 8. The major adverse events were light-headedness, nausea, and insomnia for gepirone and drowsiness and fatigue for diazepam. Clinical improvement data showed gepirone's anxiolytic response to be delayed, being significant from placebo beginning at week 6, whereas diazepam caused significantly more relief than placebo from week 1 onward. Taper results showed that only diazepam, but not gepirone, caused a temporary worsening of anxiety symptoms or rebound.

Adult↗
PubMed2002

The anxiolytic effect of the novel antipsychotic ziprasidone compared with diazepam in subjects anxious before dental surgery.

The novel atypical antipsychotic ziprasidone has a pharmacologic profile notable for potent agonism of serotonin (5-HT)1A receptors, antagonism at 5-HT1D receptors, and reuptake inhibition of norepinephrine. 5-HT1A receptor agonism, in particular, suggests anxiolytic activity, and ziprasidone has shown preliminary efficacy in treating the symptoms of anxiety associated with psychotic disorders. In this study, the anxiolytic efficacy of ziprasidone was evaluated in nonpsychotic subjects who were anxious before undergoing minor dental surgery. We compared a single oral dose of 20 mg ziprasidone (N = 30) with that of 10 mg diazepam (N = 30) and placebo (N = 30) in a randomized, parallel-group, double-blind study. The peak anxiolytic effect of ziprasidone compared with that of placebo was similar to that of diazepam but had a later onset. At 3 hours postdose, the anxiolytic effect of ziprasidone was significantly greater than that of placebo (p < 0.05) and somewhat greater than that of diazepam. Diazepam showed a significantly greater anxiolytic effect than placebo at 1 hour (p < 0.05) but not at 3 hours. The sedative effect of ziprasidone was never greater than that of placebo, whereas that of diazepam was significantly greater than that of placebo 1 to 1.5 hours postdose. Ziprasidone was generally well tolerated. Only one patient reported treatment-related adverse events (nausea and vomiting) and, unlike diazepam, ziprasidone did not cause reductions in blood pressure. Dystonia, extrapyramidal syndrome, akathisia, and postural hypotension were not seen with ziprasidone. Thus, ziprasidone may possess anxiolytic effects in addition to its antipsychotic properties.

Adolescent↗
PubMed2004

The influence of diazepam and midazolam on adenosine-induced forearm vasodilation in humans.

Adenosine is an endogenous purine with vasodilating and cardioprotective properties. Animal experiments have shown that some benzodiazepine-induced effects can be explained by potentiation of adenosine effects, via inhibition of the nucleoside transport system. The objective of this study was to determine whether the frequently used benzodiazepines diazepam and midazolam increase adenosine-induced vasodilation in the human forearm vascular bed, measured by venous occlusion plethysmography. Adenosine (0.6, 6, 20, and 60 nmol/min/dl ForeArm Volume) was infused into the brachial artery with and without concomitant separate infusion of diazepam (21 nmol/min/dl, n = 9) and midazolam (23 nmol/min/dl, n = 8). Plasma concentrations of diazepam resp. midazolam at the end of the infusion protocol averaged 0.5 +/- 0.2 microg/ml plasma (1.6 microM) for diazepam versus 1.2 +/- 0.4 microg/ml plasma (3 microM) for midazolam. Intra-arterial infusion of the benzodiazepines did not alter baseline vascular tone, and had no significant influence on the forearm vasodilator response to adenosine. The adenosine-induced relative change in Forearm Vascular Resistance (FVR) was -3 +/- 7, -48 +/- 8, -75 +/- 6, and -85 +/- 3% in the absence and 3.5 +/- 11, -54 +/- 5, -74 +/- 5, and -82 +/- 3% resp. in the presence of diazepam (P > 0.1, repeated measures ANOVA, n = 9). Likewise, in the absence resp. presence of midazolam, FVR fell by 1 +/- 6, 55 +/- 5, 74 +/- 3, and 84 +/- 2% resp. 11 +/- 11, 59 +/- 2, 80 +/- 3, and 87 +/- 2% (P > 0.1, n = 7). Intra-brachial infusion of diazepam and midazolam resulting in forearm concentrations in the high therapeutic range does not augment adenosine-induced forearm vasodilation. A possible interaction at supra-therapeutic levels of the benzodiazepines can not be excluded from the present study, but lacks clinical significance.

Adenosine↗
PubMed1999

The effect of diazepam in the recovery of rabbits from acute acetaminophen intoxication.

We have recently shown that diazepam can reduce mortality of acute iron overdose in rats. The mechanism for that effect is not yet defined. Our objective in the present study was to assess whether diazepam can similarly reduce mortality of experimental acute acetaminophen intoxication. Survival of rabbits was compared among four groups receiving 3 g/kg (body weight) of acetaminophen (LD40) orally each, followed by: 1) nothing (group I), 2) one oral dose of 140 mg/kg N-acetylcystein (NAC) an hour later (group II), 3) intramuscular injection of 7 mg/kg diazepam (group III), 4) intramuscular injection of 7 mg/kg diazepam and one oral dose of 140 mg/kg NAC an hour later (group IV). 37.5% of rabbits in group I died after 16 hours, whereas none of the rabbits in group III died, (p = 0.04). No animal died during the 96-hour observation period in groups II and IV. Two and four hours post drug administration, acetaminophen plasma concentrations (APC) were significantly lower among rabbits in group III than in group I (p = 0.0007 and 0.01, respectively) and significantly lower among rabbits in group IV than in those in group II (p<0.0001 and p = 0.03, respectively). Acetaminophen plasma concentrations 2 hours after drug administration were also significantly lower among rabbits in group III than in those in group II (p = 0.0002). Seven and 24 hours after dosage, APC tended to be higher among rabbits in group III than in those in group I, but not significantly so. Administration of diazepam without NAC did not prevent liver and renal dysfunction. We conclude that early administration of diazepam in acute experimental acetaminophen overdose in rabbits reduced APC and mortality, probably by slowing intestinal motility, which resulted in delayed acetaminophen absorption from the gastrointestinal tract.

Acetaminophen↗
PubMed2006

Interactions on mixing diazepam with methadone or buprenorphine in maintenance patients.

Benzodiazepine use by patients in methadone and buprenorphine substitution treatment is common, despite safety concerns regarding these drug interactions. The relative safety of diazepam use by methadone- or buprenorphine-treated patients has not been systematically examined. This study aimed to examine the effect of single diazepam doses, within normal therapeutic range (doses: 0, 10, and 20 mg), upon physiological, subjective, and performance measures in stable methadone and buprenorphine-treated patients. In a double-blind, randomized crossover design, methadone- or buprenorphine-treated patients were administered their normal opioid dose and either placebo, 10-, or 20-mg diazepam, in balanced order over 3 sessions. Eight methadone- and 8 buprenorphine-prescribed patients with no concurrent benzodiazepine dependence or significant comorbidity were recruited from an outpatient addiction clinic in London. Measures were taken at baseline and for 6 hours after dosing, and included physiological responses (pulse rate, blood pressure, pupil size, respiratory rate, and peripheral pO2), subjective drug effects (Addiction Research Center Inventory subscales, visual analog scales of strength of drug effect, drug-liking, and sedation), and performance measures (simple reaction time, cancellation task, digit symbol substitution task, and balance). The 10- and 20-mg diazepam doses resulted in comparable subjective experiences of greater sedation and strength of drug effects in both patient groups, and had minimal impact on physiological parameters. However, diazepam had greater peak effects on performance measures (simple reaction time, digit symbol substitution task, and cancellation time) in methadone-treated than in buprenorphine-treated patients. Diazepam may significantly alter the response to opioid substitution treatment with methadone or buprenorphine.

Adolescent↗
PubMed1982

Diazepam and suxamethonium muscle pain (a dose-response study).

Postoperative muscle pain occurred in 17.2% of patients given diazepam intravenously 5 minutes prior to suxamethonium. The incidence of muscle pain was 48% in those patients who were not given diazepam before suxamethonium. The difference is statistically significant (p less than 0.01). Five mg diazepam reduced the incidence of pain but not significantly (p = 0.30); 10 mg diazepam significantly reduced the incidence (p less than 0.05); while 15 and 20 mg diazepam showed better effects (p less than 0.01). Diazepam pretreatment also reduced the severity, frequency and duration of muscle pain. The incidence of fasciculations was significantly reduced but there was no correlation between the incidence of fasciculations and the occurrence of muscle pains.

Adult↗
PubMed1975

Immediate effects on human performance of a 1,5-genzodiazepine (clobazam) compared with the 1,4-benzodiazepines, chlordiazepoxide hydrochloride and diazepam.

1 The immediate effects on human performance of the 1,5-benzodiazepine, clobazam (20 mg), and the 1,4-benzodiazepines, chlordiazepoxide hydrochloride (20 mg) and diazepam (10 mg), were studied by adaptive tracking and measurement of reaction time. Each drug was ingested at 09.00 h and performance was measured at 09 h 30 min (0.5 h), 11 h 30 min (2.5 h), 14 h 30 min (5.5 h) and 18 h 30 min (9.5 h after ingestion). 2 With diazepam decrements in performance on adaptive tracking were observed at 0.5 h and 2.5 h and performance was enhanced at 9.5 h after ingestion. With clobazam performance at individual times did not differ significantly from control, but there was evidence of an improvement in performance during the day. There was no evidence of impaired performance on adaptive tracking after chlordiazepoxide hydrochloride. 3 Reaction time was slowed at 0.5 h and 2.5 h after diazepam and chlordiazepoxide hydrochloride. A decrease in reaction time was observed at 9.5 h after diazepam. No changes in reaction time were observed after clobazam. 4 The subjects as a group differentiated correctly between performance decrements on adaptive tracking after diazepam and the absence of performance decrements after clobazam and chlordiazepoxide hydrochloride. The persistence of the decrement in performance after diazepam was accurately assessed. 5 It is evident that the nature and persistence of impaired performance and the ability to appreciate impaired performance vary considerably between the benzodiazepines, and that the choice of a benzodiazepine should include careful consideration of performance sequelae.

Adult↗
PubMed1982

Valproic acid and diazepam interaction in vivo.

1 The effect of oral administration of sodium valproate (1500 mg daily) on the distribution and elimination kinetics of intravenously administered diazepam in six healthy volunteers has been studied. 2 During valproate administration the unbound fraction of diazepam in serum increased approximately two fold. This was accompanied by a significant increase in apparent volume of distribution and plasma clearance of diazepam. 3 There was a positive correlation between the change in free fraction and the increase in both apparent volume of distribution and plasma clearance of the drug. 4 The concentration of unbound diazepam in serum (calculated from the percent free diazepam and total serum concentration) was significantly higher during valproate administration. Both the intrinsic clearance and volume of distribution of unbound drug were significantly reduced. 5 Mean serum N-desmethyldiazepam levels were significantly lower during valproate coadministration. 6 These results suggest that valproic acid displaces diazepam from plasma protein binding sites and inhibits its metabolism.

Adult↗
PubMed1985

Responsiveness to oral diazepam in the elderly: relationship to total and free plasma concentrations.

The immediate and residual response to single doses of oral diazepam 10 mg was measured in 11 young and 12 elderly healthy volunteers using postural sway, digit symbol substitution scores and subjective ratings. The effect on postural sway was markedly accentuated in the older volunteers, but the difference between groups in the effect on the other measures used did not achieve significance. The corresponding plasma total diazepam concentrations were lower in the older subjects beyond 0.5 h post dose and the concentrations of plasma desmethyldiazepam did not differ between the groups. Diazepam plasma protein binding was significantly reduced in the elderly subjects, but the plasma free (unbound) diazepam concentrations did not exceed those in the young group. There was poor correlation between the responses measured and the concentrations of either total diazepam, desmethyldiazepam or free diazepam. The results suggest the occurrence of a non-uniform effect of age on different aspects of benzodiazepine response, and that where an accentuated effect occurs the mechanisms are substantially pharmacodynamic.

Adult↗
PubMed1992

Quantitative electroencephalography for measurement of central nervous system responses to diazepam and the benzodiazepine antagonist, flumazenil, in isoflurane-anaesthetized dogs.

Quantitative EEG was assessed in six dogs anaesthetized with 1.8% end-tidal isoflurane concentration and following diazepam (0.2 mg/kg i.v.) administration. Ventilation was controlled to maintain normocapnia. Five dogs were subsequently given the benzodiazepine antagonist, flumazenil (0.04 mg/kg i.v.), and quantitative EEG was recorded. One dog received a saline injection following diazepam (as a control) and quantitative EEG was recorded for an additional 2.5 h. Heart rate, arterial blood pressure, esophageal temperature, arterial pH and blood gas tensions, end-tidal CO2 tension and end-tidal isoflurane concentration were monitored throughout the study. A 21 lead linked-ear montage was used for recording EEG. Quantitative EEG data were stored on an optical disc for analysis at a later date. Values for absolute power of EEG were determined for theta, delta, alpha, and beta frequencies. Cardiovascular parameters remained stable throughout the study. Diazepam administration was associated with decreased absolute power in all frequencies of EEG at all electrode sites. The duration of diazepam-induced decreased absolute power of EEG was at least 3 h in one dog. Administration of flumazenil antagonized diazepam-induced decreased absolute power of EEG in all frequencies at all electrode sites. We conclude that quantitative EEG provides a relatively non-invasive, objective measure of diazepam- and flumazenil-induced changes in cortical activity during isoflurane anaesthesia.

Anesthesia, Inhalation↗
PubMed1978

Plasma free norepinephrine and epinephrine concentrations following diazepam-ketamine induction in patients undergoing cardiac surgery.

Ketamine causes cardiovascular stimulation, presumably, by increasing central sympathetic activity. This study was undertaken to find out if diazepam in appropriate doses could abolish or moderate the central sympathetic and cardiovascular stimulation following ketamine in patients undergoing cardiac surgery. Twelve patients, scheduled for valvular replacement (8) and direct aortocoronary bypass graft operations (4) were studied. After premedication with diazepam 0.15 mg/kg orally and morphine sulphate 0.15 mg/kg i.m., they were induced with diazepam 0.3 mg/kg i.v., followed 10 min later by ketamine 2 mg/kg i.v. Direct arterial pressure by a strain gauge from the radial artery and heart rate by EKG were continuously recorded. Plasma free norepinephrine, measured by Vendsalu's method, in the arterial blood was 0.39 +/- 0.03 ng/ml prior to induction, 0.39 +/- 0.03 ng/ml 10 min after diazepam and 0.42 +/- 0.05 ng/ml (P greater than 0.05) 5 min after ketamine administration. Plasma free epinephrine concentrations were 0.10 +/- 0.04 ng/ml prior to induction, 0.06 +/- 0.03 ng/ml (P less than 0.05) 10 min after diazepam and 0.01 +/- 0.003 ng/ml (P less than 0.05) 5 min after ketamine. Heart rate and systolic pressure did not change significantly throughout the study period. Diastolic pressures were elevated significantly (P less than 0.05) 5 min after ketamine administration, amounting to a 12% increase over baseline. Diazepam-ketamine induction in cardiac surgical patients did not result in clinically significant central sympathetic or cardiovascular stimulation.

Aged↗
PubMed1980

The role of diazepam and fentanyl in the production of balanced anaesthesia.

The effects of diazepam-fentanyl combinations on consciousness, superficial nociception, respiration and circulation during N2O+O2 inhalation were studied in 40 premedicated patients during induction of anaesthesia. The balance between antinociception and anaesthesia was closest to the optimum in patients receiving 0.2 mg/kg of diazepam plus 1 micrograms/kg of fentanyl; the eyelid reflex was negative in all patients and only two out of ten patients reacted to abdominal pinching. When only 0.2 mg/kg of diazepam was given with N2O+O2, the eyelid reflex was negative in all patients, but half of them reacted to pinching. When the dose of diazepam was reduced to 0.1 mg/kg and patients received 1 or 2 micrograms/kg of fentanyl, the balance between anaesthesia and antinociception was good, but 30-50% of patients had a positive eyelid reflex and reacted to pinching. No distinct respiratory depression was observed in patients given 0.2 mg/kg of diazepam, whereas seven patients given 0.1mg/kg of diazepam plus 2 micrrograms/kg of fentanyl had apnoea lasting more than 60 s associated with a significant (P less than 0.05-0.001) increase in end-tidal CO2 and PCO2 in arterialised venous blood. No significant changes were observed in blood pressure or heart rate after any of the drug combinations studied. It appears that an optimal balance between anaesthesia and antinociception with minimal side-effects during balanced general anaesthesia requires reinforcement of N2O+O2 anaesthesia not only with fentanyl but also with hypnotics for sedatives.

Adult↗
PubMed1981

Comparison of thiopentone and diazepam as induction agents of anaesthesia for Caesarean section.

Clinical effects of thiopentone (3 mg/kg body weight) and diazepam (0.3 mg/kg) were compared for elective caesarean sections in two groups of 43 and 39 women, respectively. They were given general anaesthesia in left lateral tilt. The systolic, diastolic and mean arterial pressures were moderately elevated at onset of surgery in both groups, probably indicating light anaesthesia. Later, a gradual decrease to the preinduction levels was observed. The mean injection-delivery (I-D) interval was 344 s in the thiopentone group and 339 s in the diazepam group. The I-D intervals were shorter than 10 min in 39 of the cases in the thiopentone group and 38 cases in the diazepam group. Low Apgar scores at 1 min (6 or less) occurred in five of the neonates in each group, while all had normal Apgar scores at 5 min ( 7 or mor) As judged by the Apgar scores and the acid-base status of umbilical cord blood, the effects of the induction agents on the neonatal condition were indistinguishable in the two groups. In the thiopentone group, unpleasant recollections were reported in 5 out of 40 patients (12.5%) compared to none in the diazepam group. Diazepam-nitrous oxide anaesthesia is well accepted by the mothers and is alternative to supplementing thiopentone induction with a volatile gas for patients who have previous experienced wakefulness or express fear of awareness. The main drawback with diazepam induction, however, is the slow induction of sleep. Harmful drug effects on the neonates must be expected if the dose has to be increased in order to ensure sleep.

Anesthesia, Intravenous↗
PubMed1985

The effect of diazepam pretreatment on the succinylcholine-induced rise in intraocular pressure.

The influence of diazepam on some adverse effects of succinylcholine was studied double-blind. Thirty patients (ASA I-II) were allocated to groups receiving either diazepam 0.08 mg/kg or d-tubocurarine 0.05 mg/kg 5 min before a bolus of succinylcholine, 1 mg/kg and 1.5 mg/kg, respectively. Fasciculations were more frequent in the diazepam group (80%) than in the d-tubocurarine group (13%). Relaxation, onset and duration of neuromuscular blockade were comparable in the two groups. The rise in intraocular pressure after succinylcholine and endotracheal intubation was small (0.27 kPa = 2 mmHg) but significant (P less than 0.01) after diazepam pretreatment. In this group the rise in intraocular pressure was 50% lower than the rise seen in the d-tubocurarine group (P less than 0.01). We conclude that pretreatment with diazepam 0.08 mg/kg will reduce but not prevent a rise in the intraocular pressure after succinylcholine in a rapid sequence induction. In the management of patients with penetrating eye injuries the use of succinylcholine still carries some risk even after diazepam pretreatment.

Adolescent↗
PubMed1996

Intravenous sedation for retrobulbar injection and eye surgery: diazepam and/or propofol?

Principle goals of sedation for eye surgery are to provide patient comfort and to allow the patient to stay calm during both retrobulbar injection and surgery. Insufficient sedation may not prevent the patient from moving during retrobulbar injection, whereas very deep sedation may result in respiratory complications during surgery. The aim of the present study was to evaluate the effectiveness and suitability of a combination of diazepam and propofol for sedation for both application of retrobulbar block and subsequent elective eye surgery. One-hundred and fifty patients were randomly allocated to receive either diazepam, propofol or a combination of both drugs before retrobulbar injection. Tolerance of retrobulbar injection and comfort during the surgical procedure were assessed by comfort scores using a nominal analogue scale between 1 (worst possible condition) and 6 (best conceivable condition). Side effects related to sedation were recorded. The combination of diazepam and propofol resulted in the highest comfort scores for both retrobulbar block (5.3 +/- 0.3) and the surgical procedure (5.4 +/- 0.4). Diazepam alone did not produce adequate sedation for retrobulbar block (3.1 +/- 0.3), whereas comfort scores during surgery were significantly higher (5.3 +/- 0.3) compared to propofol alone (3.6 +/- 0.4). No severe side effects induced by sedation were noted in any of the study groups. The combination of diazepam and propofol proved able to provide a reliable degree of sedation with minimal side effects for both retrobulbar block and surgery. The combination was clearly superior to the sedation induced by propofol or diazepam alone.

Adult↗
PubMed1986

Acute tolerance to diazepam in mice: pharmacokinetic considerations.

The tolerance to the hypnotic effect of diazepam developed after a single exposure to diazepam in the presence or absence of cycloheximide, which blocks liver enzyme induction, was studied. At the high dose (30-35 mg/kg) used in this study, diazepam was found to be metabolized very rapidly in mice, consistent with previous findings using a much smaller dose (5 mg/kg). There was no significant difference in the pharmacokinetics of diazepam in control and tolerant mice as observed by monitoring the plasma and brain concentrations of diazepam and N-desmethyldiazepam. It is concluded that acute tolerance to diazepam in mice may not be attributed to changes in pharmacokinetic factors.

Animals↗