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1 haracteristics (SmPC) were obtained for each sedative.
2 ally, alcohol acts as both a stimulant and a sedative.
3 idomide, which had been prescribed as a mild sedative.
4 ension or bradycardia before starting either sedative.
5 equently managed using a continuous-infusion sedative.
6 e mechanically ventilated and were receiving sedatives.
7 nes suggest minimizing dosage of opioids and sedatives.
8 d clinical outcomes associated with specific sedatives.
9 be unintentionally induced by heavy doses of sedatives.
10 to find non-benzodiazepine-based alternative sedatives.
11 people who find it hard to get to sleep take sedatives.
12 a reduces the metabolism of commonly used IV sedatives.
13 ics, 3) antidepressants, 4) street drugs, 5) sedatives, 6) poisoning (carbon monoxide, arsenic, or cy
14 s may constitute a nonneuronal mechanism for sedative action of anesthetic drugs.
15          The neuronal circuits mediating the sedative action of diazepam are unknown.
16 rs to be separate from the antipsychotic and sedative action of these medications.
17 moral pathway by which music might exert its sedative action.
18 idazolam and the IV route were the commonest sedative agent and route of administration, respectively
19 nitored anaesthetic care using propofol as a sedative agent can result in serious patient harm.
20 le of registered nurses in administering new sedative agents has led to a re-examination of the role
21             There are limited data comparing sedative agents in terms of clinical outcomes in an ICU
22                       The use of long-acting sedative agents may confound neurologic assessment.
23 tiple organ dysfunction syndrome scores, and sedative agents were recorded for each sedation interrup
24 us anxiolytic, anticonvulsant, hypnotic, and sedative agents, actions that are principally mediated v
25 aracteristics, sedative exposure, additional sedative agents, and system-level factors.
26                We assessed administration of sedative agents, ventilation time, sedation depth using
27    All trends persisted when controlling for sedative agents.
28 is exacerbated by frequent administration of sedative agents.
29 discomfort and sedation-agitation behaviors; sedative, analgesic, and neuromuscular blocking drug adm
30 odds ratio, 2.9; p < 0.001), lower amount of sedative-analgesic drugs (odds ratio, 1.9; p = 0.03), hi
31 n alpha2-adrenergic agonists, a new class of sedative/analgesic agents and their possible application
32 ation initiation, 97% respondents administer sedative/analgesic infusions, and the sedation target wa
33 in the management of drug withdrawal, and as sedative analgesics.
34 rug events reported to occur with the use of sedatives, analgesics, and antipsychotics in the intensi
35  of life-sustaining treatment and the use of sedatives, analgesics, and nonpharmacologic approaches t
36  propofol alone or in combination with other sedatives/analgesics has become popular for procedural s
37 n confounded by complicating factors such as sedative and analgesic administration.
38 omfort while minimizing the predilection for sedative and analgesic drug accumulation with prolongati
39 be severe enough to require increased use of sedative and analgesic drugs, and is among the events th
40 long been known to have anaesthetic-sparing, sedative and analgesic properties which are desirable in
41                                Propofol is a sedative and anesthetic agent that can both activate GAB
42                                  Propofol, a sedative and anesthetic drug was chosen as a model lipop
43 obarbital is a lipophilic molecule used as a sedative and antiepileptic drug that elicits a multitude
44 ing (liking and wanting) responses and lower sedative and cortisol responses in heavy vs light drinke
45 eriana officinalis used as an anxiolytic and sedative and in the treatment of insomnia.
46                        A brief comment as to sedative and opiate withdrawal follows.
47 ation following cannulation, with the use of sedative and opioid infusions.
48 ward "hibernation." The agents we utilize as sedative and pressor agents have considerable effects on
49    How critical care practitioners prescribe sedatives and analgesics and, perhaps more broadly, how
50  An evidence-based approach to administering sedatives and analgesics is necessary to optimize short-
51  ill patients receive significant amounts of sedatives and analgesics that increase their risk of dev
52       Critically ill patients are prescribed sedatives and analgesics to decrease pain and anxiety, i
53 of sedation and analgesia and total doses of sedatives and analgesics.
54 documented the advantages of pharmacological sedatives and anesthetics for use in bronchoscopy.
55                    Despite the common use of sedatives and anesthetics in the acute phase of TBI mana
56                                   The use of sedatives and antibiotics may be required to be changed
57 mmonly used ICU medications, especially some sedatives and anticholinergic medications, and keeping p
58                    Active compounds included sedatives and antipsychotic, antidepressant, and antisei
59 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
60 idepressants, antipsychotics, lithium salts, sedatives and anxiolytics, and stimulants.
61                                              Sedatives and anxiolytics, antidepressants, antipsychoti
62               As an alternative to high-dose sedatives and controlled mechanical ventilation, pharmac
63 ngton, Minnesota, USA) and novel 'soft-drug' sedatives and hypnotics (e.g. CNS-7259X and TD-4756) as
64 bilitation in routine care, including use of sedatives and lack of awareness of post-ICU cognitive im
65                                              Sedatives and opioids use was similar in the higher and
66                                              Sedatives and opioids were used in >80% of the patients
67                                   The use of sedatives and opioids, but not NMBAs, was associated wit
68                                   The use of sedatives and opioids, but not the use of NMBAs, was ass
69 outcomes included duration of stay, doses of sedatives and opioids, unintentional device removal, del
70 se of continuous infusions of opioids and/or sedatives and ventilator parameters (tidal volume per id
71 knockout mice are insensitive to the ataxic, sedative, and analgesic effects of the novel hypnotic dr
72 enetic factors that can influence analgesic, sedative, and antipsychotic response and safety in the c
73 erioperative period include sympathomimetic, sedative, and coagulopathic effects.
74             Decisions to administer opioids, sedatives, and antipsychotic medications are frequently
75  ill patients frequently receive analgesics, sedatives, and antipsychotics to optimize patient comfor
76 armacologic treatments including analgesics, sedatives, and neuromuscular blockers.
77 gical ocular complication rates, use of oral sedatives, and reported reasons to perform the surgery i
78 prescription drugs (prescription pain pills, sedatives, and tranquilliser) were the most commonly rep
79                                Propofol is a sedative, anesthetic, and antiepileptic agent that is fr
80  sleep-wake behavior are engaged by low-dose sedative anesthetics and that the mesopontine descending
81 -type compounds in animals with a history of sedative-anxiolytic/benzodiazepine self-administration.
82  been used as a pre-operative medication and sedative/anxiolytic drug.
83 ys compared with intermittent lorazepam when sedatives are interrupted daily.
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                             We also recorded sedative cost in U.S. dollars and adverse events includi
100 zole, antiprostate cancer drug bicalutamide, sedative dexmedetomidine, and two antifungals ravuconazo
101 n overview update in the diverse uses of the sedative dexmedetomidine.
102 ows that subjects rendered unresponsive with sedatives do not exhibit a stereotypic 'unconscious' res
103 ve requirements with PH and determination of sedative dose changes with PH are needed.
104 ional day 14 were treated with ketamine at a sedative dose for 2 hrs, and pups were studied at postna
105 s of righting reflex (LORR) in response to a sedative dose of ethanol (3.5 g/Kg).
106                                     A single sedative dose of THIP (6 mg/kg) to mice induced glutamat
107 ear regression analysis (dependent variable: sedative dose) was used to analyze the following indepen
108 study day, the PDM patients received 2 fewer sedative doses (reduction of 38%) and had a reduction of
109                    They also received higher sedative doses and longer exposure periods.
110  more beneficial than either method alone if sedative doses are reduced and arousal and mobility are
111                                              Sedative doses required to tolerate PH have not been wel
112 ls of sedation and significant reductions in sedative doses, especially benzodiazepines.
113 d calm) and requires failure of intermittent sedative dosing prior to starting continuous infusions.
114 r dose titrations per day, and a lower total sedative drug cost.
115                                              Sedative drug intensity and behavior varied during the c
116      Inadequate sedation was associated with sedative drug intensity and patient behavior as measured
117 e measures, consistent with its profile as a sedative drug with abuse liability.
118            Disturbance of neural activity by sedative drugs has been proposed to trigger a homeostati
119                   It has been suggested that sedative drugs may shorten life, but few studies exist c
120 lication significantly reduced the amount of sedative drugs needed to achieve a comparable degree of
121 linical practice suggests that analgesic and sedative drugs should be used prior to and during neurom
122 ess hormones and cytokines, requirements for sedative drugs, and level of sedation before and at the
123 eostatic adaptation conferring resistance to sedative drugs.
124 ptors contributes to the clinical actions of sedative drugs.
125 ination in rotarod experiments and a shorter sedative effect in loss of righting reflex assays.
126 BF cholinergic cell loss in dementia and the sedative effect of anti-cholinergic drugs have long impl
127 ereby implicating these neurons in the motor-sedative effect of diazepam.
128 drinkers, greater positive effects and lower sedative effects after alcohol consumption predicted inc
129 n dogs for their analgesic properties, their sedative effects and as adjuncts to anesthesia.
130  rewarding effects with lower sensitivity to sedative effects and cortisol reactivity, relative to li
131 righting reflex was performed to measure the sedative effects of alcohol (3.5 g/kg) and total sleepin
132 tion and had an increased sensitivity to the sedative effects of alcohol.
133 sive drinking, it was important in the acute sedative effects of alcohol.
134 es exhibit both increased sensitivity to the sedative effects of ethanol and failure to develop norma
135 bit significantly augmented responses to the sedative effects of ethanol and ketamine, but not pentob
136 s appear to be particularly sensitive to the sedative effects of ethanol as adults and insensitive to
137                           Sensitivity to the sedative effects of ethanol is inversely correlated with
138 ppy), due to its increased resistance to the sedative effects of ethanol.
139 izing actions of the inhaled anesthetics and sedative effects of halothane were reduced to the same e
140 ally isolated (SI) mice are resistant to the sedative effects of the positive allosteric GABA(A)-R mo
141 o link a molecular site in the GlyR with the sedative effects produced by intoxicating doses of ethan
142 te VLPO neurons, and may contribute to their sedative effects.
143  to achieve adequate sedation as measures of sedative efficacy.
144 itoring of anesthetic depth for titration of sedatives, en route to avoiding emetogenic and hyperalge
145                                              Sedatives, even given intermittently, substantially redu
146                                  Intravenous sedatives examined included benzodiazepines (midazolam a
147 cessed electroencephalography during coma in sedative-exposed patients is a predictor of post-coma de
148 al analog scale) and 2 aggregate measures of sedative exposure (intensity and frequency).
149 sedation-related adverse events, measures of sedative exposure (wakefulness, pain, and agitation), an
150 ents when these approaches result in reduced sedative exposure and facilitate arousal.
151 s that may be reduced by efforts to decrease sedative exposure during both daytime and nighttime hour
152  effect of invasive procedures and analgesic-sedative exposure on hippocampal growth was assessed, as
153                 Strategies aimed at reducing sedative exposure through protocols and coordination of
154 edictive, including patient characteristics, sedative exposure, additional sedative agents, and syste
155  delirium/coma-free days after adjusting for sedative exposure, age, and severity of illness.
156 s associated with deep sedation, substantial sedative exposure, and increased frequency of iatrogenic
157 ional multicomponent strategy for minimizing sedative exposure, reducing duration of mechanical venti
158 t PDM significantly reduced both measures of sedative exposure.
159 an failure, sepsis, prior mental status, and sedative exposure.
160 bidities, ventilator bundle adherence rates, sedative exposures, routes of nutrition, blood products,
161 estational age, sex, PMA, dose of analgesics/sedatives (fentanyl, morphine, midazolam), mechanical ve
162 %) were reported as the most frequently used sedatives; fentanyl (44%) and morphine (20%) the most fr
163 onist medications are the most commonly used sedatives for intensive care unit (ICU) patients, yet pr
164 ologists and other specialists administering sedatives for their own or others' procedures.
165 =48 hrs, administered a continuously infused sedative &gt;/=24 hrs, extubated, and successfully discharg
166 ration following exposure to anesthetics and sedatives has been clearly established in developing ani
167                         Some anesthetics and sedatives have been shown to cause neurotoxic effects in
168 hanol on neurons, as either a stimulant or a sedative, however remain unclear.
169  (HR, 1.22; 95% CI, 1.08 to 1.37), hypnotics/sedatives (HR, 1.21; 95% CI, 1.07 to 1.37), antidepressa
170  (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
171 e of anesthesiology are employing new potent sedative hypnotic agents to accomplish effective pediatr
172  currents and to test their contributions to sedative, hypnotic, and immobilizing anesthetic actions.
173 -4(3H)-quinazolinone, Quaalude), an infamous sedative-hypnotic and recreational drug from the 1960s-1
174 lated by the anxiolytic, anticonvulsant, and sedative-hypnotic benzodiazepines.
175           Propofol is the most commonly used sedative-hypnotic drug for noxious procedures, yet the m
176  and prolonged hypotensive, bradycardic, and sedative-hypnotic responses to alpha(2)AR stimulation.
177 RK3 (Kir3.3), is associated with less severe sedative-hypnotic withdrawal.
178 zodiazepines, which are often used for their sedative/hypnotic and anxiolytic effects.
179 n mice, but it should be applicable to other sedative/hypnotic drugs and to testing cerebellar mutant
180         However, we show that the ability of sedative/hypnotic drugs to enhance tonic inhibition in t
181 ptor numbers when considering the ability of sedative/hypnotic drugs to enhance tonic inhibition.
182 hanced by neurosteroids, antiepileptics, and sedative/hypnotic drugs.
183 o behavioral intoxication, as assayed by the sedative/hypnotic effects of ethanol.
184 iled to develop rapid tolerance to ethanol's sedative/hypnotic effects.
185 ht underlie the increased sensitivity to the sedative/hypnotic properties of ethanol but not the rewa
186 justed RR, 1.87; 95% CI, 1.70-2.06), receive sedative hypnotics concurrently (40.7% vs 7.6%, adjusted
187  for severe anxiety that was unresponsive to sedative hypnotics.
188        Particularly addressing the fields of sedatives, hypnotics and neuromuscular blockers, however
189 thdrawal from pentobarbital as well as other sedative-hypnotics (zolpidem and ethanol) versus wild-ty
190 in a wide variety of behavioral responses to sedative-hypnotics and may directly facilitate progress
191 r 2 or more antidepressants, antipsychotics, sedative-hypnotics, and antidepressant-antipsychotic com
192 mplex traits, including diverse responses to sedative-hypnotics, have been detected on distal chromos
193 R, 15.46; 99% CI, 6.77-35.31); and 2 or more sedative-hypnotics, with anxiety disorders (OR, 2.13; 99
194 novel aspects of neurobiological response to sedative-hypnotics.
195 e sedation and need for constant infusion of sedative-hypnotics.
196 ntly increasing the use of antipsychotics or sedative-hypnotics.
197 al ventilation (TV) and exposure to opioids, sedatives-hypnotics, or general anaesthetics in neonates
198  visits in which neither antidepressants nor sedative/hypnotics were prescribed.
199 eports relating to the use of each drug as a sedative in children under the age of 16.
200                 Propofol is commonly used as sedative in newborns and children.
201 plications related to the use of opioids and sedatives in an elderly population.
202 anically ventilated adult patients receiving sedatives in an ICU setting were used to develop and tes
203 xmedetomidine and propofol are commonly used sedatives in neurocritical care as they allow for freque
204 ssociated with increased dose or duration of sedatives in patients with acute lung injury.
205  information and the wide spread use of both sedatives in routine practice the pharmacovigilance plan
206                                 Delirium and sedative-induced coma are described as incremental manif
207 tween periods of awakening from sedation vs. sedative infusion were made.
208 adycardia (heart rate < 50 beats/min) during sedative infusion.
209 ructured quality improvement process, use of sedative infusions can be substantially decreased and da
210 lly ventilated patients receiving continuous sedative infusions over a 3-month period.
211 is study was to describe a protocol of daily sedative interruption and early physical and occupationa
212                     Patients underwent daily sedative interruption followed by physical and occupatio
213                                        Daily sedative interruption is not associated with an increase
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  vital signs and catecholamine levels during sedative interruption, fraction of ischemic time did not
218 ndependent variables: PH, age, gender, daily sedative interruption, type of respiratory failure, pres
219 entilation when used in the setting of daily sedative interruption.
220  levels were all significantly higher during sedative interruption.
221 xis, daily spontaneous breathing trials, and sedative interruptions, were not associated with ventila
222  titrated to maintain stable vital signs and sedative levels.
223 te-specific deletion does disrupt the normal sedative-locomotor inhibition as well as the anticonvuls
224 ng anxiety, agitation and adverse effects of sedative medication in patients undergoing weaning from
225 patients prescribed a continuous infusion of sedative medication while in the medical intensive care
226 ed on the following tenets - minimization of sedative medication, particularly benzodiazepines, delir
227 specific nursing shift and dosing level of a sedative medication.
228 rvals, during which 37% of patients received sedative medication.
229 n, and respiratory arrest after narcotic and sedative medication.
230                                              Sedative medications in both hypothermic and nonhypother
231 y of illness, severe sepsis, and exposure to sedative medications in the intensive care unit, increas
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 man primate models predictive of anxiolytic, sedative, motor, subjective, and reinforcing effects of
236              Behaviorally, SH-I-048A induced sedative, muscle relaxant and ataxic effects, reversed m
237 m, coma, sepsis, mechanical ventilation, and sedatives/opiates.
238                                   The use of sedatives, opioids, and neuromuscular blocking agents (N
239 her positive end-expiratory pressure (PEEP), sedatives, opioids, and NMBAs are used in a higher propo
240 ively collected data regarding the impact of sedatives, opioids, and NMBAs in ALI/ARDS patients on du
241 7 decreases anxiety-related behavior without sedative or addictive liabilities.
242 s of the duration of delirium and the use of sedative or analgesic agents with the outcomes were asse
243                                       Use of sedative or analgesic medications was not consistently a
244                  Both may be associated with sedative or opiate doses and pharmacokinetic or pharmaco
245                       The use of analgesics, sedatives, or extubation did not significantly influence
246 uring induction in the control group and the sedative outcome were recorded.
247     Female gender (p = .019), the absence of sedatives (p = .009), and lower Acute Physiology and Chr
248 e investigated the effect of a commonly used sedative, pentobarbital, on glial cells and their uptake
249 ver, this may be reduced during sleep and by sedatives, potent analgesics, and volatile anesthetics.
250 heir parents include the administration of a sedative premedicant, parental presence during induction
251 ia and pharmacological interventions such as sedative premedication are used to treat this clinical p
252  of benefit with routine use of lorazepam as sedative premedication in patients undergoing general an
253                                              Sedative premedication is widely administered before sur
254 g elective surgery under general anesthesia, sedative premedication with lorazepam compared with plac
255 t popular technique involves administering a sedative premedication, such as midazolam.
256  prevention to outline the differences among sedative premedications such as midazolam, clonidine, an
257 uce anxiety are effective lambdaU similar to sedative premedications, with the exception of parent pr
258 cost-effectiveness of the most commonly used sedatives prescribed for mechanically ventilated critica
259                          Given its favorable sedative properties combined with its limited effects on
260                                        Total sedative (propofol and midazolam) dose was recorded for
261 diazepine-based to a nonbenzodiazepine-based sedative regimen and reported duration of ICU length of
262          There is still a need to refine the sedative regimen for these cases.
263 hanical ventilation and who were receiving a sedative regimen that did not include opiate pain contro
264 ding benzodiazepines in favor of alternative sedative regimens and early mobilization of patients hav
265                                  While other sedative regimens continue to be examined, the use of pr
266 rther define the impact of nonbenzodiazepine sedative regimens on delirium and short-term mortality.
267     The model including bispectral index and sedative requirement correctly reclassified 15% of subje
268 s had lower bispectral index (p < 0.001) and sedative requirements (p < 0.001) during hypothermia com
269                  Bispectral index scores and sedative requirements early in the course of therapeutic
270 -protective ventilation, characterization of sedative requirements with PH and determination of sedat
271 ffer in their pharmacokinetic, stimulant, or sedative responses.
272 ibiting substance abuse-related, gating, and sedative side effects of ketamine in the drug discrimina
273 ics suffer from undesirable psychotropic and sedative side effects, as well as abuse potential.
274 s are observed in the absence of significant sedative side effects.
275 for marijuana to 0.63 (CI, 0.47 to 0.78) for sedatives; specificity was 0.93 or higher.
276 atients, due to a combination of illness and sedatives, spend a considerable amount of time in a coma
277 t alcohol use, or maximal level of cannabis, sedative, stimulant, or cocaine use.
278 epine sedative strategy, a nonbenzodiazepine sedative strategy was associated with a shorter ICU leng
279                 Compared to a benzodiazepine sedative strategy, a nonbenzodiazepine sedative strategy
280 als, all currently available anesthetics and sedatives that have been studied, such as ketamine, mida
281 se results could help with the design of new sedatives that induce a more natural sleep.
282  to the effects of pain and analgesic and/or sedative therapies and contribute to adverse outcomes.
283 iated with inadequate sedation, variation of sedative therapy intensity, and behavior over time were
284 ive care unit patients prescribed continuous sedative therapy.
285 50s, the drug thalidomide, administered as a sedative to pregnant women, led to the birth of thousand
286 entia (n = 85; P = .062 for interaction) and sedative/tranquilizer use (n = 224; P = .049 for interac
287 ine, hallucinogen, heroin, nonheroin opioid, sedative/tranquilizer, and/or solvent/inhalant use disor
288 ltiple organ dysfunction syndrome levels and sedative types.
289                  In a multivariate analysis, sedative use (p = 0.03), baseline moderate to severe shi
290                                              Sedative use and delirium status in acute lung injury pa
291                                              Sedative use increased over time, from 39.7% (38.7-40.6)
292  of out of the operating room anesthetic and sedative use will continue.
293                            However, like all sedatives, volatile agents are capable of deeply sedatin
294                                              Sedatives were administered in 85% of 18,050 four-hour i
295                                              Sedatives were also associated with increased time to ac
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%

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