ライフサイエンスコーパス: volatile anesthetic

1 ure) and chemical stimuli (signaling lipids, volatile anesthetics).

2 the presence of halothane, a clinically used volatile anesthetic.

3 also for etomidate and other intravenous and volatile anesthetics.

4 ermia, a pharmacogenetic crisis triggered by volatile anesthetics.

5 to be distinct from that of the alcohol and volatile anesthetics.

6 ed with the activity profiles of three other volatile anesthetics.

7 etic evidence points to multiple targets for volatile anesthetics.

8 t display abnormalities in their response to volatile anesthetics.

9 pharmacological antagonism of the effects of volatile anesthetics.

10 s for clinically important compounds such as volatile anesthetics.

11 ds may overlap with those of ethanol and the volatile anesthetics.

12 a greater degree than bronchus, as seen with volatile anesthetics.

13 ement of glycine receptor (GlyR) function by volatile anesthetics.

14 complexes may represent a general target for volatile anesthetics.

15 en proximal and distal airways, as seen with volatile anesthetics.

16 a1 GlyR subunit was tested for modulation by volatile anesthetics.

17 ans and may represent a molecular target for volatile anesthetics.

18 ique effects on sensitivity to the different volatile anesthetics.

19 e involved in the response of these cells to volatile anesthetics.

20 omplex I is a primary mechanism of action of volatile anesthetics.

21 TLR7-mediated activation was not affected by volatile anesthetics.

22 oute to avoiding emetogenic and hyperalgesic volatile anesthetics.

23 amic nucleus (CMT) are important targets for volatile anesthetics.

24 tially lethal genetic condition triggered by volatile anesthetics.

25 rane potential and is the primary target for volatile anesthetics.

26 d for MH diagnostic in vitro testing) and to volatile anesthetics.

27 cated in functional tolerance to alcohol and volatile anesthetics.

28 ivated T-channels) are potently inhibited by volatile anesthetics.

29 ) with designed specific binding pockets for volatile anesthetics.

30 o the induction of preconditioning effect by volatile anesthetics.

31 eep and by sedatives, potent analgesics, and volatile anesthetics.

32 le I(K(ACh)) channels, indicating that these volatile anesthetics act on channel open-close kinetics.

33 l use, the neuronal mechanisms through which volatile anesthetics act to produce unconsciousness rema

34 tion might be the primary mechanism by which volatile anesthetics act, rather than an untoward second

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

36 The mechanisms of volatile anesthetic action remain among the most perplex

37 K9) tandem-pore potassium channels provide a volatile anesthetic-activated and Galpha(q) protein- and

38 Volatile anesthetics affect all cells and tissues tested

39 of pharmacological postconditioning with the volatile anesthetic agent sevoflurane (n = 48), intermit

40 Volatile anesthetic agent use in the intensive care unit

41 Volatile anesthetic agent, 1-chloro-1,2,2-trifluorocyclo

42 Isoflurane, a volatile anesthetic agent, has been recognized for its p

43 Three other volatile anesthetic agents show a similar pattern.

44 oflurane, and enflurane, three commonly used volatile anesthetic agents, affect glutamate receptor-mo

45 and vomiting or motion sickness, young age, volatile anesthetic agents, nitrous oxide, and the admin

46 tors, cyclosporine A, radiocontrast dyes and volatile anesthetic agents.

47 the mechanism by which preconditioning with volatile anesthetics alleviates ischemic injury remains

48 ail clamp stimulus in mice anesthetized with volatile anesthetics also did not differ between genotyp

49 Volatile anesthetics alter tissue excitability by decrea

50 otection to ischemia, reduced sensitivity to volatile anesthetics, altered perception of pain, and a

51 )Ala(291), a water-accessible residue, alter volatile anesthetic and ethanol potentiation of GABA-ind

52 how here that a pair of structurally similar volatile anesthetic and nonimmobilizer (nonanesthetic),

53 nstrated that a pair of structurally similar volatile anesthetic and nonimmobilizer, 1-chloro-1,2,2-t

54 s the notion that low affinity drugs such as volatile anesthetics and alcohols can cause significant

55 no acid residues important for the action of volatile anesthetics and alcohols in these receptors.

56 a(2+) leak and desensitized the mice to both volatile anesthetics and heat.

57 ayed rectifier Kv1 channels to modulation by volatile anesthetics and highlight an arousal suppressin

58 urates, and neuroactive steroids, as well as volatile anesthetics and long-chain alcohols, all enhanc

59 or studying the specific interaction between volatile anesthetics and membrane proteins at the molecu

60 vated K(+) current was strongly inhibited by volatile anesthetics and mGluR activation.

61 ation of intraoperative fever is impaired by volatile anesthetics and muscle relaxants.

62 rrect evaluation of binding kinetics between volatile anesthetics and neuronal receptors.

63 or a variety of modulatory agents, including volatile anesthetics and neurotransmitters/hormones, the

64 ations in minimum alveolar concentrations of volatile anesthetics and subcutaneous lidocaine efficacy

65 a severe reaction triggered by inhalational volatile anesthetics and succinylcholine in genetically

66 In this review, we outline the history of volatile anesthetics and their effect on kidney function

67 Given that isoflurane is a widely used volatile anesthetic, and is used for inhalational long-t

68 d between isoflurane, a clinically important volatile anesthetic, and membrane-bound nicotinic acetyl

69 Recent studies suggest that alcohols, volatile anesthetics, and inhaled drugs of abuse, which

70 Volatile anesthetics appear to suppress effector functio

71 ctural features of protein binding sites for volatile anesthetics are being explored using a defined

72 Volatile anesthetics are commonly used during surgery.

73 their ability to antagonize propofol and two volatile anesthetics, as well as their interaction with

74 As yet, the direct effect of volatile anesthetics at physiological relevant concentra

75 t a diverse range of noxious and non-noxious volatile anesthetics, at clinically relevant concentrati

76 Competition experiments indicate that volatile anesthetics, at low concentrations, share the s

77 Administration of volatile anesthetics before prolonged coronary artery oc

78 STD was able to identify that volatile anesthetics bind to bovine serum albumin, oleic

79 were used in this study to characterize the volatile anesthetic binding sites in gramicidin A (gA) i

80 The structural features of volatile anesthetic binding sites on proteins are being

81 The direct measure of volatile anesthetic binding to protein is complicated by

82 graphy for the purpose of directly measuring volatile anesthetic binding to protein, and show that it

83 The techniques to measure directly volatile anesthetic binding to proteins are still under

84 ases the affinity (Kd = 0.71 +/- 0.04 mM) of volatile anesthetic binding to the designed bundle core

85 he buried cavity, as a dominant attribute of volatile anesthetic-binding sites found in a limited num

86 acid, Gly-819, is critical for the action of volatile anesthetics, but not of ethanol or pentobarbita

87 ajor recent findings examining mechanisms of volatile anesthetic cardioprotection.

88 hyperthermia (MH), a genetic sensitivity to volatile anesthetics, causes functional instability of t

89 A) is significantly quenched by halothane, a volatile anesthetic common in clinical practice.

90 Studies have shown that volatile anesthetics compete for luciferin binding to th

91 Median end-tidal volatile anesthetic concentration was significantly lowe

92 ctivation of raphe neuronal TASK channels by volatile anesthetics could play a role in their immobili

93 Volatile anesthetics did not attenuate glycocalyx sheddi

94 Other volatile anesthetics, diethyl ether and diisopropyl ethe

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

96 findings support therapeutic applications of volatile anesthetics during the intraoperative and posto

97 Sedation with volatile anesthetics during therapeutic hypothermia may

98 horylation function as a primary mediator of volatile anesthetic effect.

99 We determined volatile anesthetic effects on Na(+) currents mediated b

100 l anesthesia through intravenous delivery of volatile anesthetics, eliminating the need for the use o

101 ed from concentration-response curves of the volatile anesthetic enflurane constructed in the presenc

102 lation of GABAA and glycine receptors by the volatile anesthetic enflurane.

103 A(A) receptor subunits mediating alcohol and volatile anesthetic enhancement of receptor function.

104 gets for many general anesthetics, including volatile anesthetics, etomidate, propofol, and barbitura

105 the setting of triggering factors including volatile anesthetics, exercise, and high environmental t

106 A growing body of evidence indicates that volatile anesthetics exert protective effects against is

107 sedation, minimal alveolar concentration of volatile anesthetic, fatigue, active time, and respirato

108 tion in the gene gas-1 alters sensitivity to volatile anesthetics, fecundity, and life span in the ne

109 Volatile anesthetics, frequently administered in surgica

110 hat presents as a hypermetabolic response to volatile anesthetic gases, where susceptible persons may

111 ot associated with reduced administration of volatile anesthetic gases.

112 have previously shown that low levels of the volatile anesthetic halothane activate the Ca-ATPase in

113 The volatile anesthetic halothane directly activated a curre

114 ormed to investigate the partitioning of the volatile anesthetic halothane from an aqueous phase into

115 The addition of volatile anesthetic halothane to gA in SDS with a channe

116 was reduced by acid and was augmented by the volatile anesthetic halothane, which are all hallmarks o

117 e hydrophobic core is capable of binding the volatile anesthetic halothane.

118 has demonstrated that the halogenated alkane volatile anesthetics halothane and chloroform bind to th

119 tein, we investigated the interaction of the volatile anesthetic, halothane, with the Rho GDP dissoci

120 In this randomized study, we examined if volatile anesthetics have an effect on acute graft injur

121 Although immunomodulatory effects of volatile anesthetics have been growingly appreciated, th

122 Volatile anesthetics have been reported to provide prote

123 In addition, volatile anesthetics have been shown to accelerate posti

124 Volatile anesthetics have been shown to protect myocardi

125 Volatile anesthetics have been shown to reduce ischemic

126 ubiquitin metabolism in cellular response to volatile anesthetics: (i) mutations in the ZZZ1 gene ren

127 onditioning with isoflurane, a commonly used volatile anesthetic in clinical practice, reduces neuron

128 is study to determine whether the potency of volatile anesthetics in inducing neuropreconditioning is

129 indicates that certain general anesthetics, volatile anesthetics in particular, depress excitatory s

130 ed the role of ion channels/transporters and volatile anesthetics in the biofilm formation by E. faec

131 ctional pathway that controls sensitivity to volatile anesthetics in the nematode Caenorhabditis eleg

132 in the mechanisms of action of a variety of volatile anesthetics in yeast and that ubiquitin metabol

133 Volatile anesthetics including isoflurane affect all cel

134 Volatile anesthetics, including isoflurane, have anti-in

135 These compounds did not antagonize the volatile anesthetics, indicating some selectivity amongs

136 cent studies suggest that modern halogenated volatile anesthetics induce potent anti-inflammatory, an

137 All four volatile anesthetics induced a concentration-dependent p

138 dney function, briefly review the studies on volatile anesthetic-induced renal protection, and summar

139 These results suggest that ethanol and volatile anesthetics inhibit mGluR5 because they promote

140 Alcohols and volatile anesthetics inhibit peripheral nicotinic acetyl

141 s studies have demonstrated that ethanol and volatile anesthetics inhibit the function of some metabo

142 is glutamate, and recent studies found that volatile anesthetics inhibit the function of the alpha-a

143 New lines of evidence suggest that volatile anesthetics interact specifically with proteins

144 ated by identification of the low millimolar volatile anesthetic interaction site of the calcium sens

145 0 peptide in the single monolayers, with the volatile anesthetic introduced into the moist vapor envi

146 e preconditioning-induced neuroprotection by volatile anesthetics is not agent-specific.

147 ng of the preferential interactions given by volatile anesthetics is quite poor.

148 The mechanism of action of volatile anesthetics is unknown.

149 A brief exposure to the volatile anesthetic isoflurane (preconditioning) induces

150 In conclusion, the volatile anesthetic isoflurane and the intravenous anest

151 In septic mice, the commonly used volatile anesthetic isoflurane attenuated the production

152 We have demonstrated that the widely used volatile anesthetic isoflurane blocks the activation-dep

153 A prior exposure to the volatile anesthetic isoflurane has been shown to induce

154 R is highly susceptible to inhibition by the volatile anesthetic isoflurane in electrophysiology meas

155 The volatile anesthetic isoflurane is capable of inducing pr

156 Different from volatile anesthetic isoflurane, sevoflurane exposure sig

157 ypnotic, and anesthetic drugs, including the volatile anesthetic isoflurane.

158 er Saccharomyces cerevisiae resistant to the volatile anesthetic isoflurane.

159 Volatile anesthetics isoflurane and sevoflurane directly

160 Our reporter assay showed that volatile anesthetics isoflurane and sevoflurane increase

161 The binding sites of volatile anesthetics isoflurane and sevoflurane were loc

162 The volatile anesthetics isoflurane, sevoflurane and desflur

163 ngs to explore the actions of a prototypical volatile anesthetic, isoflurane (Iso), on recombinant hu

164 The volatile anesthetic, isoflurane, protected ACM from hypo

165 Volatile anesthetics like halothane and enflurane are of

166 It is conceivable that volatile anesthetics may contribute to postoperative cog

167 Volatile anesthetics may not inhibit this extracellular

168 herefore, the renal protective properties of volatile anesthetics may provide clinically useful thera

169 A molecular understanding of volatile anesthetic mechanisms of action will require st

170 This study examined volatile anesthetic-mediated protection against intestin

171 d summarize the basic cellular mechanisms of volatile anesthetic-mediated protection against ischemic

172 h alpha-1 and alpha-2 subunits, within which volatile anesthetics might bind.

173 mpared with the usual care group, the median volatile anesthetic minimum alveolar concentration was 0

174 Alcohols and volatile anesthetics modulate the function of cys-loop l

175 d for the electronic detection of archetypal volatile anesthetic molecules such as diethyl ether and

176 target of a large variety of agents such as volatile anesthetics, neuroprotective agents, and antide

177 ttributed to the differential sensitivity to volatile anesthetics of specific Na(v) subtypes preferen

178 l recordings were used to examine effects of volatile anesthetic on TASK currents in cortical neurons

179 e potential impact of an ion transporter and volatile anesthetic on this process.

180 ly improved for investigating the effects of volatile anesthetics on Ca(2+) binding characteristics o

181 sites of action for ethanol, inhalants, and volatile anesthetics on glycine receptors and illustrate

182 ing was antagonized by application of either volatile anesthetics or another GlyR modulator, zinc.

183 ate when carriers are exposed to halogenated volatile anesthetics or depolarizing muscle relaxants.

184 eletal muscle thermogenesis upon exposure to volatile anesthetics or heat.

185 de documentation, ventilator management, and volatile anesthetic overuse.

186 Volatile anesthetics, particularly the new generation of

187 We examined the hypothesis that opioids and volatile anesthetics potentiate cardiac K(ATP) channel o

188 The volatile anesthetic preconditioning-induced neuroprotect

189 Opioids and volatile anesthetics produce marked cardioprotective eff

190 millions of patients, the mechanism by which volatile anesthetics produce reversible loss of consciou

191 Volatile anesthetics provide myocardial preconditioning

192 age in the cortex, and postconditioning with volatile anesthetics provides neuroprotective actions th

193 toxic effects of several clinically utilized volatile anesthetics, recent studies suggest that modern

194 ergic agonist, produces sedation and reduces volatile anesthetic requirements.

195 ermia (MH), a pharmacogenetic sensitivity to volatile anesthetics resulting in massive intracellular

196 Across phylogeny, volatile anesthetics selectively inhibit mitochondrial c

197 putative chaperone proteins that can modify volatile anesthetic sensitivity and disrupt coordinated

198 nematode C. elegans for animals with altered volatile anesthetic sensitivity identified a mutant in a

199 stomatin-like protein deficiency as follows: volatile anesthetic sensitivity, uncoordinated locomotio

200 ndent oxidative phosphorylation capacity and volatile anesthetic sensitivity.

201 Volatile anesthetics serve as useful probes of a conserv

202 The volatile anesthetic sevoflurane is a common general anes

203 The volatile anesthetic sevoflurane reduces neutrophil apopt

204 Ethanol and the volatile anesthetics share many features including effec

205 Slices prepared using volatile anesthetics showed the same degree of damage du

206 Paradoxically, volatile anesthetics such as halothane inhibit these cha

207 Electrophysiology measurements suggest that volatile anesthetics such as isoflurane inhibit NaV by s

208 We demonstrated in the past that volatile anesthetics such as sevoflurane attenuate ische

209 yeast cells is inhibited by the five common volatile anesthetics tested (isoflurane, halothane, enfl

210 ains, zzz1 mutants are resistant to all five volatile anesthetics tested, suggesting there are simila

211 ntrations, female mice are more resistant to volatile anesthetics than males.

212 Isoflurane is a volatile anesthetic that has a vasodilating effect on ce

213 As a model of the protein targets for volatile anesthetics, the dimeric four-alpha-helix bundl

214 Despite the widespread clinical use of volatile anesthetics, their mechanisms of action remain

215 ulatory site or sites, and they suggest that volatile anesthetics, through perturbations at a single

216 is a dominantly inherited disorder in which volatile anesthetics trigger aberrant Ca(2+) release in

217 ons of a model membrane in the presence of a volatile anesthetic using a coarse-grain model.

218 To identify genes controlling volatile anesthetic (VA) action, we have screened throug

219 nding interactions were used to characterize volatile anesthetic (VA) binding sites and unoccupied po

220 assium channels are known to be modulated by volatile anesthetic (VA) drugs and play important roles

221 developed to study the direct effects of the volatile anesthetic (VA) halothane on the enzyme kinetic

222 or defining the molecular mechanisms whereby volatile anesthetics (VA) disrupt nervous system functio

223 Relaxation of intraparenchymal airways to volatile anesthetics varied by topographic location.

224 ate the character of the interaction between volatile anesthetics (VAs) and the plasma membrane Ca2+-

225 Volatile anesthetics (VAs) are widely used in medicine,

226 Volatile anesthetics (VAs) cause profound neurological e

227 Volatile anesthetics (VAs) disrupt nervous system functi

228 Xenopus oocytes to determine the effects of volatile anesthetics (VAs) on currents through each spec

229 The mechanisms by which volatile anesthetics (VAs) produce their effects (loss o

230 by their distinctive inhibitory response to volatile anesthetics (VAs), molecular details governing

231 Volatile anesthetics (VAs), such as isoflurane, induce a

232 xide (N(2)O, also known as laughing gas) and volatile anesthetics (VAs), the original and still most

233 To identify sites of action of volatile anesthetics, we are studying genes in a functio

234 To investigate the mechanism of action of volatile anesthetics, we are studying mutants of the yea

235 The volatile anesthetics were introduced into a preassembled

236 fied mechanism shared by the interactions of volatile anesthetics with targets in the CNS.

237 Interactions of volatile anesthetics with the central nervous system are

238 is the first demonstration that opioids and volatile anesthetics work in conjunction to confer prote

239 Not only will understanding how volatile anesthetics work yield better and safer anesthe