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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.
16 ine 1.0 mg/kg (n = 20), and a single dose of midazolam 0.045 mg/kg (active placebo) (n = 19).
17 0.006), and high-dose fentanyl plus low-dose midazolam (0.007).
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
20 on of ketamine hydrochloride (0.5 mg/kg) and midazolam (0.045 mg/kg).
21 ravenous infusion of ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg).
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
24                           Microinjections of midazolam (10 and 100 microM solutions) into the cNTS di
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
27 % (34-56%); ketamine (saline), 46% (34-58%); midazolam, 18% (6-30%); saline, 1% (0-11%).
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
34 infused lorazepam (7% vs. 15%, p = .037) and midazolam (30% vs. 81%, p < .0001).
35 h 95% CI) yielded similar results: ketamine (midazolam), 45% (34-56%); ketamine (saline), 46% (34-58%
36                                              Midazolam (48%) and propofol (19%) were reported as the
37        Late awakening was more frequent with midazolam (58% vs 45%) and was associated with higher ra
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 <
41                                Compared with midazolam, a single ketamine infusion elicited a signifi
42                 In the acute setting of RSE, midazolam achieves clinical seizure control at a mean of
43 ction of two anesthetic agents, Morphine and Midazolam, acting simultaneously in the same individual.
44 nsisted of 50 microg of fentanyl and 1 mg of midazolam administered intravenously.
45         Delirium occurrence was unrelated to midazolam administration, cumulative doses, or serum lev
46      The opposite pattern was observed under midazolam administration, suggesting that when recollect
47            An intravenous infusion of either midazolam alone or co-sedation was administered by a nur
48 iable sedation and is easier to titrate than midazolam alone, without significant difference in the r
49 ne as compared with rats receiving saline or midazolam alone.
50               Preoperative administration of midazolam, alone or combined with other pharmacologic ag
51            Co-administration of morphine and midazolam also exacerbated morphine-induced hyperactive
52 mparison of single infusions of ketamine and midazolam (an active placebo control).
53       In rat hippocampal slices, we compared midazolam, an anesthetic BDZ, with clonazepam, an antico
54 sual search task, once after an injection of midazolam, an anesthetic that induces temporary amnesia,
55                    There were 2,250 propofol-midazolam and 1,054 propofol-lorazepam matched patients.
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
58            288 abstracts were identified for midazolam and 16 for clonidine with full texts obtained
59            Time to reach 50% complete mature midazolam and 1`-hydroxymidazolam metabolite/4`-hydroxym
60 eutic success was 56% (61 of 109) for buccal midazolam and 27% (30 of 110) for rectal diazepam (perce
61 portal venous blood samples were assayed for midazolam and [15N3]midazolam.
62                                    When both midazolam and barbiturates have failed, use of isofluran
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
65 ation of a single dose of 5 and 10 mg/kg for midazolam and desipramine, respectively.
66 rage titrated dosages of 3.3 and 12.1 mg for midazolam and diazepam, respectively.
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
69                                      We used midazolam and fexofenadine to assess CYP3A (intestinal a
70 tion of mechanical ventilation compared with midazolam and improved patients' ability to communicate
71                    Comparison of propofol to midazolam and lorazepam in adult ICU patients.
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
74 midazolam exposure; delirium is unrelated to midazolam and may be linked to inflammatory status.
75                                              Midazolam and morphine are often used in pediatric inten
76                        All patients received midazolam and nalbuphine intravenously.
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
80 s' ability to communicate pain compared with midazolam and propofol.
81 -up in performance across blocks in both the midazolam and saline conditions.
82                                              Midazolam and the IV route were the commonest sedative a
83       Thirty-three studies provided data for midazolam and two for clonidine.
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
87 ially after the application of high doses of midazolam, and in case of impaired drug metabolism.
88  of delirium, use of fentanyl and open-label midazolam, and nursing assessments.
89 e were abolished by gabazine, insensitive to midazolam, and partially blocked by 20 microM Zn2+, cons
90            The additional doses of fentanyl, midazolam, and propofol required for CAE were 0.05, 1.9
91 duced the need for concomitant sedation with midazolam, and reduced the levels of circulating unbound
92 m-controlled), ketamine (saline-controlled), midazolam, and saline.
93 .3% vs. 78.8%; P < 0.001) when compared with midazolam- and lorazepam-treated patients, respectively.
94                                              Midazolam appears to be able to bind to P450 3A4 in two
95               Buccal and intranasal forms of midazolam are emerging as suitable alternatives to recta
96 nclude that higher doses of propofol but not midazolam are required to sedate patients managed with P
97                   Rectal diazepam and buccal midazolam are used for emergency treatment of acute febr
98 this study was to infer the effectiveness of midazolam as a comparator in preserving the blind in ket
99                            Studies that used midazolam as a comparator yielded smaller effects of ket
100 ervention studies that used either saline or midazolam as a control treatment.
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
103             The network depressant action of midazolam at low concentrations was absent in slices fro
104       YPFP-NH(2) inhibited the oxidations of midazolam at two different positions (1'- and 4-) with 2
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
108 te but not for TRH binding, was critical for midazolam binding.
109 onsistent with the competitive antagonism of midazolam binding.
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
112                                              Midazolam, but not clonazepam, also augmented a form of
113                                              Midazolam, but not clonazepam, increased neurosteroid le
114 iated CYP3A4 expression and CYP3A4-catalyzed midazolam clearance in human primary hepatocytes.
115                                The estimated midazolam clearance was 0.61 L/min/70kg.
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
118 rences among sedative premedications such as midazolam, clonidine, and dexmedetomidine.
119 onproprietary drugs (haloperidol, bufuralol, midazolam, clozapine, terfenadine, erlotinib, olanzapine
120 counted for by greater improvement following midazolam compared to saline.
121 ied TRH-R1 to generate a model of the TRH-R1/midazolam complex.
122                                         When midazolam concentration was increased, it depressed neur
123  binding rates for varying both P450 3A4 and midazolam concentrations revealed discordance in the par
124                 Systemic and cerebral venous midazolam concentrations were measured at 0.5, 1, 2, 3,
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
128 as found to be a regioselective inhibitor of midazolam CYP3A metabolism.
129                                              Midazolam depressed neuronal activity at a low concentra
130 es that have been studied, such as ketamine, midazolam, diazepam, clonazepam, propofol, pentobarbital
131 heduled periodontal surgeries under IVS with midazolam, diazepam, or placebo control.
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
135                                        Total midazolam dose predicted decreased hippocampal volumes (
136    By univariate linear regression analysis, midazolam dose was dependent on age, morphine dose, and
137                 Total sedative (propofol and midazolam) dose was recorded for the first three days of
138  first coma was associated with fentanyl and midazolam doses (p=0.03 and p=0.01, respectively).
139 mine doses ranged from 0.5 to 0.54 mg/kg and midazolam doses ranged from 0.02 to 0.045 mg/kg.
140   The maximum serum concentration after oral midazolam dosing was significantly different between the
141        The results suggest that diazepam and midazolam each may have advantages for IVS.
142 y ICU benzodiazepine dose of > or = 75 mg of midazolam equivalent (RR 2.1, 95% CI 1.1-3.5).
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
145                  These results indicate that midazolam exacerbated morphine tolerance through a spina
146                                              Midazolam exposure was associated with macro- and micros
147         Coma is associated with fentanyl and midazolam exposure; delirium is unrelated to midazolam a
148                 Bolus dosing of fentanyl and midazolam fails to reduce the intracranial hypertension
149  medications, including propofol, etomidate, midazolam, fentanyl, ketamine, and nitrous oxide.
150 (14)C]TETS and [(3)H]EBOB binding, including midazolam, flurazepam, avermectin Ba1, baclofen, isoguva
151                                         Oral midazolam for children and patient-controlled propofol s
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
157 eks of the trial, compared with 10.7% in the midazolam group (intent-to-treat analysis).
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
160 ater improvement in the MADRS score than the midazolam group 24 hours after treatment.
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
166 igned to the sevoflurane group and 25 to the midazolam group.
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
169                                              Midazolam has a clinically active metabolite, 1-hydroxym
170  (stage of early status epilepticus), buccal midazolam has become an important out-of-hospital treatm
171                                         When midazolam has failed to control RSE, the evidence points
172 entanyl, chloral hydrate, pentobarbital, and midazolam hydrochloride--by using the Fisher exact test.
173  strongly correlated with CYP3A4 content and midazolam hydroxylation activity.
174 ounted for 31% of the variability in hepatic midazolam hydroxylation activity.
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
177 a single intravenous infusion of ketamine or midazolam in a 2:1 ratio (N=73).
178           We analyzed dosing of propofol and midazolam in patients undergoing PH through a retrospect
179                                       Use of midazolam in preterm neonates, particularly those not un
180 uces the systemic clearances of fentanyl and midazolam in rats after cardiac arrest through alteratio
181 valuated the comparative value of continuous midazolam in secondary analyses.
182 as no difference between dexmedetomidine and midazolam in time at targeted sedation level in mechanic
183           Isoflurane sedation was changed to midazolam in two nonsurviving patients because of hemody
184 e, we have determined that propofol, but not midazolam, increases the efficacy of piperidine-4-sulpho
185 ience, yet only one of these was affected by midazolam-induced amnesia.
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
188                                              Midazolam infusion did not affect systemic hemodynamics
189 otal intensive care unit costs compared with midazolam infusion for intensive care unit sedation, pri
190                                              Midazolam infusion preceded by a high bolus dose in newb
191 reased brain perfusion and metabolism during midazolam infusion.
192 ere randomly assigned to receive ketamine or midazolam infusion.
193  fear learning when administrated 1 d before midazolam injection.
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
196 tion of 1-hydroxymidazolam to the effects of midazolam is controversial.
197                                           As midazolam is more potent than its metabolite 1-hydroxymi
198                                              Midazolam is primarily metabolized by the CYP3A4/CYP3A5
199                           The benzodiazepine midazolam is widely used in critical care medicine.
200 r clinical effects are thus likely caused by midazolam itself.
201 ents (propofol group), and other agents like midazolam, lorazepam, and pentobarbital were used in the
202         sedation; anxiolysis; critical care; midazolam; lorazepam; propofol; benzodiazepines; intensi
203 n coadministration, geometric mean values of midazolam maximal observed serum concentration and area
204                                              Midazolam may be used for shorter procedures for faster
205                        Alternatives, such as midazolam, may offer advantages in particular circumstan
206                         Intravenous and oral midazolam (MDZ) clearances were used to measure the in v
207                                              Midazolam (MDZ) is metabolized by CYP3A4 to two hydroxyl
208                                              Midazolam (MDZ) oxidation by recombinant CYP3A4 purified
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
211 ination profiles of several drugs, including midazolam, metoprolol, and tolbutamide.
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
221  meaningful differences between propofol and midazolam on costs or measures of effectiveness.
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
224 odes of ileus with co-sedation compared with midazolam-only (2 vs. 0).
225                            Compared with the midazolam-only group, the co-sedation group had fewer ho
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
229 ere ARDS onset to receive either intravenous midazolam or inhaled sevoflurane for 48 hours.
230              When preceded by nitrous oxide, midazolam or normocapnia, the risk of inducing epileptif
231                      Long-term sedation with midazolam or propofol in intensive care units (ICUs) has
232 amine use as a sedative for intubation, with midazolam or propofol use as the reference.
233 -1.5 kg) randomly assigned to receive either midazolam or vehicle (5% dextrose) infusion for 6 hrs.
234                    Participants who injected midazolam or were in prison during open-label follow-up
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
236 ith continuously infused sedation (propofol, midazolam, or lorazepam).
237 sedative or to receive usual care (propofol, midazolam, or other sedatives).
238               Sedation with dexmedetomidine, midazolam, or propofol; daily sedation stops; and sponta
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
244                       Under the influence of midazolam, participants did not show facilitation in sea
245                           Dexmedetomidine vs midazolam patients had more hypotension (51/247 [20.6%]
246 nonheritable and heritable factors affecting midazolam pharmacokinetic in pediatric subjects with pri
247 8861 polymorphism are relevant predictors of midazolam pharmacokinetic variables.
248  impact of inflammation and organ failure on midazolam pharmacokinetics was developed using NONMEM 7.
249 sed the effect of PF-00562271 on single-dose midazolam PK in a subgroup of patients.
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
255                                              Midazolam provides rapid and reliable amnesia, even when
256                              Dexmedetomidine/midazolam ratio in time at target sedation was 1.07 (95%
257  -0.43], P < 0.00001, I = 61.1, N = 554) and midazolam requirement (pooled SMD -1.07 [95% CI -1.70 to
258  group (p = .021), with similar morphine and midazolam requirements (p = .317).
259 ation of the benzodiazepine receptor agonist midazolam, resulted in a dose-dependent inhibition of su
260       The patient was treated with ketamine, midazolam, ribavirin, and amantadine.
261                                              Midazolam selectively influenced the putative ERP-correl
262                                    Moreover, midazolam shortened cortical up states at low, but not a
263 nd that the GABAA agonists phenobarbital and midazolam significantly increased status epilepticus-ass
264                              Triazolam, oral midazolam, St. John's Wort, carbamazepine and pimozide,
265  both saline (t(353) = 7.41, p < 0.0001) and midazolam (t(353) = 4.59, p < 0.0001).
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
269                            Concentrations of midazolam, the 1' (1`-hydroxymidazolam metabolite) and 4
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
273                                              Midazolam use did not decrease and was statistically hig
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
278                                              Midazolam via the IV route with or without oral route is
279               The inhibition at 50 microg/kg midazolam was 65+/-11% compared to the baseline response
280                                         More midazolam was administered in the placebo recipients tha
281                                     However, midazolam was found to cause a greater incidence of amne
282                                              Midazolam was given to 576 (9%) of 6680 neonates and 536
283 orally, the maximum plasma concentration for midazolam was increased by 2.5-fold, and the clearance d
284                                       Buccal midazolam was more effective than rectal diazepam for ch
285 djusted for with logistic regression, buccal midazolam was more effective than rectal diazepam.
286 ial tested the hypothesis that intramuscular midazolam was noninferior to intravenous lorazepam by a
287                    The systemic clearance of midazolam was significantly greater (P <.05) in healthy
288                       The bioavailability of midazolam was significantly higher (P <.05) in cirrhotic
289 , dextromethorphan, and oral and intravenous midazolam) was administered to 18 RYGB recipients and 18
290                        Simultaneous doses of midazolam were given intravenously (0.05 mg/kg) and oral
291                                 Fentanyl and midazolam were independently administered by intravenous
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
294 it P450 3A4-mediated oxidative metabolism of midazolam with an IC(50) value of 71 microM.
295                     The MIDEX trial compared midazolam with dexmedetomidine in ICUs of 44 centers in
296 we examined whether (1) co-administration of midazolam with morphine would exacerbate morphine tolera
297 olam with intravenous placebo or intravenous midazolam with oral placebo before surgery.
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

 
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