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

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

5 etic evidence points to multiple targets for volatile anesthetics.

6 t display abnormalities in their response to volatile anesthetics.

7 pharmacological antagonism of the effects of volatile anesthetics.

8 s for clinically important compounds such as volatile anesthetics.

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

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

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

12 complexes may represent a general target for volatile anesthetics.

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

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

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

16 ique effects on sensitivity to the different volatile anesthetics.

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

18 oute to avoiding emetogenic and hyperalgesic volatile anesthetics.

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

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

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

22 cated in functional tolerance to alcohol and volatile anesthetics.

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

24 ) with designed specific binding pockets for volatile anesthetics.

25 o the induction of preconditioning effect by volatile anesthetics.

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

27 also for etomidate and other intravenous and volatile anesthetics.

28 ermia, a pharmacogenetic crisis triggered by volatile anesthetics.

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

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

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

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

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

34 Volatile anesthetics affect all cells and tissues tested

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

36 Volatile anesthetic agent use in the intensive care unit

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

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

39 Three other volatile anesthetic agents show a similar pattern.

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

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

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

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

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

45 Volatile anesthetics alter tissue excitability by decrea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Volatile anesthetics appear to suppress effector functio

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

66 Volatile anesthetics are commonly used during surgery.

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

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

69 Administration of volatile anesthetics before prolonged coronary artery oc

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

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

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

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

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

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

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

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

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

79 ajor recent findings examining mechanisms of volatile anesthetic cardioprotection.

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

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

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

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

84 Volatile anesthetics did not attenuate glycocalyx sheddi

85 Other volatile anesthetics, diethyl ether and diisopropyl ethe

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

87 Sedation with volatile anesthetics during therapeutic hypothermia may

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

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

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

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

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

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

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

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

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

97 ot associated with reduced administration of volatile anesthetic gases.

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

99 The volatile anesthetic halothane directly activated a curre

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

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

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

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

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

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

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

107 Volatile anesthetics have been reported to provide prote

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

109 Volatile anesthetics have been shown to protect myocardi

110 Volatile anesthetics have been shown to reduce ischemic

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

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

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

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

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

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

117 Volatile anesthetics including isoflurane affect all cel

118 Volatile anesthetics, including isoflurane, have anti-in

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

120 All four volatile anesthetics induced a concentration-dependent p

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

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

123 Alcohols and volatile anesthetics inhibit peripheral nicotinic acetyl

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

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

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

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

128 0 peptide in the single monolayers, with the volatile anesthetic introduced into the moist vapor envi

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

130 The mechanism of action of volatile anesthetics is unknown.

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

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

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

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

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

136 The volatile anesthetic isoflurane is capable of inducing pr

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

138 er Saccharomyces cerevisiae resistant to the volatile anesthetic isoflurane.

139 The volatile anesthetics isoflurane, sevoflurane and desflur

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

141 The volatile anesthetic, isoflurane, protected ACM from hypo

142 Volatile anesthetics like halothane and enflurane are of

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

144 Volatile anesthetics may not inhibit this extracellular

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

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

147 This study examined volatile anesthetic-mediated protection against intestin

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

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

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

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

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

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

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

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

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

157 Volatile anesthetics, particularly the new generation of

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

159 The volatile anesthetic preconditioning-induced neuroprotect

160 Opioids and volatile anesthetics produce marked cardioprotective eff

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

162 Volatile anesthetics provide myocardial preconditioning

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

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

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

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

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

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

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

170 ndent oxidative phosphorylation capacity and volatile anesthetic sensitivity.

171 Volatile anesthetics serve as useful probes of a conserv

172 Ethanol and the volatile anesthetics share many features including effec

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

174 Paradoxically, volatile anesthetics such as halothane inhibit these cha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 Volatile anesthetics (VAs) cause profound neurological e

192 Volatile anesthetics (VAs) disrupt nervous system functi

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

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

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

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

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

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

199 The volatile anesthetics were introduced into a preassembled

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

201 Interactions of volatile anesthetics with the central nervous system are

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

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