ライフサイエンスコーパス: dexmedetomidine

1 ing alpha2 adrenergic receptor (AR) agonist (dexmedetomidine).

2 3.0 +/- 0.2 to 19.1 +/- 0.8 Hz (20 microg/kg dexmedetomidine).

3 is needed to evaluate the clinical impact of dexmedetomidine.

4 edications such as midazolam, clonidine, and dexmedetomidine.

5 More adverse effects were associated with dexmedetomidine.

6 nes (midazolam and lorazepam), propofol, and dexmedetomidine.

7 ewer agents such as etomidate, propofol, and dexmedetomidine.

8 w update in the diverse uses of the sedative dexmedetomidine.

9 es, mechanism of action, and side effects of dexmedetomidine.

10 anagement include clonidine, tizanidine, and dexmedetomidine.

11 ay, intraoperative steroid bolus, and use of dexmedetomidine.

12 pamezole, reversed the functional effects of dexmedetomidine.

13 onferred by known alpha(2A)AR drugs, such as dexmedetomidine.

14 ofol, and time to recovery was shortest with dexmedetomidine.

15 ness and recovery using the alpha(2)-agonist dexmedetomidine.

16 ssign patients to receive either intravenous dexmedetomidine (0.1 mug/kg per h, from intensive care u

17 lly ventilated adults with sepsis to receive dexmedetomidine (0.2 to 1.5 ug per kilogram of body weig

18 Dexmedetomidine (0.2-1.4 microg/kg per hour [n = 244]) o

19 otocol with lorazepam and were randomized to dexmedetomidine 1.2 mug/kg/hr (high dose), 0.4 mug/kg/hr

20 e biological activity of the present series, dexmedetomidine (1), and conformationally restrained ana

21 patients given placebo to 17% in those given dexmedetomidine: 1.48 (97.8% CI 0.99-2.23).

22 e, and after subsequent injection of saline, dexmedetomidine (100 mug/kg IV), or clonidine (200 mug/k

23 Dexmedetomidine (100 mug/kg, i.p.) prevented and reverse

24 atment with a sublingual film formulation of dexmedetomidine 120 mug or 180 mug, compared with placeb

25 mechanical ventilation appeared shorter with dexmedetomidine (123 hours [IQR, 67-337]) vs midazolam (

26 ylephrine (-25 +/- 4 versus -45 +/- 5%), and dexmedetomidine (-22 +/- 4 versus -44 +/- 3%) were all s

27 14%] of 350 patients) than in patients given dexmedetomidine (23 [7%] of 350 patients; 0.44, 0.26-0.7

28 mic administration of the alpha2-AR agonists dexmedetomidine (25 mug/kg, i.v.) and clonidine (100 mug

29 placebo (62 [18%] of 350 patients) than with dexmedetomidine (34 [10%] of 350 patients; 0.50, 0.32-0.

30 urred in 35.7% of patients taking 180 mug of dexmedetomidine, 34.9% taking 120 mug, and 17.5% taking

31 5) vs. benzodiazepines (31.1%, 30.7-31.5) or dexmedetomidine (4.0%, 3.8-4.2).

32 4 hours [IQR, 92-380]; P = .03) but not with dexmedetomidine (97 hours [IQR, 45-257]) vs propofol (11

33 The effects of dexmedetomidine, a highly selective alpha(2)-adrenocepto

34 e investigated whether prophylactic low-dose dexmedetomidine, a highly selective alpha2 adrenoceptor

35 We found that dexmedetomidine, a specific agonist of alpha-2 AR was ve

36 Dexmedetomidine abolished these increases, whereas intra

37 During the group comparison phase, dexmedetomidine achieved a higher percentage of time in

38 Similarly, dexmedetomidine administered after lipopolysaccharide ca

39 A causal link between dexmedetomidine administration and elevated temperature

40 Some hours after dexmedetomidine administration to wild-type mice there i

41 ry hypothesis tested was that intraoperative dexmedetomidine administration would reduce postoperativ

42 lly the same for natural sleep and following dexmedetomidine administration, but a sudden change in p

43 pared the effects of select survival agents (dexmedetomidine, alfaxalone, and propofol) on urodynamic

44 Dexmedetomidine allowed for the preservation of satisfac

45 ions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (alpha(2)-agonist) during moderate rhyth

46 ions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (alpha(2)-agonist) during rhythmic handg

47 release), phenylephrine (alpha1-agonist) and dexmedetomidine (alpha2-agonist) were assessed.

48 nnulated rats and their hypnotic response to dexmedetomidine (an alpha2 agonist) was determined.

49 Dexmedetomidine, an a2 adrenoceptor agonist that is used

50 Dexmedetomidine, an alpha(2)-agonist available for ICU s

51 Dexmedetomidine, an alpha-2-adrenergic agonist, causes a

52 Dexmedetomidine, an alpha2 adrenergic agonist, is a usef

53 Dexmedetomidine, an alpha2-adrenergic agonist, is not ap

54 Dexmedetomidine, an alpha2-adrenergic agonist, produces

55 1 (<1%) of 391 patients given dexmedetomidine and 1 (<1%) of 387 patients given placeb

56 illation was 121 (30%) in 397 patients given dexmedetomidine and 134 (34%) in 395 patients given plac

57 A total of 342 patients (105 dexmedetomidine and 237 propofol) were included in the a

58 ned, 794 were analysed, with 400 assigned to dexmedetomidine and 398 assigned to placebo.

59 21 (5%) of 394 patients given dexmedetomidine and 8 (2%) of 396 patients given placebo

60 Propofol was then replaced by dexmedetomidine and a second set of data was obtained af

61 Fourteen patients in both the placebo-dexmedetomidine and acetaminophen-propofol groups (46% a

62 e significantly greater than those following dexmedetomidine and atipamezole.

63 Dexmedetomidine and etomidate are the subjects of invest

64 ces on heart rate (HR) during isoproterenol, dexmedetomidine and glycopyrrolate were given.

65 This investigation compared the actions of dexmedetomidine and halothane on the processed EEG and o

66 There was no difference between dexmedetomidine and midazolam in time at targeted sedati

67 nts were not statistically different between dexmedetomidine and placebo (159 mg vs 181 mg).

68 erence in postoperative delirium between the dexmedetomidine and placebo groups (12.2% [23 of 189] vs

69 rs of initiating study drug were similar for dexmedetomidine and placebo groups, respectively.

70 ups (46% and 45%) and 7 in the acetaminophen-dexmedetomidine and placebo-propofol groups (24% and 23%

71 Dexmedetomidine and propofol are commonly used sedatives

72 ns: In patients 65 years of age sedated with dexmedetomidine and propofol combination, preferentially

73 cts in neurocritical care patients receiving dexmedetomidine and propofol.

74 Modern anesthetic medications such as dexmedetomidine and proven techniques such as awake fibe

75 ess (LOC) with the alpha2-adrenergic agonist dexmedetomidine and return of consciousness (ROC) in a f

76 A conjunction analysis across the propofol, dexmedetomidine and sevoflurane groups confirmed the tha

77 duced with alpha2-adrenergic agonists (e.g., dexmedetomidine) and sleep homeostasis both depend on th

78 9.6 +/- 0.7 to 5.9 +/- 0.8 Hz (20 microg/kg dexmedetomidine), and 95% power frequency from 23.0 +/-

79 outcomes, none were significantly worse with dexmedetomidine, and several showed statistically signif

80 iprostate cancer drug bicalutamide, sedative dexmedetomidine, and two antifungals ravuconazole and po

81 However, heart rate was not decreased in the dexmedetomidine arm.

82 The use of dexmedetomidine as the sole or primary sedative agent in

83 longer than the next calendar day to receive dexmedetomidine as the sole or primary sedative or to re

84 After excluding controls exposed to dexmedetomidine at a later time in the hospitalization,

85 d to early goal-directed sedation received a dexmedetomidine-based algorithm targeted to light sedati

86 urgery population has also been studied with dexmedetomidine because of its adequate sedation and les

87 Monitoring for bradycardia is needed with dexmedetomidine but the occurrence may be lessened with

88 Dexmedetomidine can decrease emergence agitation and has

89 Furthermore, dexmedetomidine cannot induce high-power delta oscillati

90 Dexmedetomidine, clonidine, or propofol IV sedation.

91 alysis with a 6-month time horizon comparing dexmedetomidine-, clonidine-, and propofol-based IV seda

92 etamine during anesthetic induction and with dexmedetomidine compared with other sedation strategies

93 , smaller DeltaHR, decreased reflexes) under dexmedetomidine, compared to propofol and alfaxalone.

94 The nonsubtype-selective alpha2 agonist dexmedetomidine completely blocked the contractile respo

95 l hypothesis that central sympatholysis with dexmedetomidine constitutes a highly effective counterme

96 enable self-administration, we suggest that dexmedetomidine could serve as a sedative-hypnotic drug

97 The results indicate that dexmedetomidine decreases both GABAergic and glycinergic

98 At the clinically relevant doses, dexmedetomidine decreases cerebral blood flow and cerebr

99 by the Valsalva manoeuvre were lower during dexmedetomidine (Delta 2 +/- 1 to Delta 0 +/- 2 AP clust

100 ared with 1125 controls, the group receiving dexmedetomidine demonstrated significantly fewer tachyar

101 The administration of dexmedetomidine (DEX) at a low dose (2 microg/kg bolus i

102 Dexmedetomidine (DEX) has been shown to decrease the pro

103 Dexmedetomidine (DEX) may provide a sedation level that

104 The alpha-2 adrenergic agonist dexmedetomidine (Dex), 3-300 microg/kg, i.p., decreased

105 Dexmedetomidine (Dex), a potent, selective alpha-2 adren

106 Dexmedetomidine (DEX), a selective alpha2 receptor (adra

107 itional analgesics in PCA were replaced with dexmedetomidine (Dex), an alpha-2 agonist widely used fo

108 Dexmedetomidine (DEX; Precedex) is an alpha-2 adrenergic

109 pproaches, outcomes in patients who received dexmedetomidine did not differ from outcomes in those wh

110 rtheless, these reports indicate that use of dexmedetomidine does not interfere with electrophysiolog

111 Intraoperative dexmedetomidine does not prevent postoperative delirium.

112 Dexmedetomidine dosage was 0.7 +/- 0.2 mug/kg/hr.

113 rine and the highly selective alpha2 agonist dexmedetomidine each reversed the VLPO depolarization in

114 The concurrent release of dexmedetomidine enhanced the efficacy of released local

115 ction (measured using VAS) was improved with dexmedetomidine (estimated score difference vs midazolam

116 uch more common than with benzodiazepines or dexmedetomidine, even for patients mechanically ventilat

117 Although dexmedetomidine exposure in the immediate postoperative

118 Early dexmedetomidine exposure was associated with lower DRS (

119 Compared with unexposed patients, early dexmedetomidine exposure was not associated with better

120 Early dexmedetomidine exposure was not associated with improve

121 However, intraoperative use of dexmedetomidine for prevention of delirium has not been

122 ilation in the ICU, those who received early dexmedetomidine for sedation had a rate of death at 90 d

123 Anesthesiologists are evaluating the use of dexmedetomidine for sedation of children and new reports

124 Adjunctive dexmedetomidine for severe alcohol withdrawal maintains

125 As recently developed dexmedetomidine formulations enable self-administration,

126 tive delirium was significantly lower in the dexmedetomidine group (32 [9%] of 350 patients) than in

127 More patients in the dexmedetomidine group (42% vs 31%; P = .61) were able to

128 ized incorrectly, leaving 39 patients in the dexmedetomidine group and 32 patients in the placebo gro

129 event occurred in 566 of 1948 (29.1%) in the dexmedetomidine group and in 569 of 1956 (29.1%) in the

130 versus before study drug was greater in the dexmedetomidine group compared with the placebo group (-

131 rate adjustments occurred more often in the dexmedetomidine group compared with the placebo group (5

132 nd low-dose groups were combined as a single dexmedetomidine group for primary analysis with secondar

133 rescribed level of sedation, patients in the dexmedetomidine group received supplemental propofol (64

134 More adverse events were reported in the dexmedetomidine group than in the usual-care group.

135 Bradycardia occurred more frequently in the dexmedetomidine group versus placebo group (25% vs 0%, p

136 e 12-month time to death was 363 days in the dexmedetomidine group vs 188 days in the lorazepam group

137 time within the target RASS range (77.3% for dexmedetomidine group vs 75.1% for midazolam group; diff

138 The 28-day mortality in the dexmedetomidine group was 17% vs 27% in the lorazepam gr

139 rol group) were compared with nonresponders (dexmedetomidine group).

140 be randomized to either the propofol or the dexmedetomidine group.

141 rdia and hypotension were more common in the dexmedetomidine group.

142 Propofol and dexmedetomidine had the highest bladder pressure slopes

143 Dexmedetomidine has been demonstrated to provide a succe

144 Dexmedetomidine has been used effectively for sedation d

145 Dexmedetomidine has unique properties as sedative agent

146 Clonidine and dexmedetomidine have many similar or superior qualities

147 Propofol and dexmedetomidine have not been rigorously tested in compa

148 fol, mortality was similar over 180 days for dexmedetomidine (HR, 0.98 [95% CI, 0.77-1.24]) and cloni

149 on of, the loss of righting reflex following dexmedetomidine; hypnotic response had normalized 8 d af

150 ies; the PRODEX trial compared propofol with dexmedetomidine in 31 centers in 6 European countries an

151 medetomidine only, and 2,639 (0.6%) received dexmedetomidine in addition to opioid and/or benzodiazep

152 The MIDEX trial compared midazolam with dexmedetomidine in ICUs of 44 centers in 9 European coun

153 The findings support the use of dexmedetomidine in patients such as these.

154 examine the short- and long-term effects of dexmedetomidine in premature and critically ill infants.

155 However, the off-label use of dexmedetomidine in premature infants has increased 50-fo

156 application of an alpha-2-adrenergic agonist dexmedetomidine in the anesthetic management of function

157 is responsible for the hypnotic response to dexmedetomidine in the locus coeruleus of the rat.

158 managed with an antipsychotic and, possibly, dexmedetomidine in treatment-refractory cases.

159 spread use of alpha2 agonists (clonidine and dexmedetomidine) in pediatric critical care sedation.

160 mouse lightly anesthetized with isoflurane, dexmedetomidine increased behavioral arousal and reduced

161 Dexmedetomidine increased ventilator-free hours at 7 day

162 Dexmedetomidine, increasingly used for long-term sedatio

163 st, phenylephrine, or full alpha(2)-agonist, dexmedetomidine, indicated that the behavioral effects o

164 These results provide a mechanism for dexmedetomidine induced bradycardia and has implications

165 Thus, we hypothesized that dexmedetomidine-induced altered arousal would manifest w

166 of age (n = 15, 6 males) at baseline, during dexmedetomidine-induced altered arousal, and recovery st

167 Thus, sleep homeostasis and dexmedetomidine-induced sedation require PO galanin neur

168 Dexmedetomidine induces sedation via different central n

169 Dexmedetomidine infusion (0.5 microg/kg/h) during surger

170 Dexmedetomidine infusion elicited shorter sympathetic AP

171 etic tone during cardiac surgery, a low-dose dexmedetomidine infusion has been utilized.

172 Dexmedetomidine infusion inhibited the recruitment of la

173 Participants were given either dexmedetomidine infusion or saline placebo started befor

174 , using multivariable regression, escalating dexmedetomidine infusion rate was associated with increa

175 h individualized targeted sedation, use of a dexmedetomidine infusion resulted in more days alive wit

176 ne to 0.30 +/- 0.25 mug/kg/min 4 hours after dexmedetomidine infusion, increasing again to 0.42 +/- 0

177 Dexmedetomidine infusion, initiated at anaesthetic induc

178 Before and after dexmedetomidine infusion, sedative doses remained unchan

179 uvre (20 s, 40 mmHg) during baseline and the dexmedetomidine infusion.

180 nd set of data was obtained after 4 hours of dexmedetomidine infusion.

181 Dexmedetomidine is a relatively new representative for p

182 Dexmedetomidine is a selective alpha2 adrenoreceptor ago

183 Dexmedetomidine is a useful medication with many clinica

184 Dexmedetomidine is an anesthetic that alters the level o

185 ot associated with delirium, and that use of dexmedetomidine is associated with a lower delirium prev

186 Dexmedetomidine is commonly used after congenital heart

187 The combination of buspirone and dexmedetomidine is comparably effective while avoiding t

188 Dexmedetomidine is emerging as an effective therapeutic

189 antipsychotics, barbiturates, propofol, and dexmedetomidine) is detailed.

190 We anesthetized the rats with dexmedetomidine/isoflurane and infused paramagnetic cont

191 The roles of clonidine, dexmedetomidine, ketamine and nalbuphine in the treatmen

192 Propofol, dexmedetomidine, ketamine and remifentanil may be used i

193 tral medial thalamus, occurs at the point of dexmedetomidine loss of righting reflex.

194 troduced into the critical care unit such as dexmedetomidine may also provide a greater ability to ac

195 Conversely, increasing dexmedetomidine may be associated with increased mortali

196 edation with propofol to the alpha-2 agonist dexmedetomidine may decrease norepinephrine doses in sep

197 evidence indicates that the alpha(2) agonist dexmedetomidine may have distinct advantages.

198 Dexmedetomidine may increase vasopressor sensitivity, wh

199 Sedation with dexmedetomidine, midazolam, or propofol; daily sedation

200 Dexmedetomidine/midazolam ratio in time at target sedati

201 us dexmedetomidine (n = 3), lorazepam versus dexmedetomidine (n = 1), midazolam versus propofol (n =

202 s enrolling 1,235 patients: midazolam versus dexmedetomidine (n = 3), lorazepam versus dexmedetomidin

203 on was 1.09 (95% CI, 0.96-1.25; P = .20) for dexmedetomidine (n = 457) vs propofol (n = 471) and was

204 ssigned to receive either placebo (n=350) or dexmedetomidine (n=350).

205 medetomidine, n = 227; propofol, n = 214, vs dexmedetomidine, n = 223).

206 -protocol population (midazolam, n = 233, vs dexmedetomidine, n = 227; propofol, n = 214, vs dexmedet

207 r more than 24 hours (midazolam, n = 251, vs dexmedetomidine, n = 249; propofol, n = 247, vs dexmedet

208 medetomidine, n = 249; propofol, n = 247, vs dexmedetomidine, n = 251).

209 ntinued for up to 6 hours (acetaminophen and dexmedetomidine: n = 29; placebo and dexmedetomidine: n

210 hen and dexmedetomidine: n = 29; placebo and dexmedetomidine: n = 30; acetaminophen and propofol: n =

211 In critically ill patients, neither dexmedetomidine nor clonidine was superior to propofol i

212 ll voltage clamp methodology, the actions of dexmedetomidine on excitatory glutamatergic and inhibito

213 ndomly administered halothane or intravenous dexmedetomidine (on separate days).

214 s and benzodiazepines, 1.573 (0.4%) received dexmedetomidine only, and 2,639 (0.6%) received dexmedet

215 Patients were sedated with dexmedetomidine or lorazepam for as many as 120 hours.

216 andomly assigned 1:1, stratified by site, to dexmedetomidine or normal saline placebo.

217 ntly recommend targeting light sedation with dexmedetomidine or propofol for adults receiving mechani

218 Use of dexmedetomidine or propofol rather than a benzodiazepine

219 for 48 hours and postoperative sedation with dexmedetomidine or propofol starting at chest closure an

220 e in neurocritical care patients who receive dexmedetomidine or propofol.

221 Continuous sedation with dexmedetomidine or propofol.

222 led trial that randomly assigned patients to dexmedetomidine or saline placebo infused during surgery

223 aine (2 mg/kg) alone and in combination with dexmedetomidine or saline.

224 Bedside nursing staff administered dexmedetomidine (or placebo) initially at a rate of 0.5

225 urrent controlled data suggest that use of a dexmedetomidine- or propofol-based sedation regimen rath

226 ce issued conditional recommendations to use dexmedetomidine over propofol for sedation, provide enha

227 min while on propofol 8 hours after stopping dexmedetomidine (p < 0.005).

228 4 (-4 to -3) during, and -4 (-4 to -4) after dexmedetomidine (p = 0.07).

229 Halothane and dexmedetomidine produced differing effects on level of c

230 d a lack of response to tail clamping, while dexmedetomidine produced profound sedation, with preserv

231 Dexmedetomidine produces sedation while maintaining a de

232 Dexmedetomidine progressively de-recruited sympathetic A

233 hasone, rivastigmine, risperidone, ketamine, dexmedetomidine, propofol, and clonidine) reduced the ri

234 et sedation was 1.07 (95% CI, 0.97-1.18) and dexmedetomidine/propofol, 1.00 (95% CI, 0.92-1.08).

235 ng large AP clusters with shorter latencies, dexmedetomidine reduced AP latency across remaining clus

236 Dexmedetomidine reduced baroreflex gain, most strongly f

237 Dexmedetomidine reduced duration of mechanical ventilati

238 Dexmedetomidine reduced mean pressure (92 +/- 7 to 80 +/

239 Dexmedetomidine reduced sympathetic AP discharge (126 +/

240 acetaminophen, combined with IV propofol or dexmedetomidine, reduced in-hospital delirium vs placebo

241 aluate whether an intraoperative infusion of dexmedetomidine reduces postoperative delirium.

242 study coprimarily aimed to establish whether dexmedetomidine reduces the incidence of new-onset atria

243 evel of sedation, switching from propofol to dexmedetomidine resulted in a reduction of catecholamine

244 Sedation with dexmedetomidine resulted in more days alive without deli

245 Continuous sedation with dexmedetomidine results in significantly lower total int

246 cardia (heart rate <50/min) were higher with dexmedetomidine (RR, 1.62 [95% CI, 1.36-1.93]) and cloni

247 warranted to delineate an optimal regimen of dexmedetomidine sedation and any dose-related influence

248 to determine the safety and effectiveness of dexmedetomidine sedation compared to the standard used p

249 ibing respiratory and hemodynamic aspects of dexmedetomidine sedation have also been published.

250 Emerging literature suggests that dexmedetomidine sedation in critical care units is assoc

251 Dexmedetomidine should not be infused to reduce atrial f

252 In addition, dexmedetomidine showed (5) longer time to analgesic requ

253 In the study conditions, dexmedetomidine shows to be useful as a rescue drug for

254 r non-cardiac surgery, prophylactic low-dose dexmedetomidine significantly decreases the occurrence o

255 Compared with LA alone, dexmedetomidine significantly prolonged sensory and moto

256 Patients sedated with dexmedetomidine spent more time within 1 RASS point of t

257 clinically used alpha(2)-adrenergic agonist dexmedetomidine that enhances EEG slow-wave activity, in

258 to light by co-delivering a second compound, dexmedetomidine, that potentiates the effect of delivere

259 With dexmedetomidine, the changes occurred simultaneously in

260 creased from 0.69 +/- 0.72 mug/kg/min before dexmedetomidine to 0.30 +/- 0.25 mug/kg/min 4 hours afte

261 edge, this report describes the first use of dexmedetomidine to facilitate opioid withdrawal in child

262 Administration of dexmedetomidine to facilitate the discontinuation of opi

263 l sedation and local anesthesia, addition of dexmedetomidine to intravenous anesthesia, and defining

264 The Dexmedetomidine to Lessen ICU Agitation (DahLIA) study w

265 in the intensive care unit, the addition of dexmedetomidine to standard care compared with standard

266 The administration of the alpha 2-agonist, dexmedetomidine, to HTM cells resulted in a 90% inhibiti

267 n time to extubation was 1.9 days shorter in dexmedetomidine-treated patients (3.7 days [95% CI, 3.1

268 At comparable sedation levels, dexmedetomidine-treated patients spent less time on the

269 um during treatment was 54% (n = 132/244) in dexmedetomidine-treated patients vs 76.6% (n = 93/122) i

270 Dexmedetomidine-treated patients were more likely to dev

271 ere randomized to receive either propofol or dexmedetomidine until unresponsiveness.

272 , the study examined the correlation between dexmedetomidine use and postoperative cognitive change.

273 Clinical experience of dexmedetomidine use in functional neurosurgery is limite

274 gery, we examined for an association between dexmedetomidine use in the immediate postoperative perio

275 y, there are no large studies characterizing dexmedetomidine use in US neonatal intensive care units

276 Dexmedetomidine use increased from 0.003% in 2010 to 0.1

277 Early sedation with dexmedetomidine versus usual care.

278 Dexmedetomidine vs midazolam patients had more hypotensi

279 e care units (NICUs) or comparing the use of dexmedetomidine vs opioids in infants.

280 es, agitation occurred at a higher rate with dexmedetomidine vs propofol (risk ratio [RR], 1.54 [95%

281 Patients receiving dexmedetomidine vs propofol had no significant differenc

282 For dexmedetomidine vs propofol, only breakthrough analgesia

283 For dexmedetomidine vs propofol, there were 0.0008 QALYs (95

284 function trial, which compared sedation with dexmedetomidine vs. lorazepam in mechanically ventilated

285 Direct cost of dexmedetomidine was 17 times greater than haloperidol, b

286 Early dexmedetomidine was administered in 77 of the patients (

287 Dexmedetomidine was administered in the immediate postop

288 cluding drug acquisition cost, sedation with dexmedetomidine was associated with a median total inten

289 dine at a later time in the hospitalization, dexmedetomidine was associated with increased odds of br

290 Compared with LA alone, dexmedetomidine was associated with prolonged (1) motor

291 The most notable adverse effect of dexmedetomidine was bradycardia.

292 Dexmedetomidine was effective in blocking these sympatho

293 4 (3.5%) standard sedation patient-days when dexmedetomidine was given.

294 For each trial, we tested whether dexmedetomidine was noninferior to control with respect

295 receiving prolonged mechanical ventilation, dexmedetomidine was not inferior to midazolam and propof

296 nced baseline characteristics, allocation to dexmedetomidine was significantly associated with earlie

297 Dexmedetomidine was subsequently discontinued and the pa

298 Propofol and dexmedetomidine were the most commonly restricted medica

299 label use, and the potential side effects of dexmedetomidine with long-term use needs further evaluat

300 ese procedures can be provided by the use of dexmedetomidine, with or without the addition of remifen