ライフサイエンスコーパス: anesthetics

1 chemical stimuli (signaling lipids, volatile anesthetics).

2 arlson comorbidity index, and treatment with anesthetics).

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

4 are used clinically as analgesics and local anesthetics.

5 mmalian brain, are major targets for general anesthetics.

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

7 nctionally inhibited by isoflurane and other anesthetics.

8 are targeted by benzodiazepines and general anesthetics.

9 diverse experimental conditions and types of anesthetics.

10 esthetics is very similar to that of general anesthetics.

11 electronic structure of proteins by general anesthetics.

12 pressure, temperature, signaling lipids, and anesthetics.

13 ity profiles of membranes in the presence of anesthetics.

14 dditivity of the effect of general and local anesthetics.

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

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

17 ree the puzzling structural heterogeneity of anesthetics.

18 tional targets for some neurosteroid general anesthetics.

19 voiding emetogenic and hyperalgesic volatile anesthetics.

20 investigate molecular mechanisms of general anesthetics.

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

22 a variety of therapeutics, including general anesthetics.

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

24 to maintain variable levels of resistance to anesthetics.

25 ntial and is the primary target for volatile anesthetics.

26 diagnostic in vitro testing) and to volatile anesthetics.

27 thal genetic condition triggered by volatile anesthetics.

28 changes with age are modulated by inhalation anesthetics.

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

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

31 the greater and lesser occipital nerves with anesthetics.

32 side effects associated with conventional IV anesthetics.

33 s system function and the actions of general anesthetics.

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

35 animals resistant to systemically delivered anesthetics.

36 at potentiates the effect of delivered local anesthetics.

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

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

39 s targets and putative mechanisms of general anesthetics across biology and identify key substrates t

40 e review the behavioral endpoints of general anesthetics across species and propose the isolation of

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

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

43 A new study shows that anesthetics activate an endogenous analgesia neural ense

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

45 These noxious anesthetics activate transient receptor potential ankyri

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

47 re complications after subconjunctival local anesthetics administration.

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

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

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

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

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

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

54 For example, the local anesthetics ambroxol and lidocaine block both Na(V)1.7 a

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

56 samide receptor overlaps receptors for local anesthetics and batrachotoxin.

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

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

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

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

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

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

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

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

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

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

67 nostic related groups codes, blood pressure, anesthetics and narcotics administered, surgical and ane

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

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

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

71 Our structural analysis using photoactivable anesthetics and rigid docking simulation showed that iso

72 Some anesthetics and sedatives have been shown to cause neuro

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

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

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

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

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

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

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

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

81 erse group of 3alpha-OH steroids that act as anesthetics, anti-epileptics, and anti-depressants.

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

83 terial hypertension) and is an off target of anesthetics, antiparkinsonian drugs, and selective serot

84 Although anesthetics appear to activate microglia, the increased

85 Inhaled anesthetics are a chemically diverse collection of hydro

86 Propofol, etomidate, and barbiturate anesthetics are allosteric coagonists at pentameric alph

87 General anesthetics are both neuroprotective and neurotoxic with

88 Inhalational anesthetics are bronchodilators with immunomodulatory ef

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

90 been no empirical demonstration that general anesthetics are capable of functional quantum interactio

91 Volatile anesthetics are commonly used during surgery.

92 Anesthetics are generally associated with sedation, but

93 General anesthetics are known to cause depression of the freezin

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

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

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

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

98 General anesthetics are routinely used in clinical practice to i

99 val zebrafish respond to inhalational and IV anesthetics at concentrations similar to mammals.

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

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

102 se range of noxious and non-noxious volatile anesthetics, at clinically relevant concentrations, inhi

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

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

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

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

107 oline carboxamides interacted with the local anesthetics binding site.

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

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

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

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

112 This is the first illustration that anesthetics can affect the binding of nucleic acids to t

113 generally associated with sedation, but some anesthetics can also increase brain and motor activity-a

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

115 e lines of evidence demonstrate that general anesthetics can co-opt the neural circuits regulating ar

116 first experimental evidence that halogenated anesthetics can directly undergo quantum interaction mec

117 future studies to further determine whether anesthetics can induce behavioral hyperactivity via incr

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

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

120 How general anesthetics cause loss of consciousness is unknown.

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

122 Here we show that inhaled anesthetics (chloroform and isoflurane) activate TREK-1

123 en considerable focus on the hypothesis that anesthetics co-opt the neural mechanisms regulating slee

124 nding of the mechanisms of action of general anesthetics, coincident with progress in structural biol

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

126 provide a survey of the effects of different anesthetics, demonstrating that short exposure to diethy

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

128 Volatile anesthetics did not attenuate glycocalyx shedding in hum

129 We previously reported that volatile anesthetics directly bound to TLR2 and TLR4 and attenuat

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

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

132 General anesthetics during surgery are presumed to block pain by

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

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

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

136 Local anesthetics effectively suppress pain sensation, but mos

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

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

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

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

141 activation was not attenuated by intravenous anesthetics, except for a high concentration of propofol

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

143 Intravenous anesthetics exert a component of their actions via poten

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

145 General anesthetics exert their effects on the central nervous s

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

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

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

149 to network function and suggest that general anesthetics - from single cells to complex brains - crea

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

151 Lengthy use of general anesthetics (GAs) causes neurobehavioral deficits in the

152 General anesthetics (GAs) exert their effects through endogenous

153 Several general anesthetics (GAs) produce pain or irritation upon admini

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

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

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

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

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

159 lthough immunomodulatory effects of volatile anesthetics have been growingly appreciated, the molecul

160 Anesthetics have been linked to widespread neuronal cell

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

162 Volatile anesthetics have been reported to provide protection aga

163 Several anesthetics have been reported to suppress the transcrip

164 Anesthetics have both anti-inflammatory and proinflammat

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

166 but causal investigations of potent inhaled anesthetics have not been conducted.

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

168 modulators such as barbiturates and steroid anesthetics have provided insight into the modes of acti

169 General anesthetics have revolutionized medicine by facilitating

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

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

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

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

174 tion-based and individual-based responses to anesthetics in mice and zebrafish.

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

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

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

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

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

180 Local anesthetics in the form of creams, gels and sprays have

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

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

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

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

185 Volatile anesthetics, including isoflurane, have anti-inflammator

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

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

188 ow that both noxious and non-noxious general anesthetics inhibit agonist-evoked transient receptor po

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

190 We conclude that anesthetics inhibit TRPA1 by interacting at a site disti

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

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

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

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

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

196 The subconjunctival anesthesia with local anesthetics is considered as a low-risk procedure allowi

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

198 preferential interactions given by volatile anesthetics is quite poor.

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

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

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

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

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

204 Volatile anesthetics isoflurane and sevoflurane directly target a

205 Our reporter assay showed that volatile anesthetics isoflurane and sevoflurane increased the act

206 The binding sites of volatile anesthetics isoflurane and sevoflurane were located near

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

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

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

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

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

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

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

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

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

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

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

218 General anesthetics may control cell survival via their effects

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

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

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

222 on by aryl sulfonamides and by classic local anesthetics might show an interaction mediated by their

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

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

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

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

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

228 ugs of abuse (methamphetamine and fentanyl), anesthetics, neurotoxins, the pesticide paraquat, and he

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

230 the pharmacological effects of commonly used anesthetics nor with methadone, naloxone, oxycodone, or

231 All mutations reduced the log(d) values for anesthetics occupying both abutting and nonabutting pock

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

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

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

235 The effects of anesthetics on central energetic metabolism remain poorl

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

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

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

239 l evidence informing the distinct effects of anesthetics on metastasis of breast cancers through chan

240 implication for inhibitory action of general anesthetics on pLGICs.

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

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

243 ould be critical to understand the impact of anesthetics on sepsis pathophysiology.

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

245 study sets the foundation for the effect of anesthetics on TLR9 and will pave the way for future stu

246 upon tissue injury, we examined the role of anesthetics on TLR9 function.

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

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

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

250 The GABAergic anesthetics pentobarbital and propofol were also effecti

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

252 All currently available general anesthetics produce potentially deadly side effects.

253 Furthermore, the results indicate that the anesthetics propofol and pentobarbital interact with par

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

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

256 Volatile anesthetics provide myocardial preconditioning in corona

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

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

259 underlying different functional responses to anesthetics remain elusive.

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

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

262 Volatile anesthetics serve as useful probes of a conserved biolog

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

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

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

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

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

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

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

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

271 General anesthetics, such as chloroform, isoflurane, diethyl eth

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

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

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

275 General anesthetics suppress CNS activity by modulating the func

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

277 recover more slowly from certain injectable anesthetics than other dog breeds.

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

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

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

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

282 ., anxiolytics, anticonvulsants, and general anesthetics) that act as positive allosteric modulators

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 complicate the ability to appropriately dose anesthetics to each individual.

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

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

288 Even with co-administration of local anesthetics, traditional injection still causes pain to

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 The role of anesthetics used during surgery in cancer metastasis and

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

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

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

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

296 For 100 y, anesthetics were speculated to target cellular membranes

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

298 and scientific interest in developing local anesthetics with prolonged durations of effect from sing

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