ライフサイエンスコーパス: sedative

1 ve usual care (propofol, midazolam, or other sedatives).

2 ension or bradycardia before starting either sedative.

3 equently managed using a continuous-infusion sedative.

4 haracteristics (SmPC) were obtained for each sedative.

5 idomide, which had been prescribed as a mild sedative.

6 d may be affected by choice of analgesic and sedative.

7 ally, alcohol acts as both a stimulant and a sedative.

8 a reduces the metabolism of commonly used IV sedatives.

9 nes suggest minimizing dosage of opioids and sedatives.

10 d clinical outcomes associated with specific sedatives.

11 be unintentionally induced by heavy doses of sedatives.

12 e mechanically ventilated and were receiving sedatives.

13 ICU and administered with analgesics and/or sedatives.

14 ine vasopressor infusions, but unaffected by sedatives.

15 to find non-benzodiazepine-based alternative sedatives.

16 people who find it hard to get to sleep take sedatives.

17 ics, 3) antidepressants, 4) street drugs, 5) sedatives, 6) poisoning (carbon monoxide, arsenic, or cy

18 s may constitute a nonneuronal mechanism for sedative action of anesthetic drugs.

19 The neuronal circuits mediating the sedative action of diazepam are unknown.

20 oss-of-righting reflex (a measure of alcohol sedative actions), and on blood PF-5190457 concentration

21 Dexmedetomidine has unique properties as sedative agent and might reduce the risk of each complic

22 idazolam and the IV route were the commonest sedative agent and route of administration, respectively

23 nitored anaesthetic care using propofol as a sedative agent can result in serious patient harm.

24 observations support ketamine use as a safe sedative agent for intubation in hemodynamically-unstabl

25 se of dexmedetomidine as the sole or primary sedative agent in patients undergoing mechanical ventila

26 There are limited data comparing sedative agents in terms of clinical outcomes in an ICU

27 The use of long-acting sedative agents may confound neurologic assessment.

28 tiple organ dysfunction syndrome scores, and sedative agents were recorded for each sedation interrup

29 us anxiolytic, anticonvulsant, hypnotic, and sedative agents, actions that are principally mediated v

30 aracteristics, sedative exposure, additional sedative agents, and system-level factors.

31 We assessed administration of sedative agents, ventilation time, sedation depth using

32 All trends persisted when controlling for sedative agents.

33 is exacerbated by frequent administration of sedative agents.

34 discomfort and sedation-agitation behaviors; sedative, analgesic, and neuromuscular blocking drug adm

35 odds ratio, 2.9; p < 0.001), lower amount of sedative-analgesic drugs (odds ratio, 1.9; p = 0.03), hi

36 ation initiation, 97% respondents administer sedative/analgesic infusions, and the sedation target wa

37 in the management of drug withdrawal, and as sedative analgesics.

38 rug events reported to occur with the use of sedatives, analgesics, and antipsychotics in the intensi

39 of life-sustaining treatment and the use of sedatives, analgesics, and nonpharmacologic approaches t

40 propofol alone or in combination with other sedatives/analgesics has become popular for procedural s

41 n confounded by complicating factors such as sedative and analgesic administration.

42 ngth of ICU and hospital stays, and doses of sedative and analgesic drugs administered were recorded.

43 be severe enough to require increased use of sedative and analgesic drugs, and is among the events th

44 long been known to have anaesthetic-sparing, sedative and analgesic properties which are desirable in

45 Propofol is a sedative and anesthetic agent that can both activate GAB

46 Propofol, a sedative and anesthetic drug was chosen as a model lipop

47 ing (liking and wanting) responses and lower sedative and cortisol responses in heavy vs light drinke

48 In addition to their sedative and hypotensive effect, their curare-like activ

49 eriana officinalis used as an anxiolytic and sedative and in the treatment of insomnia.

50 A brief comment as to sedative and opiate withdrawal follows.

51 ation following cannulation, with the use of sedative and opioid infusions.

52 ward "hibernation." The agents we utilize as sedative and pressor agents have considerable effects on

53 How critical care practitioners prescribe sedatives and analgesics and, perhaps more broadly, how

54 ill patients receive significant amounts of sedatives and analgesics that increase their risk of dev

55 Critically ill patients are prescribed sedatives and analgesics to decrease pain and anxiety, i

56 of sedation and analgesia and total doses of sedatives and analgesics.

57 documented the advantages of pharmacological sedatives and anesthetics for use in bronchoscopy.

58 Despite the common use of sedatives and anesthetics in the acute phase of TBI mana

59 The use of sedatives and antibiotics may be required to be changed

60 mmonly used ICU medications, especially some sedatives and anticholinergic medications, and keeping p

61 after an intentional overdose of concomitant sedatives and antidepressants) and one attributable to l

62 Active compounds included sedatives and antipsychotic, antidepressant, and antisei

63 ely, compared with 3.6 (95% CI, 3.2-4.1) for sedatives and anxiolytics, 2.9 (95% CI, 2.3-3.5) for sti

64 idepressants, antipsychotics, lithium salts, sedatives and anxiolytics, and stimulants.

65 Sedatives and anxiolytics, antidepressants, antipsychoti

66 As an alternative to high-dose sedatives and controlled mechanical ventilation, pharmac

67 bilitation in routine care, including use of sedatives and lack of awareness of post-ICU cognitive im

68 Sedatives and opioids use was similar in the higher and

69 Sedatives and opioids were used in >80% of the patients

70 The use of sedatives and opioids, but not NMBAs, was associated wit

71 The use of sedatives and opioids, but not the use of NMBAs, was ass

72 outcomes included duration of stay, doses of sedatives and opioids, unintentional device removal, del

73 The later peak misuse trajectory for sedatives and tranquilisers crested at an older age (35

74 se of continuous infusions of opioids and/or sedatives and ventilator parameters (tidal volume per id

75 enetic factors that can influence analgesic, sedative, and antipsychotic response and safety in the c

76 Decisions to administer opioids, sedatives, and antipsychotic medications are frequently

77 ill patients frequently receive analgesics, sedatives, and antipsychotics to optimize patient comfor

78 armacologic treatments including analgesics, sedatives, and neuromuscular blockers.

79 gical ocular complication rates, use of oral sedatives, and reported reasons to perform the surgery i

80 prescription drugs (prescription pain pills, sedatives, and tranquilliser) were the most commonly rep

81 Propofol is a sedative, anesthetic, and antiepileptic agent that is fr

82 sleep-wake behavior are engaged by low-dose sedative anesthetics and that the mesopontine descending

83 -type compounds in animals with a history of sedative-anxiolytic/benzodiazepine self-administration.

84 General anesthetics and sedatives are used in millions of children every year to

85 dverse events and route of administration of sedatives as well as image quality.

86 in the search for anticonvulsants devoid of sedative, ataxic, and amnestic side effects.

87 to have anxiolytic-like effects with reduced sedative/ataxic liabilities.

88 ked by systemic treatment with the novel non-sedative benzodiazepine site agonist HZ166 in neuropathi

89 Among those receiving the sedatives, benzodiazepine and propofol doses were increa

90 tics has a role in the effects of analgesic, sedative, beta-blocker, local anesthetic, antiemetic, an

91 e, an alpha2 adrenergic agonist, is a useful sedative but can also cause significant bradycardia.

92 re widely used as anti-pruritics and central sedatives, but demonstrate only modest anti-inflammatory

93 preexisting cognitive impairment, and use of sedatives; but to date, the relationship between race an

94 arily an anaesthetic agent, but its use in a sedative capacity has resulted in the extensive off-labe

95 and presents therapeutic properties, such as sedative, carminative and antispasmodic, also being incl

96 The economic implications of sedative choice in the management of patients receiving

97 4-21] days; P = .01), were exposed to fewer sedative classes (median, 2 [IQR, 2-3] classes vs 3 [IQR

98 edation, receipt of three or more preweaning sedative classes, higher nursing workload, and more one-

99 zole, antiprostate cancer drug bicalutamide, sedative dexmedetomidine, and two antifungals ravuconazo

100 n overview update in the diverse uses of the sedative dexmedetomidine.

101 ows that subjects rendered unresponsive with sedatives do not exhibit a stereotypic 'unconscious' res

102 ional day 14 were treated with ketamine at a sedative dose for 2 hrs, and pups were studied at postna

103 s of righting reflex (LORR) in response to a sedative dose of ethanol (3.5 g/Kg).

104 A single sedative dose of THIP (6 mg/kg) to mice induced glutamat

105 study day, the PDM patients received 2 fewer sedative doses (reduction of 38%) and had a reduction of

106 They also received higher sedative doses and longer exposure periods.

107 more beneficial than either method alone if sedative doses are reduced and arousal and mobility are

108 faster from the administration of ataxic and sedative doses of ethanol.

109 Before and after dexmedetomidine infusion, sedative doses remained unchanged (propofol 2.6 +/- 1.2

110 ls of sedation and significant reductions in sedative doses, especially benzodiazepines.

111 d calm) and requires failure of intermittent sedative dosing prior to starting continuous infusions.

112 Sedative drug intensity and behavior varied during the c

113 Inadequate sedation was associated with sedative drug intensity and patient behavior as measured

114 uggest exposures to anesthetic agents and/or sedative drugs (AASDs) in children under three years old

115 Additionally, known sedative drugs cause loss of spontaneous larval movement

116 Disturbance of neural activity by sedative drugs has been proposed to trigger a homeostati

117 It has been suggested that sedative drugs may shorten life, but few studies exist c

118 linical practice suggests that analgesic and sedative drugs should be used prior to and during neurom

119 ess hormones and cytokines, requirements for sedative drugs, and level of sedation before and at the

120 h after arrest to allow for the clearance of sedative drugs.

121 eostatic adaptation conferring resistance to sedative drugs.

122 eroids, and various GABAergic anesthetic and sedative drugs.

123 onist treatment (OAT) may also be prescribed sedative drugs.

124 ptors contributes to the clinical actions of sedative drugs.

125 CBD had a dose-dependent sedative effect but did not have an impact on motor perf

126 ination in rotarod experiments and a shorter sedative effect in loss of righting reflex assays.

127 BF cholinergic cell loss in dementia and the sedative effect of anti-cholinergic drugs have long impl

128 ereby implicating these neurons in the motor-sedative effect of diazepam.

129 drinkers, greater positive effects and lower sedative effects after alcohol consumption predicted inc

130 rewarding effects with lower sensitivity to sedative effects and cortisol reactivity, relative to li

131 thout affecting analgesic, anti-scratch, and sedative effects and motor incoordination.

132 effects in Scn1a(+/-) mice without apparent sedative effects in vivo.

133 righting reflex was performed to measure the sedative effects of alcohol (3.5 g/kg) and total sleepin

134 d alcohol consumption and sensitivity to the sedative effects of alcohol in male NBCn1 knockout mice.

135 tion and had an increased sensitivity to the sedative effects of alcohol.

136 sive drinking, it was important in the acute sedative effects of alcohol.

137 es exhibit both increased sensitivity to the sedative effects of ethanol and failure to develop norma

138 bit significantly augmented responses to the sedative effects of ethanol and ketamine, but not pentob

139 s appear to be particularly sensitive to the sedative effects of ethanol as adults and insensitive to

140 Sensitivity to the sedative effects of ethanol is inversely correlated with

141 ppy), due to its increased resistance to the sedative effects of ethanol.

142 izing actions of the inhaled anesthetics and sedative effects of halothane were reduced to the same e

143 o link a molecular site in the GlyR with the sedative effects produced by intoxicating doses of ethan

144 te VLPO neurons, and may contribute to their sedative effects.

145 perthermia-induced seizures without apparent sedative effects.

146 itoring of anesthetic depth for titration of sedatives, en route to avoiding emetogenic and hyperalge

147 Sedatives, even given intermittently, substantially redu

148 Intravenous sedatives examined included benzodiazepines (midazolam a

149 cessed electroencephalography during coma in sedative-exposed patients is a predictor of post-coma de

150 al analog scale) and 2 aggregate measures of sedative exposure (intensity and frequency).

151 sedation-related adverse events, measures of sedative exposure (wakefulness, pain, and agitation), an

152 ents when these approaches result in reduced sedative exposure and facilitate arousal.

153 s that may be reduced by efforts to decrease sedative exposure during both daytime and nighttime hour

154 effect of invasive procedures and analgesic-sedative exposure on hippocampal growth was assessed, as

155 Strategies aimed at reducing sedative exposure through protocols and coordination of

156 edictive, including patient characteristics, sedative exposure, additional sedative agents, and syste

157 delirium/coma-free days after adjusting for sedative exposure, age, and severity of illness.

158 s associated with deep sedation, substantial sedative exposure, and increased frequency of iatrogenic

159 ional multicomponent strategy for minimizing sedative exposure, reducing duration of mechanical venti

160 t PDM significantly reduced both measures of sedative exposure.

161 an failure, sepsis, prior mental status, and sedative exposure.

162 bidities, ventilator bundle adherence rates, sedative exposures, routes of nutrition, blood products,

163 estational age, sex, PMA, dose of analgesics/sedatives (fentanyl, morphine, midazolam), mechanical ve

164 %) were reported as the most frequently used sedatives; fentanyl (44%) and morphine (20%) the most fr

165 The primary exposure was ketamine use as a sedative for intubation, with midazolam or propofol use

166 onist medications are the most commonly used sedatives for intensive care unit (ICU) patients, yet pr

167 dorsing the use of high doses of opioids and sedatives for pain control, regardless of the risk that

168 =48 hrs, administered a continuously infused sedative >/=24 hrs, extubated, and successfully discharg

169 ration following exposure to anesthetics and sedatives has been clearly established in developing ani

170 Some anesthetics and sedatives have been shown to cause neurotoxic effects in

171 hanol on neurons, as either a stimulant or a sedative, however remain unclear.

172 (HR, 1.22; 95% CI, 1.08 to 1.37), hypnotics/sedatives (HR, 1.21; 95% CI, 1.07 to 1.37), antidepressa

173 (HR, 1.33; 95% CI, 1.16 to 1.52), hypnotics/sedatives (HR, 1.24; 95% CI, 1.07 to 1.43), GI drugs (HR

174 szopiclone (Lunesta(R)), a nonbenzodiazepine sedative hypnotic, increased N2 spindle density (number/

175 currents and to test their contributions to sedative, hypnotic, and immobilizing anesthetic actions.

176 -4(3H)-quinazolinone, Quaalude), an infamous sedative-hypnotic and recreational drug from the 1960s-1

177 lated by the anxiolytic, anticonvulsant, and sedative-hypnotic benzodiazepines.

178 Propofol is the most commonly used sedative-hypnotic drug for noxious procedures, yet the m

179 tivating effects of low dose ethanol and the sedative-hypnotic effects of a high dose, while reduced

180 aling also altered the acute stimulatory and sedative-hypnotic effects of ethanol.

181 and prolonged hypotensive, bradycardic, and sedative-hypnotic responses to alpha(2)AR stimulation.

182 RK3 (Kir3.3), is associated with less severe sedative-hypnotic withdrawal.

183 zodiazepines, which are often used for their sedative/hypnotic and anxiolytic effects.

184 However, we show that the ability of sedative/hypnotic drugs to enhance tonic inhibition in t

185 ptor numbers when considering the ability of sedative/hypnotic drugs to enhance tonic inhibition.

186 hanced by neurosteroids, antiepileptics, and sedative/hypnotic drugs.

187 iled to develop rapid tolerance to ethanol's sedative/hypnotic effects.

188 ht underlie the increased sensitivity to the sedative/hypnotic properties of ethanol but not the rewa

189 justed RR, 1.87; 95% CI, 1.70-2.06), receive sedative hypnotics concurrently (40.7% vs 7.6%, adjusted

190 for severe anxiety that was unresponsive to sedative hypnotics.

191 thdrawal from pentobarbital as well as other sedative-hypnotics (zolpidem and ethanol) versus wild-ty

192 in a wide variety of behavioral responses to sedative-hypnotics and may directly facilitate progress

193 Use of sedative-hypnotics before surgery is common, but its eff

194 ombination with opioids, preoperative use of sedative-hypnotics increases the risk of adverse outcome

195 r 2 or more antidepressants, antipsychotics, sedative-hypnotics, and antidepressant-antipsychotic com

196 mplex traits, including diverse responses to sedative-hypnotics, have been detected on distal chromos

197 R, 15.46; 99% CI, 6.77-35.31); and 2 or more sedative-hypnotics, with anxiety disorders (OR, 2.13; 99

198 novel aspects of neurobiological response to sedative-hypnotics.

199 al ventilation (TV) and exposure to opioids, sedatives-hypnotics, or general anaesthetics in neonates

200 visits in which neither antidepressants nor sedative/hypnotics were prescribed.

201 eports relating to the use of each drug as a sedative in children under the age of 16.

202 Propofol is commonly used as sedative in newborns and children.

203 up, these drugs were administered as primary sedatives in 60%, 12%, and 20% of the patients, respecti

204 anically ventilated adult patients receiving sedatives in an ICU setting were used to develop and tes

205 xmedetomidine and propofol are commonly used sedatives in neurocritical care as they allow for freque

206 information and the wide spread use of both sedatives in routine practice the pharmacovigilance plan

207 Delirium and sedative-induced coma are described as incremental manif

208 tween periods of awakening from sedation vs. sedative infusion were made.

209 adycardia (heart rate < 50 beats/min) during sedative infusion.

210 ructured quality improvement process, use of sedative infusions can be substantially decreased and da

211 lly ventilated patients receiving continuous sedative infusions over a 3-month period.

212 is study was to describe a protocol of daily sedative interruption and early physical and occupationa

213 Patients underwent daily sedative interruption followed by physical and occupatio

214 Coordinating delirium assessments with daily sedative interruption will improve such assessments' abi

215 rium that persists despite a short period of sedative interruption) is unknown.

216 delirium (delirium that abates shortly after sedative interruption) occurs with the same frequency an

217 entilation when used in the setting of daily sedative interruption.

218 levels were all significantly higher during sedative interruption.

219 xis, daily spontaneous breathing trials, and sedative interruptions, were not associated with ventila

220 titrated to maintain stable vital signs and sedative levels.

221 te-specific deletion does disrupt the normal sedative-locomotor inhibition as well as the anticonvuls

222 ng anxiety, agitation and adverse effects of sedative medication in patients undergoing weaning from

223 Perioperative music can reduce opioid and sedative medication requirement, potentially improving p

224 patients prescribed a continuous infusion of sedative medication while in the medical intensive care

225 ed on the following tenets - minimization of sedative medication, particularly benzodiazepines, delir

226 specific nursing shift and dosing level of a sedative medication.

227 rvals, during which 37% of patients received sedative medication.

228 Sedative medications in both hypothermic and nonhypother

229 y of illness, severe sepsis, and exposure to sedative medications in the intensive care unit, increas

230 with a limited neurologic examination due to sedative medications until hospital day 10.

231 experience) and expanded (based on doses of sedative medications) definitions of CS failure were use

232 Alternatives to sedative medications, such as music, may alleviate the a

233 pioids, benzodiazepines, propofol, and other sedative medications.

234 ety of drugs undergoing metabolism, only the sedative midazolam (MDZ) serves as a marker substrate fo

235 Behaviorally, SH-I-048A induced sedative, muscle relaxant and ataxic effects, reversed m

236 m, coma, sepsis, mechanical ventilation, and sedatives/opiates.

237 The use of sedatives, opioids, and neuromuscular blocking agents (N

238 her positive end-expiratory pressure (PEEP), sedatives, opioids, and NMBAs are used in a higher propo

239 ively collected data regarding the impact of sedatives, opioids, and NMBAs in ALI/ARDS patients on du

240 7 decreases anxiety-related behavior without sedative or addictive liabilities.

241 s of the duration of delirium and the use of sedative or analgesic agents with the outcomes were asse

242 Use of sedative or analgesic medications was not consistently a

243 Both may be associated with sedative or opiate doses and pharmacokinetic or pharmaco

244 ing a dose that did not produce accompanying sedative or thermoregulatory effects that could concomit

245 ceive dexmedetomidine as the sole or primary sedative or to receive usual care (propofol, midazolam,

246 three drug classes (opioids, stimulants, and sedatives or tranquilisers) from adolescence into adulth

247 The use of analgesics, sedatives, or extubation did not significantly influence

248 uring induction in the control group and the sedative outcome were recorded.

249 Female gender (p = .019), the absence of sedatives (p = .009), and lower Acute Physiology and Chr

250 e investigated the effect of a commonly used sedative, pentobarbital, on glial cells and their uptake

251 of benefit with routine use of lorazepam as sedative premedication in patients undergoing general an

252 Sedative premedication is widely administered before sur

253 g elective surgery under general anesthesia, sedative premedication with lorazepam compared with plac

254 prevention to outline the differences among sedative premedications such as midazolam, clonidine, an

255 uce anxiety are effective lambdaU similar to sedative premedications, with the exception of parent pr

256 cost-effectiveness of the most commonly used sedatives prescribed for mechanically ventilated critica

257 disposal system for deactivating three model sedative prescription medications.

258 Given its favorable sedative properties combined with its limited effects on

259 diazepine-based to a nonbenzodiazepine-based sedative regimen and reported duration of ICU length of

260 ding benzodiazepines in favor of alternative sedative regimens and early mobilization of patients hav

261 rther define the impact of nonbenzodiazepine sedative regimens on delirium and short-term mortality.

262 The model including bispectral index and sedative requirement correctly reclassified 15% of subje

263 s had lower bispectral index (p < 0.001) and sedative requirements (p < 0.001) during hypothermia com

264 Bispectral index scores and sedative requirements early in the course of therapeutic

265 ffer in their pharmacokinetic, stimulant, or sedative responses.

266 ibiting substance abuse-related, gating, and sedative side effects of ketamine in the drug discrimina

267 ics suffer from undesirable psychotropic and sedative side effects, as well as abuse potential.

268 s are observed in the absence of significant sedative side effects.

269 for marijuana to 0.63 (CI, 0.47 to 0.78) for sedatives; specificity was 0.93 or higher.

270 atients, due to a combination of illness and sedatives, spend a considerable amount of time in a coma

271 t alcohol use, or maximal level of cannabis, sedative, stimulant, or cocaine use.

272 epine sedative strategy, a nonbenzodiazepine sedative strategy was associated with a shorter ICU leng

273 Compared to a benzodiazepine sedative strategy, a nonbenzodiazepine sedative strategy

274 als, all currently available anesthetics and sedatives that have been studied, such as ketamine, mida

275 se results could help with the design of new sedatives that induce a more natural sleep.

276 ved regarding the days free of analgesics or sedatives, the duration of night sleep, and the occurren

277 to the effects of pain and analgesic and/or sedative therapies and contribute to adverse outcomes.

278 iated with inadequate sedation, variation of sedative therapy intensity, and behavior over time were

279 ive care unit patients prescribed continuous sedative therapy.

280 50s, the drug thalidomide, administered as a sedative to pregnant women, led to the birth of thousand

281 e usual-care group and required supplemental sedatives to achieve the prescribed level of sedation.

282 entia (n = 85; P = .062 for interaction) and sedative/tranquilizer use (n = 224; P = .049 for interac

283 ine, hallucinogen, heroin, nonheroin opioid, sedative/tranquilizer, and/or solvent/inhalant use disor

284 ltiple organ dysfunction syndrome levels and sedative types.

285 In a multivariate analysis, sedative use (p = 0.03), baseline moderate to severe shi

286 Sedative use and delirium status in acute lung injury pa

287 Sedative use increased over time, from 39.7% (38.7-40.6)

288 e for tracheal intubation, compared to other sedative use, is associated with a lower risk of post-in

289 no observed adverse effect of the additional sedatives used.

290 However, like all sedatives, volatile agents are capable of deeply sedatin

291 The use of analgesics and sedatives was assessed daily.

292 Sedatives were administered in 85% of 18,050 four-hour i

293 Sedatives were also associated with increased time to ac

294 motherapy, inotropes, vasoactive agents, and sedatives were the most frequently proposed needed thera

295 Sedated patients had received more sedatives, whereas doses of morphine and antipsychotics

296 Evaluation II score and cumulative doses of sedatives while comatose.

297 nned to compare midazolam and clonidine, two sedatives widely used within PICUs neither of which bein

298 aneous awakening trials (ie, interruption of sedatives) with daily spontaneous breathing trials resul

299 ning trials (SATs)-ie, daily interruption of sedatives-with spontaneous breathing trials (SBTs).

300 The commonly used sedative zolpidem tartrate was implicated in 11.5% (95%