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1 Ds that lack a 3'-imidazo substituent (e.g., midazolam).
2 ously (0.05 mg/kg) and orally (3 mg of [15N3]midazolam).
3 ncreased in rats receiving both morphine and midazolam.
4 ve placebo control condition, the anesthetic midazolam.
5 e have many similar or superior qualities to midazolam.
6 ulness and LOC induced by the benzodiazepine midazolam.
7 dence interval, $2314-$17,045) compared with midazolam.
8 inistering a sedative premedication, such as midazolam.
9 ing propofol and 13 of 64 patients receiving midazolam.
10 samples were assayed for midazolam and [15N3]midazolam.
11 imal adverse events compared with placebo or midazolam.
12 of some inflammatory markers, compared with midazolam.
13 elihood of heavy drinking days compared with midazolam.
14 with continuous infusions of sufentanil and midazolam.
15 the NAc is necessary for the preference for midazolam.
18 ne (0.2-1.4 microg/kg per hour [n = 244]) or midazolam (0.02-0.1 mg/kg per hour [n = 122]) titrated t
19 ine (0.71 mg/kg, N=17) or the active control midazolam (0.025 mg/kg, N=23), provided during the secon
22 vs 4.4 +/- 1.3 hours, P < 0.0001), and oral midazolam (0.5 +/- 0.2 vs 0.7 +/- 0.4 hours, P < 0.01).
23 esults, CYP3A catalytic activity measured as midazolam 1'- and 4-hydroxylation in liver microsomes fr
25 s associated with higher mean daily doses of midazolam (102 mg/d vs 82 mg/d; P = .04) and fentanyl (m
26 dexmedetomidine (123 hours [IQR, 67-337]) vs midazolam (164 hours [IQR, 92-380]; P = .03) but not wit
28 xmedetomidine (estimated score difference vs midazolam, 19.7 [95% CI, 15.2-24.2]; P < .001; and vs pr
29 slices the BZ agonists chlordiazepoxide and midazolam (2 and 50 microM) did not significantly enhanc
30 0 microg [cryoablation group]; P < .001) and midazolam (2.9 mg [RF group] vs 1.6 mg [cryoablation gro
31 administered with morphine (10mg/kg, s.c.), midazolam (2mg/kg, i.p.), and chelerythrine chloride (a
32 .), followed 30min later by either saline or midazolam (2mg/kg, intraperitoneal, i.p.), for 14 days b
33 ved supplemental propofol (64% of patients), midazolam (3%), or both (7%) during the first 2 days aft
35 h 95% CI) yielded similar results: ketamine (midazolam), 45% (34-56%); ketamine (saline), 46% (34-58%
38 (CAM-ICU+) received continuous infusions of midazolam (59% vs. 32%, p < .05) or fentanyl (57% vs. 32
39 eiving magnesium required significantly less midazolam (7.1 mg/kg per day [0.1-47.9] vs 1.4 mg/kg per
40 1.5 to 48.9 +/- 8.95 mL/min/kg; p < .05) and midazolam (89.2 +/- 12.5 to 73.6 +/- 12.1 mL/min/kg; p <
43 ction of two anesthetic agents, Morphine and Midazolam, acting simultaneously in the same individual.
48 iable sedation and is easier to titrate than midazolam alone, without significant difference in the r
54 sual search task, once after an injection of midazolam, an anesthetic that induces temporary amnesia,
56 current study was to compare the actions of midazolam and 1-hydroxymidazolam on network activity of
57 bation (14.1% of subjects with intramuscular midazolam and 14.4% with intravenous lorazepam) and recu
60 eutic success was 56% (61 of 109) for buccal midazolam and 27% (30 of 110) for rectal diazepam (perce
63 is small and a trial was planned to compare midazolam and clonidine, two sedatives widely used withi
64 CI: 0.4-0.9) for ketamine (midazolam) versus midazolam and d = 1.8 (95% CI: 1.4-2.2) for ketamine (sa
67 azepines (alpha2(H101R) mice) did not prefer midazolam and did not show midazolam-induced reward enha
68 ically ventilated patients, co-sedation with midazolam and fentanyl by constant infusion provides mor
70 tion of mechanical ventilation compared with midazolam and improved patients' ability to communicate
72 sedatives examined included benzodiazepines (midazolam and lorazepam), propofol, and dexmedetomidine.
73 ctive benzodiazepine receptor full agonists, midazolam and lorazepam, in rhesus monkeys trained to se
77 nil, midazolam and propofol versus fentanyl, midazolam and propofol in 272 outpatients undergoing dia
78 ilation, dexmedetomidine was not inferior to midazolam and propofol in maintaining light to moderate
79 double-blinded clinical trial of alfentanil, midazolam and propofol versus fentanyl, midazolam and pr
84 s were sedated using continuous infusions of midazolam and/or fentanyl; no changes in ventilator sett
85 hat combined injectable (fentanyl-fluanisone/midazolam) and volatile (isoflurane) anesthetics in mice
86 eiving morphine alone or in combination with midazolam, and chelerythrine prevented the development o
89 e were abolished by gabazine, insensitive to midazolam, and partially blocked by 20 microM Zn2+, cons
91 duced the need for concomitant sedation with midazolam, and reduced the levels of circulating unbound
93 .3% vs. 78.8%; P < 0.001) when compared with midazolam- and lorazepam-treated patients, respectively.
96 nclude that higher doses of propofol but not midazolam are required to sedate patients managed with P
98 this study was to infer the effectiveness of midazolam as a comparator in preserving the blind in ket
101 as a marked loss in first-pass metabolism of midazolam as a result of diminished intestinal CYP3A act
102 entanyl as their first-line opioid (66%) and midazolam as their first-line benzodiazepine (86%) and p
105 o standard sedation received propofol and/or midazolam-based sedation as clinically appropriate.
106 vehicle levels in monkeys maintained under a midazolam baseline, but not under a cocaine baseline ove
107 smembrane helix 7 (7.39), were important for midazolam binding but another, Tyr-282 in transmembrane
110 molecular model of the complex suggest that midazolam binds to TRH-R1 within a transmembrane helical
111 Simulation of the binding of the ligands midazolam, bromocriptine, testosterone, and ketoconazole
116 The final model suggested a decrease in midazolam clearance with increase in alanine transaminas
117 flammation and organ failure strongly reduce midazolam clearance, a surrogate marker of CYP3A-mediate
119 onproprietary drugs (haloperidol, bufuralol, midazolam, clozapine, terfenadine, erlotinib, olanzapine
123 binding rates for varying both P450 3A4 and midazolam concentrations revealed discordance in the par
125 ing ketamine with an active placebo control, midazolam, conducted at a single site (Icahn School of M
126 larger in saline-controlled studies than in midazolam-controlled studies (t(276) = 2.32, p = 0.02).
127 were compared across four groups: ketamine (midazolam-controlled), ketamine (saline-controlled), mid
130 es that have been studied, such as ketamine, midazolam, diazepam, clonazepam, propofol, pentobarbital
132 ippocampal growth (beta = -0.31, p = 0.003), midazolam dose (beta = -0.27, p = 0.03), and surgery (be
133 , 1.67; 95% CI, 1.005-2.767; p = 0.047), and midazolam dose (hazard ratio, 0.998; 95% CI, 0.997-1.0;
134 tients (42.5+/-16.2 vs. 27.0+/-15.3; p=.02); Midazolam dose did not differ between PH and non-PH pati
136 By univariate linear regression analysis, midazolam dose was dependent on age, morphine dose, and
140 The maximum serum concentration after oral midazolam dosing was significantly different between the
143 ve care unit benzodiazepine dose > 100 mg of midazolam-equivalent agent (relative risk 2.4, 95% confi
144 hydroxymidazolam could add to the effects of midazolam, especially after the application of high dose
150 (14)C]TETS and [(3)H]EBOB binding, including midazolam, flurazepam, avermectin Ba1, baclofen, isoguva
152 oints included the total dose of concomitant midazolam for sedation and quantitative plasma venom lev
153 and after administration of fentanyl and/or midazolam for the treatment of episodic intracranial hyp
154 ation in children is best achieved with oral midazolam formulated in flavoured syrups, and the inhala
155 ter for the ketamine group compared with the midazolam group (95% CI=2.33, 7.59; Cohen's d=0.75).
156 y 1 for the ketamine group compared with the midazolam group (estimate=7.65, 95% CI=1.36, 13.94), and
158 higher in the sevoflurane group than in the midazolam group (mean +/- SD, 205 +/- 56 vs. 166 +/- 59,
159 s 55% for the ketamine group and 30% for the midazolam group (odds ratio=2.85, 95% CI=1.14, 7.15; num
161 atment were 1.2 minutes in the intramuscular-midazolam group and 4.8 minutes in the intravenous-loraz
162 of 448 subjects (73.4%) in the intramuscular-midazolam group and in 282 of 445 (63.4%) in the intrave
163 was lower in the ketamine group than in the midazolam group by 7.95 points (95% confidence interval
164 e (dropout or use cocaine) compared with the midazolam group, and craving scores were 58.1% lower in
165 in the sevoflurane group, compared with the midazolam group, and no serious adverse event was observ
167 77.3% for dexmedetomidine group vs 75.1% for midazolam group; difference, 2.2% [95% confidence interv
168 acokinetic studies in vivo demonstrated that midazolam half-life, C(max), and area under the concentr
170 (stage of early status epilepticus), buccal midazolam has become an important out-of-hospital treatm
172 entanyl, chloral hydrate, pentobarbital, and midazolam hydrochloride--by using the Fisher exact test.
175 er research indicates that the amnestic drug midazolam impairs recollection more than familiarity.
176 Participants were randomized to ketamine or midazolam in a 2:1 fashion under double-blind conditions
180 uces the systemic clearances of fentanyl and midazolam in rats after cardiac arrest through alteratio
182 as no difference between dexmedetomidine and midazolam in time at targeted sedation level in mechanic
184 e, we have determined that propofol, but not midazolam, increases the efficacy of piperidine-4-sulpho
186 e cortical areas lasting for >300 ms, during midazolam-induced LOC, TMS-evoked activity was local and
187 e) did not prefer midazolam and did not show midazolam-induced reward enhancement in ICSS, in contras
189 otal intensive care unit costs compared with midazolam infusion for intensive care unit sedation, pri
194 the mechanism of inverse agonism effected by midazolam involves its direct interaction with Trp-279,
195 ubjects in status epilepticus, intramuscular midazolam is at least as safe and effective as intraveno
201 ents (propofol group), and other agents like midazolam, lorazepam, and pentobarbital were used in the
203 n coadministration, geometric mean values of midazolam maximal observed serum concentration and area
209 ugs undergoing metabolism, only the sedative midazolam (MDZ) serves as a marker substrate for the in
210 of analgesics/sedatives (fentanyl, morphine, midazolam), mechanical ventilation, hypotension, and sur
212 ion was analyzed in per-protocol population (midazolam, n = 233, vs dexmedetomidine, n = 227; propofo
213 to moderate sedation for more than 24 hours (midazolam, n = 251, vs dexmedetomidine, n = 249; propofo
214 and 27 recommend intranasal benzodiazepines (midazolam, n = 27; lorazepam, n = 3); pediatric protocol
215 30 recommend intramuscular benzodiazepines (midazolam, n = 30; lorazepam, n = 8; diazepam, n = 3), a
216 ocols recommend intravenous benzodiazepines (midazolam, n = 33; lorazepam, n = 23; diazepam, n = 24),
217 drugs commonly used in pediatric anesthesia (midazolam, nitrous oxide, and isoflurane) in doses suffi
218 24 hours was greater with ketamine than with midazolam (odds ratio, 2.18; 95% CI, 1.21 to 4.14), with
219 rly goal-directed sedation patients received midazolam on 6 of 173 (3.5%) versus 4 of 114 (3.5%) stan
220 esults, finasteride abolished the effects of midazolam on contextual fear learning when administrated
222 on (ICSS) paradigm to evaluate the impact of midazolam on reward enhancement, we demonstrated that mi
223 noted in the co-sedation group compared with midazolam-only (0.4 +/- 0.1 and 1.0 +/- 0.2, respectivel
226 e did not observe significant differences in midazolam or 1'-hydroxymidazolam clearance or area under
227 in rhesus monkeys trained to self-administer midazolam or cocaine, under a progressive-ratio schedule
228 effects of intravenous sedation (IVS) using midazolam or diazepam during periodontal procedures on p
233 -1.5 kg) randomly assigned to receive either midazolam or vehicle (5% dextrose) infusion for 6 hrs.
235 adherent than were those who did not inject midazolam (OR 2.2, 95% CI 1.2-4.3; p=0.02) or were not i
239 n propofol-treated patients as compared with midazolam- or lorazepam-treated patients (risk ratio, 0.
240 the hepatic CYP3A activity, but the reduced midazolam oral bioavailability suggests that moderate al
241 ased after administration of fentanyl and/or midazolam (overall aggregate mean Deltaarea under the cu
242 n of high-dose fentanyl (p = 0.02), low-dose midazolam (p = 0.006), and high-dose fentanyl plus low-d
243 essed patients within 24 hours compared with midazolam, partially independently of antidepressant eff
246 nonheritable and heritable factors affecting midazolam pharmacokinetic in pediatric subjects with pri
248 impact of inflammation and organ failure on midazolam pharmacokinetics was developed using NONMEM 7.
250 n (median age, 5.1 mo [range, 0.02-202 mo]), midazolam plasma (n = 532), cytokine (e.g., IL-6, tumor
251 /-4.7 vs. 2.0+/-1.8 ng/mL, p=0.0001) as were midazolam plasma levels (1050+/-2232 vs. 168+/-249 ng/mL
252 -bottle choice drinking paradigm to evaluate midazolam preference and an intracranial self-stimulatio
253 ding ketamine, isoflurane, nitrous oxide and midazolam, produced increased neurodegeneration in 7-day
254 had therapy with: thiopental, pentobarbital, midazolam, propofol, ketamine, inhalational anaesthetics
257 -0.43], P < 0.00001, I = 61.1, N = 554) and midazolam requirement (pooled SMD -1.07 [95% CI -1.70 to
259 ation of the benzodiazepine receptor agonist midazolam, resulted in a dose-dependent inhibition of su
263 nd that the GABAA agonists phenobarbital and midazolam significantly increased status epilepticus-ass
266 s in the HFOV group received higher doses of midazolam than did patients in the control group (199 mg
267 riven by a comparatively larger effect under midazolam than saline (t(111) = 5.40, p < 0.0001), where
268 ravenous infusion of ketamine (0.5 mg/kg) or midazolam (the control condition) during a 5-day inpatie
270 ding site for a competitive inverse agonist, midazolam, three of the four residues that directly cont
271 ne-treated patients vs 76.6% (n = 93/122) in midazolam-treated patients (difference, 22.6% [95% CI, 1
272 the in vivo pharmacokinetics of fentanyl and midazolam, two clinically relevant cytochrome P450 3A su
274 ncluded six trials enrolling 1,235 patients: midazolam versus dexmedetomidine (n = 3), lorazepam vers
275 ), lorazepam versus dexmedetomidine (n = 1), midazolam versus propofol (n = 1), and lorazepam versus
276 as there was no difference between ketamine (midazolam) versus ketamine (saline) (t(177) = 0.65, p =
277 was d = 0.7 (95% CI: 0.4-0.9) for ketamine (midazolam) versus midazolam and d = 1.8 (95% CI: 1.4-2.2
283 orally, the maximum plasma concentration for midazolam was increased by 2.5-fold, and the clearance d
286 ial tested the hypothesis that intramuscular midazolam was noninferior to intravenous lorazepam by a
289 , dextromethorphan, and oral and intravenous midazolam) was administered to 18 RYGB recipients and 18
292 tion in PTSD symptom severity, compared with midazolam, when assessed 24 hours after infusion (mean d
293 e verb-generation task, and the GABA agonist midazolam (which increases neural inhibition) improves s
296 we examined whether (1) co-administration of midazolam with morphine would exacerbate morphine tolera
298 olled trial was undertaken to compare buccal midazolam with rectal diazepam for emergency-room treatm
299 trial compared the efficacy of intramuscular midazolam with that of intravenous lorazepam for childre
300 d binding of the substrates testosterone and midazolam, with K(i) values similar to the spectral bind