ライフサイエンスコーパス: anesthetics

1 chemical stimuli (signaling lipids, volatile anesthetics).

2 e fifth transmembrane domain (S5) in sensing anesthetics.

3 pressure, temperature, signaling lipids, and anesthetics.

4 ity profiles of membranes in the presence of anesthetics.

5 dditivity of the effect of general and local anesthetics.

6 tate and not by local specific action of the anesthetics.

7 lay a crucial role in the actions of general anesthetics.

8 ree the puzzling structural heterogeneity of anesthetics.

9 tional targets for some neurosteroid general anesthetics.

10 voiding emetogenic and hyperalgesic volatile anesthetics.

11 investigate molecular mechanisms of general anesthetics.

12 eus (CMT) are important targets for volatile anesthetics.

13 a variety of therapeutics, including general anesthetics.

14 ase C (PKC) activity is modulated by general anesthetics.

15 animals resistant to systemically delivered anesthetics.

16 to maintain variable levels of resistance to anesthetics.

17 ntial and is the primary target for volatile anesthetics.

18 diagnostic in vitro testing) and to volatile anesthetics.

19 at potentiates the effect of delivered local anesthetics.

20 changes with age are modulated by inhalation anesthetics.

21 oxicity caused by low and high-potency local anesthetics.

22 nd-gated ion channels are targets of general anesthetics.

23 ated by clinically relevant doses of general anesthetics.

24 mechanism of receptor-channel modulation by anesthetics.

25 or needle placement and application of local anesthetics.

26 linically relevant concentrations of inhaled anesthetics.

27 functional tolerance to alcohol and volatile anesthetics.

28 t to determine the best method for titrating anesthetics.

29 validating this model system for injectable anesthetics.

30 studying the potential neurotoxic effects of anesthetics.

31 ts elicited by GABA, similar to many general anesthetics.

32 he thalamus are cellular targets for general anesthetics.

33 ognition of both inhalational and injectable anesthetics.

34 etized with pungent compared with nonpungent anesthetics.

35 f the severed axon regrows in the absence of anesthetics.

36 in, and myosin light chain as targets of the anesthetics.

37 are used clinically as analgesics and local anesthetics.

38 mmalian brain, are major targets for general anesthetics.

39 s had active pacemakers at the time of their anesthetics.

40 nctionally inhibited by isoflurane and other anesthetics.

41 are targeted by benzodiazepines and general anesthetics.

42 diverse experimental conditions and types of anesthetics.

43 esthetics is very similar to that of general anesthetics.

44 electronic structure of proteins by general anesthetics.

45 biotics (49.6%), muscle relaxants, latex and anesthetics (15%), nonsteroidal anti-inflammatory drugs

46 ch helps explain how closely related inhaled anesthetics achieve specific actions and suggests strate

47 An alternative hypothesis proposes that anesthetics act on one or more brainstem or diencephalic

48 e neuronal mechanisms through which volatile anesthetics act to produce unconsciousness remain obscur

49 others such as zinc, alcohols, and volatile anesthetics acting on multiple members.

50 Here we exploit the observation that pungent anesthetics activate mammalian but not Drosophila TRPA1.

51 These noxious anesthetics activate transient receptor potential ankyri

52 US$ 13-30 per cases multiplied by 25 million anesthetics administered annually in the USA has the pot

53 general anesthetics, barbiturates, and local anesthetics all display the same effect on melting trans

54 eta3Met-227 in betaM1 established that these anesthetics also bind to a homologous site, most likely

55 However, little is known about how anesthetics alter neural activity during the transition

56 et, since the molecular targets of many such anesthetics alter the model dynamics in a manner similar

57 osters great difficulty in understanding how anesthetics alter this conscious state.

58 to ischemia, reduced sensitivity to volatile anesthetics, altered perception of pain, and a depressio

59 tory, cytostatics, diuretics, beta blockers, anesthetics, analgesics, antiepileptics, antidepressants

60 ted inhibition is a property of most general anesthetics and a candidate for a molecular mechanism of

61 samide receptor overlaps receptors for local anesthetics and batrachotoxin.

62 r many therapeutic agents, including general anesthetics and benzodiazepines, which enhance receptor

63 , interindividual variations in responses to anesthetics and consequences of exposure to anesthetic d

64 randomized to receive a TAP block with local anesthetics and dexamethasone, PILA with dexamethasone,

65 es the anti-inflammatory properties of local anesthetics and discusses the benefits seen when used sy

66 get of allosteric modulators such as general anesthetics and ethanol and is a major locus for hyperek

67 target of many drugs including some general anesthetics and ethanol.

68 unconsciousness) which is induced by general anesthetics and ethanol.

69 ifier Kv1 channels to modulation by volatile anesthetics and highlight an arousal suppressing role of

70 dered much less cardiotoxic than other local anesthetics and is used commonly as infusions for intrac

71 nd neuroactive steroids, as well as volatile anesthetics and long-chain alcohols, all enhance GABA(A)

72 "on-pathway" targets for anthracene general anesthetics and may also represent functional targets fo

73 xious and vasorelaxant properties of general anesthetics and may prove useful in understanding effect

74 rse cardiac pharmacotoxicity caused by local anesthetics and other lipophilic drugs.

75 consequences to exposure of stimuli, such as anesthetics and perioperative stress.

76 a broad range of chemically diverse general anesthetics and related nonanesthetics on lipid bilayer

77 neurons, immobilizing actions of the inhaled anesthetics and sedative effects of halothane were reduc

78 General anesthetics and sedatives are used in millions of childr

79 Neurodegeneration following exposure to anesthetics and sedatives has been clearly established i

80 Some anesthetics and sedatives have been shown to cause neuro

81 In animals, all currently available anesthetics and sedatives that have been studied, such a

82 The currently dominant theory is that anesthetics and similar molecules act by binding to Cys-

83 minimum alveolar concentrations of volatile anesthetics and subcutaneous lidocaine efficacy have bee

84 ydrogen bond between the oxygen atoms of the anesthetics and the hydroxyl of Tyr-236.

85 s review, we outline the history of volatile anesthetics and their effect on kidney function, briefly

86 r small molecule inhibitors, including local anesthetics and TTX.

87 other relevant channels sensitive to general anesthetics and, as shown here, to barbiturates, at clin

88 der typically triggered by potent inhalation anesthetics and/or the depolarizing muscle relaxant succ

89 many depressants, including benzodiazepines, anesthetics, and alcohol.

90 a group of gases including anesthetics, non-anesthetics, and anesthetic/convulsants on tubulin dynam

91 c toxicity, local tissue toxicity from local anesthetics, and inflammation.

92 in also binds propofol and related GABAergic anesthetics, and that the same binding site mediates rec

93 sodium channels are inhibited by many local anesthetics, antiarrhythmics, and antiepileptic drugs.

94 Although anesthetics appear to activate microglia, the increased

95 General anesthetics are both neuroprotective and neurotoxic with

96 Inhalational anesthetics are bronchodilators with immunomodulatory ef

97 Cumulatively, this work demonstrates that anesthetics are capable of directly activating endogenou

98 Volatile anesthetics are commonly used during surgery.

99 General anesthetics are known to cause depression of the freezin

100 Although general anesthetics are known to modulate the activity of ligand

101 imal fMRI and neurovascular studies, however anesthetics are known to profoundly affect neural and va

102 Repeatable responses of PL FBI-OFET to anesthetics are produced in a concentration range that r

103 Because anesthetics are rarely given alone, we ask whether addit

104 General anesthetics are routinely used in clinical practice to i

105 al activity into EEG signals, the effects of anesthetics at a systems level, and the neural correlate

106 As yet, the direct effect of volatile anesthetics at physiological relevant concentrations on

107 he potential binding mode of noxious general anesthetics at TRPA1.

108 us, displacement of 1-AMA from HSAF by other anesthetics attenuates the fluorescence signal and allow

109 We show here that general anesthetics, barbiturates, and local anesthetics all dis

110 ject to dynamic modulation by agents such as anesthetics, barbiturates, and neurosteroids, the cellul

111 reasoning, and that exposure to two or more anesthetics before age 2 nearly doubles the risk for an

112 Propofol and other intravenous general anesthetics bind at the betaM3-alphaM1 subunit interface

113 upports the hypothesis that some intravenous anesthetics bind in the betaM3-alphaM1 subunit interface

114 sal that these structurally distinct general anesthetics bind to sites in GABA(A)Rs in the transmembr

115 WT SoCal5 and SoCal5 with the local anesthetics binding site mutated (F1760A) could be expre

116 oline carboxamides interacted with the local anesthetics binding site.

117 Recognition that dissociative anesthetics block the N-methyl-D-aspartate (NMDA) recept

118 ne receptors (nAChRs) are targets of general anesthetics, but functional sensitivity to anesthetic in

119 ion channels (pLGICs) are targets of general anesthetics, but molecular mechanisms underlying anesthe

120 p receptors are molecular targets of general anesthetics, but the knowledge of anesthetic binding to

121 are modulated by halogenated inhaled general anesthetics, but the underlying molecular mechanisms are

122 trast to the mostly positively charged local anesthetics, but their open/inactivated-state blocking a

123 tates induced by five classes of intravenous anesthetics by relating their behavioral and physiologic

124 own that recognition of inhalational general anesthetics by the model protein apoferritin closely mir

125 ive techniques be developed so that existing anesthetics can be used with minimum risk of neurotoxic

126 es indicate that early postnatal exposure to anesthetics can lead to lasting deficits in learning and

127 Postconditioning with inhalational anesthetics can reduce ischemia-reperfusion brain injury

128 surgical depths of anesthesia, inhalational anesthetics cause a loss of motor response to painful st

129 These data indicate that inhalational anesthetics cause activation of RTN neurons, which serve

130 How general anesthetics cause loss of consciousness is unknown.

131 General anesthetics cause sedation, hypnosis, and immobilization

132 Exposure of young animals to commonly used anesthetics causes neurotoxicity including impaired neur

133 ic regional anesthesia (over 46,000 regional anesthetics) demonstrate overall safety and lack of majo

134 We show that anesthetics depress the critical temperature (Tc) of the

135 Volatile anesthetics did not attenuate glycocalyx shedding in hum

136 eceptor (NMDAR) antagonists are dissociative anesthetics, drugs of abuse, and are of therapeutic inte

137 an effective dose equivalent of inhalational anesthetics during surgery (derived from mean end-tidal

138 support therapeutic applications of volatile anesthetics during the intraoperative and postoperative

139 Sedation with volatile anesthetics during therapeutic hypothermia may be a feas

140 transplant patients underwent 118 subsequent anesthetics during which they received neostigmine and g

141 Local anesthetics effectively suppress pain sensation, but mos

142 sia through intravenous delivery of volatile anesthetics, eliminating the need for the use of large a

143 d that the degree of potentiation by general anesthetics (etomidate, propofol, and isoflurane) was gr

144 otic and amnestic actions of the intravenous anesthetics, etomidate and propofol.

145 many general anesthetics, including volatile anesthetics, etomidate, propofol, and barbiturates.

146 ane, desflurane) and i.v. (propofol) general anesthetics excite peripheral sensory nerves to cause pa

147 Intravenous anesthetics exert a component of their actions via poten

148 General anesthetics exert many of their CNS actions by binding t

149 General anesthetics exert their effects on the central nervous s

150 One emerging possibility is that anesthetics exert their hypnotic effects by hijacking en

151 as exploit the TRPV1 pore to deliver charged anesthetics for neuronal silencing.

152 advantages of pharmacological sedatives and anesthetics for use in bronchoscopy.

153 Anesthetics, for example, induce considerable tolerance,

154 lar substrates for select actions of inhaled anesthetics; for immobilization, which is spinally media

155 l can speed the removal of potent inhalation anesthetics from anesthesia workstations.

156 Owing to the lack of alternative anesthetics, further animal studies into the mechanism a

157 rature supports the idea that common general anesthetics (GAs) cause long-term cognitive changes and

158 General anesthetics (GAs) have transformed surgery through their

159 que does not involve any potentially harmful anesthetics, gases or cooling procedures.

160 dine enhanced the efficacy of released local anesthetics, greatly increasing the number of triggerabl

161 At 3.0 T, the addition of steroids and anesthetics had minimal effect on signal intensity curve

162 Their efficacy as anesthetics has been shown to correlate both with their

163 for isoflurane and 10 muM for propofol; both anesthetics have a lower affinity for the allosteric sit

164 is randomized study, we examined if volatile anesthetics have an effect on acute graft injury and cli

165 Anesthetics have been linked to widespread neuronal cell

166 PURPOSE OF REVIEW: Although general anesthetics have been provided effectively for many year

167 Volatile anesthetics have been reported to provide protection aga

168 Several anesthetics have been reported to suppress the transcrip

169 s including hypoxia, hypocapnia, and certain anesthetics have been suggested to contribute to Alzheim

170 Anesthetics have both anti-inflammatory and proinflammat

171 Local anesthetics have many beneficial properties, and promisi

172 We conclude that general anesthetics have minimal effects on bilayer properties a

173 the effects that n-alcohols and other liquid anesthetics have on the two-dimensional miscibility crit

174 General anesthetics have revolutionized medicine by facilitating

175 , followed by alcohol, marijuana or cocaine, anesthetics/hypnotics, and oral opioids.

176 the primary pharmacologic effect of general anesthetics in a behavioral phenotype we termed "optoane

177 , and therefore have implications for use of anesthetics in AD patients, pending human study confirma

178 ospective studies to demonstrate the role of anesthetics in brain protection if any as well as define

179 ypnotic sensitivity to two other intravenous anesthetics in HCN1 knock-out mice matched effects on HC

180 anisone/midazolam) and volatile (isoflurane) anesthetics in mice.

181 ntributed to countless apparently uneventful anesthetics in neurologically at-risk patients.

182 Dosing studies of local anesthetics in peripheral nerve blockade suggest that ma

183 binding, which may mimic changes elicited by anesthetics in physiologic targets like ion channels.

184 The choice of local anesthetics in regional anesthesia depends on desired on

185 Despite the common use of sedatives and anesthetics in the acute phase of TBI management, their

186 ss of intersubunit binding sites for general anesthetics in the alpha1beta3gamma2 GABAAR transmembran

187 es of intersubunit-binding sites for general anesthetics in the GABAAR transmembrane domain.

188 ing the utilization and outcomes of regional anesthetics in this population.

189 The trend toward smaller doses of local anesthetics in ultrasound-guided regional anesthesia imp

190 Previous studies show that general anesthetics including isoflurane activate VLPO neurons,

191 Intravenous anesthetics, including etomidate, propofol, barbiturates

192 Volatile anesthetics, including isoflurane, have anti-inflammator

193 receptors, are the targets for many general anesthetics, including volatile anesthetics, etomidate,

194 ies suggest that modern halogenated volatile anesthetics induce potent anti-inflammatory, antinecroti

195 We recently observed that several n-alcohol anesthetics inhibit heterogeneity in plasma-membrane-der

196 uggest that halogenated inhalational general anesthetics interact with gates and pore regions of thes

197 etermine whether other structural classes of anesthetics interact with the etomidate binding site.

198 ral pressure that arise from partitioning of anesthetics into the bilayer.

199 derstanding of the mechanisms and effects of anesthetics is a critically important part of neuroscien

200 evidence that epidural analgesia with local anesthetics is associated with faster resolution of post

201 Generally the protein target for anesthetics is assumed to be neuronal membrane receptors

202 A common endpoint of general anesthetics is behavioral unresponsiveness, which is com

203 he inhibition of K-Shaw2 channels by general anesthetics is governed by interactions between binding

204 etailed action mechanism of volatile general anesthetics is still unknown despite their effect has be

205 pentameric ion channels by alkylphenol-based anesthetics is sufficient to induce modulation of activi

206 Thus, the thermodynamic behavior of local anesthetics is very similar to that of general anestheti

207 e neuroprotective benefit of intra-operative anesthetics is widely described and routinely aimed to i

208 role of pore block inhibition by the general anesthetics isoflurane and propofol of the prokaryotic p

209 icant impact on the uptake of the inhalation anesthetics isoflurane, sevoflurane, and desflurane when

210 concentration-response of TASK-3 to several anesthetics (isoflurane, desflurane, sevoflurane, haloth

211 In the process of developing safer general anesthetics, isomers of anesthetic ethers and barbiturat

212 adaptation directly counters some effects of anesthetics, it also causes long-lasting enhancement of

213 Among anesthetics, ketamine is remarkable in that it induces p

214 uency discharges of excitable cells by local anesthetics (LA) is largely determined by drug-induced p

215 als comparing epidural analgesia (with local anesthetics, lasting for >/= 24 hours postoperatively) w

216 one, and methylprednisolone) and three local anesthetics (lidocaine, ropivacaine, and bupivacaine) we

217 a cream, and (iii) the analysis of the local anesthetics, lidocaine and prilocaine, in a gel and a cr

218 Additionally, all three anesthetics masked potentially important features of the

219 The results therefore indicate that anesthetics may be potentially harmful not only in very

220 rmalities, raising substantial concerns that anesthetics may cause similar cell death in young childr

221 It is conceivable that volatile anesthetics may contribute to postoperative cognitive de

222 General anesthetics may control cell survival via their effects

223 that the binding sites of local and general anesthetics may overlap.

224 the renal protective properties of volatile anesthetics may provide clinically useful therapeutic in

225 Recent evidence suggests that anesthetics might cause persistent deficits in cognitive

226 lts indicate that several classes of general anesthetics modulate etomidate binding to the GABA(A)R:

227 The structural mechanisms underlying how anesthetics modulate pLGIC function remain largely unkno

228 Halogenated inhaled anesthetics modulate voltage-gated ion channels by unkno

229 Because of their roles as general anesthetics, n-alcohols are perhaps the best-studied amp

230 f a large variety of agents such as volatile anesthetics, neuroprotective agents, and antidepressants

231 tly known modulators of GABA function (e.g., anesthetics, neurosteroids or ethanol).

232 ate the effect of a group of gases including anesthetics, non-anesthetics, and anesthetic/convulsants

233 iewed literature regarding the role of local anesthetics, NSAIDs, gabapentinoids, and acetaminophen,

234 nd the documentation of participation in the anesthetics of 20 trauma patients.

235 uires only that residents participate in the anesthetics of 20 trauma patients.

236 The effects of general anesthetics on apoptosis and autophagy are closely integ

237 The effects of anesthetics on central energetic metabolism remain poorl

238 understanding of the effect of inhalational anesthetics on fetal cardiac function and some insight i

239 A kinetic model of the effect of agonist and anesthetics on ligand-gated ion channels, developed in e

240 hat hexadecanol acts oppositely to n-alcohol anesthetics on membrane mixing and antagonizes ethanol-i

241 implication for inhibitory action of general anesthetics on pLGICs.

242 tients to try to mitigate the effects of the anesthetics on postoperative cognitive function.

243 may prove useful in understanding effects of anesthetics on related ion channels.

244 The implied existence of a receptor site for anesthetics on the GABA(A)R protein was supported by ide

245 to shed light on the mechanism of action of anesthetics on these important ion channels.

246 ding of analgesia devoid of the influence of anesthetics or restraints.

247 n these data that sedation with inhalational anesthetics outside of the operating room may likewise h

248 GABA, allosteric ligands such as the general anesthetics pentobarbital and etomidate can activate the

249 The GABAergic anesthetics pentobarbital and propofol were also effecti

250 sity functional theory, we show that general anesthetics perturb and extend the highest occupied mole

251 asal activity with the allosterically acting anesthetics propofol, pentobarbital, or alfaxalone.

252 We propose that liquid general anesthetics provide an experimental tool for lowering cr

253 Volatile anesthetics provide myocardial preconditioning in corona

254 e cortex, and postconditioning with volatile anesthetics provides neuroprotective actions that depend

255 ects of several clinically utilized volatile anesthetics, recent studies suggest that modern halogena

256 underlying different functional responses to anesthetics remain elusive.

257 s consistent with the high concentrations of anesthetics required to achieve clinical effects.

258 de that the inhibition of K-Shaw2 by general anesthetics results from allosteric interactions between

259 The mechanism(s) by which anesthetics reversibly suppress consciousness are incomp

260 Volatile anesthetics serve as useful probes of a conserved biolog

261 Interestingly, we show that anesthetics share with the antagonist A-967079 a potenti

262 ABA(A)Rs) are believed to be key targets for anesthetics, sleep-promoting drugs, neurosteroids, and a

263 inhibited by general anesthetics, suggesting anesthetics stabilize a closed channel state, but in ane

264 s work suggested that n-alcohols and inhaled anesthetics stabilize the closed state of the Shaw2 volt

265 Alkanols and halogenated inhaled anesthetics such as halothane and isoflurane inhibit the

266 Paradoxically, volatile anesthetics such as halothane inhibit these channels.

267 hysiology measurements suggest that volatile anesthetics such as isoflurane inhibit NaV by stabilizin

268 l circuitry, it has also been suggested that anesthetics such as propofol induce loss of consciousnes

269 We demonstrated in the past that volatile anesthetics such as sevoflurane attenuate ischemia-reper

270 sults suggest that propofol and other common anesthetics, such as etomidate and ketamine, may target

271 tic pLGIC homologue, is inhibited by general anesthetics, suggesting anesthetics stabilize a closed c

272 ts were found using three different types of anesthetics, suggesting that they are caused by the netw

273 General anesthetics suppress CNS activity by modulating the func

274 ve been shown to be sensitive to all general anesthetics tested thus far.

275 have a larger reservoir of potent inhalation anesthetics than did their predecessors.

276 The choices of anesthetics that are available are considered and a new

277 tylphenol, two structural analogs of general anesthetics that are hydrophobic but have no anesthetic

278 arbiturate, [(3)H]R-mTFD-MPAB, photoreactive anesthetics that bind with high selectivity to distinct

279 o explore the preclinical efficacy of common anesthetics that function by reducing the TXA-mediated i

280 Our model generalizes to other anesthetics that include GABA as a target, since the mol

281 ction and duration of anesthesia produced by anesthetics that suppress Glu neurotransmission.

282 Injectable local anesthetics that would last for many days could have a m

283 channel function is activated by halogenated anesthetics through binding at a putative anesthetic-bin

284 ite or sites, and they suggest that volatile anesthetics, through perturbations at a single site, inc

285 The addition of steroids and/or anesthetics to gadolinium solutions for MR arthrography

286 he patient with epilepsy are the capacity of anesthetics to modulate or potentiate seizure activity a

287 Docking these anesthetics to the original GLIC crystal structure and t

288 At 1.5 T, the addition of steroids and anesthetics to the saline solutions had no impact on the

289 inantly inherited disorder in which volatile anesthetics trigger aberrant Ca(2+) release in skeletal

290 nimize POCD in the choice and development of anesthetics used during surgeries for patients suffering

291 tential protective and harmful effect of the anesthetics used needs to be considered as well.

292 Volatile anesthetics (VAs) cause profound neurological effects, i

293 The mechanisms by which volatile anesthetics (VAs) produce their effects (loss of conscio

294 Volatile anesthetics (VAs), such as isoflurane, induce a general

295 , which is sensitive to a variety of general anesthetics, we performed multiple molecular dynamics si

296 N current (i.e., suppression by inhalational anesthetics, weak rectification, inhibition by extracell

297 onstrated that essentially all commonly used anesthetics, when used alone or in combination, enhance

298 anism shared by the interactions of volatile anesthetics with targets in the CNS.

299 ee of success, little is known regarding how anesthetics work after the events of binding.

300 We show that the general anesthetics xenon, sulfur hexafluoride, nitrous oxide, a