ライフサイエンスコーパス: isoflurane

1 eling using photoactivatable isoflurane (azi-isoflurane).

2 so required for activation by chloroform and isoflurane.

3 activity and general anesthetic state under isoflurane.

4 e commonly used volatile general anesthetic, isoflurane.

5 intain incubation and allow anesthesia using isoflurane.

6 of equianesthetic doses of pentobarbital or isoflurane.

7 hage-vehicle, and subarachnoid hemorrhage+2% isoflurane.

8 -sleep-active VLPO neurons are unaffected by isoflurane.

9 the magnitude of this cell death response to isoflurane.

10 in age from P14 to P206 were sedated with 1% isoflurane.

11 ted hemi-parkinsonian rats anesthetized with isoflurane.

12 esence and absence of the general anesthetic isoflurane.

13 raining over 2.5 weeks while anesthetized by isoflurane.

14 e are 10 and 25 times, respectively, that of isoflurane.

15 trations of volatile anaesthetics, including isoflurane.

16 commercially acquired and anaesthetised with isoflurane.

17 seleit solution, with or without propofol or isoflurane.

18 : after 1 hr of propofol discontinuation and isoflurane 0.8%; step 3: after 1 hr of propofol at the s

19 f deep pharmacologically-induced coma (PIC): isoflurane (1.25%-1.5%) and induced hypoglycemic coma.

20 orce from low doses (propofol, 27 +/- 6 muM; isoflurane, 1.0 +/- 0.1%) to moderate doses (propofol, 8

21 order efficacy: halothane (207% [202-212]) > isoflurane (169% [161-176]) > sevoflurane (164% [150-177

22 ) to moderate doses (propofol, 87 +/- 4 muM; isoflurane, 3.0 +/- 0.25%), without significant alterati

23 at had training sessions and were exposed to isoflurane 30 min later had freezing behavior similar to

24 Isoflurane (300 mum) significantly inhibited, while fent

25 ng combinations: Isoflurane (5%)+O(2) (95%); Isoflurane (5%)+N(2)O (75%)+O(2) (25%) and N(2)O (75%)+O

26 er protocol with the following combinations: Isoflurane (5%)+O(2) (95%); Isoflurane (5%)+N(2)O (75%)+

27 rats were randomly assigned to receive 1.8% isoflurane/70% nitrous oxide (N(2)O) anesthesia for 4h o

28 Here, we examined the effects of isoflurane, a commonly-used general anesthetic, which wa

29 resumption of consciousness associated with isoflurane, a potent halogenated ether in common clinica

30 Isoflurane, a volatile anesthetic agent, has been recogn

31 dies show that general anesthetics including isoflurane activate VLPO neurons, and may contribute to

32 how that inhaled anesthetics (chloroform and isoflurane) activate TREK-1 through disruption of phosph

33 Whole cell recordings revealed that the isoflurane-activated background potassium current observ

34 ngle-cell multiplex RT-PCR conducted on both isoflurane-activated, putative sleep-promoting VLPO neur

35 -159, and similar results were observed with isoflurane activation of wild-type TASK-3.

36 Moreover, isoflurane affected neuronal plasticity by facilitating

37 d when paraoxon-treated rats were exposed to isoflurane after SE.

38 ated structural and dynamical modulations by isoflurane aid in the understanding of the underlying me

39 Isoflurane also entered the channel after the pore was d

40 Isoflurane also impaired the cognitive functions of 10-w

41 Isoflurane also increased firing rate of RTN chemosensit

42 Isoflurane also induced autophagy in mouse in vivo as sh

43 anti-epileptogenic interventions were used; isoflurane anaesthesia and losartan.

44 Early treatments with either isoflurane anaesthesia or losartan prevented early micro

45 emale animals and appeared to be enhanced by isoflurane anaesthesia.

46 mically-defined midbrain dopamine neurons in isoflurane-anaesthetized adult mice.

47 re also calculated, and shown to be 3 mM for isoflurane and 10 muM for propofol; both anesthetics hav

48 Rats were anesthetized with 1.5% isoflurane and 95% oxygen.

49 The urodynamic parameters under isoflurane and alpha-chloralose were also examined in te

50 e therefore set out to assess the effects of isoflurane and desflurane on mitochondrial function, cyt

51 hways are critical in the TCR, and ketamine, isoflurane and fentanyl differentially alter the synapti

52 amines the mechanisms of action of ketamine, isoflurane and fentanyl on the synaptic TCR responses in

53 r antecedent neuronal activity, we show that isoflurane and halothane increase the number of active n

54 rectly depolarized by the general anesthetic isoflurane and hyperpolarized by norepinephrine, a wake-

55 In primary mouse cortical neurons, both isoflurane and hypoxic preconditioning induced autophagy

56 Isoflurane and hypoxic preconditioning protected against

57 plore the role of SPK2-mediated autophagy in isoflurane and hypoxic preconditioning.

58 e anesthetized the rats with dexmedetomidine/isoflurane and infused paramagnetic contrast (Gd-DOTA) i

59 One month later mice were anaesthetized with isoflurane and isometric force-producing capacity was re

60 rysanthemi, can be functionally inhibited by isoflurane and other anesthetics.

61 These results indicate that isoflurane and propofol anesthesia affect postnatal hipp

62 Isoflurane and propofol anesthesia altered postnatal hip

63 Isoflurane and propofol are known to depress cardiac con

64 urthermore, molecular modeling predicts that isoflurane and propofol bind to this pocket by forming H

65 block inhibition by the general anesthetics isoflurane and propofol of the prokaryotic pentameric ch

66 s hypothesis, we investigated the effects of isoflurane and propofol on new cell proliferation and co

67 Affinities of isoflurane and propofol to the allosteric site are also

68 both single and double occupancy binding of isoflurane and propofol to the GLIC pore.

69 Met-956 selectively abolishes activation by isoflurane and propofol without affecting actions of A-9

70 ction and uncovered the molecular targets of isoflurane and propofol.

71 t are critical for the inhibitory effects of isoflurane and propofol.

72 ics and rigid docking simulation showed that isoflurane and sevoflurane bound to both TLR9 dimer inte

73 Volatile anesthetics isoflurane and sevoflurane directly target and attenuate

74 orter assay showed that volatile anesthetics isoflurane and sevoflurane increased the activation of T

75 The binding sites of volatile anesthetics isoflurane and sevoflurane were located near critical re

76 59W, V136E, and L122D were resistant to both isoflurane and TCE activation.

77 Isoflurane and TCE likely share commonalities in their m

78 ether we induced anesthesia with urethane or isoflurane and whether awake mice were stationary or run

79 on using an anesthetic conserving device and isoflurane, and 322 received standard IV sedation.

80 eterologous expression systems, sevoflurane, isoflurane, and desflurane at subsurgical concentrations

81 er anesthetic for AD patients as compared to isoflurane, and elucidate the potential mitochondria-ass

82 We also showed that the general anesthetic isoflurane, and to a lesser extent propofol, reverses TX

83 , insulin and glucose (6 mU/g, 1 mg/g) under isoflurane, and under ketamine-xylazine anesthesia to su

84 nder isoflurane, ketamine/xylazine, ketamine/isoflurane, and urethane anesthesia demonstrated that th

85 anesthetic combinations (ketamine/xylazine, isoflurane, and urethane) markedly suppressed calcium tr

86 a and a more pronounced ability to exit both isoflurane- and sevoflurane-induced unconscious states.

87 urons stabilizes the wake state against both isoflurane- and sevoflurane-induced unconsciousness.

88 to determine the effects of laparotomy under isoflurane anesthesia (Anesthesia/Surgery) on these beha

89 rhesus macaques were exposed for 5 hours to isoflurane anesthesia according to current clinical stan

90 ice display a partial resistance to entering isoflurane anesthesia and a more pronounced ability to e

91 lly, hypoactive shifts in neuronal activity (isoflurane anesthesia and CaMKIIa Gi DREADD activation)

92 measure baseline sleep loss and responses to isoflurane anesthesia at 1% and 2%.

93 the hippocampus after a clinically relevant isoflurane anesthesia exposure conducted at an early pos

94 A brief burst-suppressing isoflurane anesthesia has been shown to rapidly alleviat

95 trained state and demonstrate the effects of isoflurane anesthesia on radiotracer uptake.

96 Isoflurane anesthesia produced learning impairment in ag

97 We show that a single isoflurane anesthesia produces antidepressant-like behav

98 Optical imaging experiments in mice under isoflurane anesthesia showed that both cortical spreadin

99 Sprague-Dawley rats under isoflurane anesthesia were exposed to a series of 3 sub-

100 Awake tissue Po2 is about half that under isoflurane anesthesia, and within the cortex, vascular a

101 Under isoflurane anesthesia, the mice were subjected to intest

102 In resting newborn piglets (n=6) on isoflurane anesthesia, we measured a median total cerebr

103 raphy (EEG) activation under continuous deep isoflurane anesthesia.

104 Five rhesus macaques were tested under isoflurane anesthesia.

105 f age and C57BL/6 age-matched controls under isoflurane anesthesia.

106 VLPO neurons themselves is not required for isoflurane anesthesia.

107 und that GABA-mediated tone decreases during isoflurane anesthesia.

108 2), after sino-aortic denervation, or during isoflurane anesthesia.

109 o accelerated behavioral emergence from deep isoflurane anesthesia; this was prevented with beta or a

110 fentanyl-fluanisone/midazolam) and volatile (isoflurane) anesthetics in mice.

111 Isoflurane anesthetized and intubated pigs were randomiz

112 hysiologically defined slow calcium waves in isoflurane anesthetized rats.

113 rophenol (DNP) were compared using 16.4 T in isoflurane anesthetized wild type (WT) and HD mice at 9

114 re scanned under the awake (n = 6 scans) and isoflurane-anesthetized (n = 4 scans) conditions.

115 Isoflurane-anesthetized adult male wild-type C57B/6 or a

116 Dynamic PET was performed for 60 min on 23 isoflurane-anesthetized male C57BL/6 mice after intraven

117 In isoflurane-anesthetized male rats, trigeminal ganglia we

118 lly microinjected into the DMH/PeF region of isoflurane-anesthetized male Sprague-Dawley rats (n = 19

119 binding potential (BPND) would be higher in isoflurane-anesthetized monkeys.

120 mins of untreated ventricular fibrillation, isoflurane-anesthetized pigs received 5 mins of either s

121 In protocol A, 24 isoflurane-anesthetized pigs underwent 15 mins of untrea

122 bon fibers in the cervical vagus nerve of 22 isoflurane-anesthetized rats.

123 Preclinical PET studies were performed with isoflurane-anesthetized rats.

124 the ventro-postero-lateral (VPL) nucleus in isoflurane-anesthetized rats.

125 blood sampling were obtained for 4 groups of isoflurane-anesthetized Wistar rats: controls (n = 7); p

126 ects on leak channels; a similar anesthetic, isoflurane, appears to work a different way.

127 the observation that the synaptic targets of isoflurane are located in local cortical circuits rather

128 esponses and encourage further evaluation of isoflurane as a rapid-acting antidepressant devoid of th

129 than wild-type (WT) mice, while the percent isoflurane at which hypnosis and immobility occurred was

130 At 24 hrs, isoflurane attenuated neuronal cell death in the cortex,

131 mice, the commonly used volatile anesthetic isoflurane attenuated the production of 5-lipoxygenase p

132 teins with meta-Azi-propofol (AziPm) and Azi-isoflurane (Azi-iso) and molecular docking were also use

133 obed by photolabeling using photoactivatable isoflurane (azi-isoflurane).

134 tudies prove that the neurons depolarized by isoflurane belong to the subpopulation of VLPO neurons r

135 onsistent with their functional responses to isoflurane, beta2 but not alpha7 showed pronounced dynam

136 Isoflurane binding introduced strong anticorrelated moti

137 Mutagenesis of the alpha'1 helix showed that isoflurane binding sites at the betaI domain were signif

138 studies suggested the existence of multiple isoflurane binding sites in NaV, but experimental bindin

139 An extensive search for isoflurane binding sites in the nicotinic acetylcholine

140 Isoflurane binding sites on the full ectodomain LFA-1 we

141 Two isoflurane binding sites were identified using photolabe

142 Point mutations were introduced around isoflurane binding sites.

143 osteric to the ICAM-1 binding site, and that isoflurane binding stabilizes LFA-1 in the closed confor

144 (19)F probes in NMR experiments to quantify isoflurane binding to the bacterial voltage-gated sodium

145 olecular dynamics simulations suggested that isoflurane binding was more stable in the resting than i

146 the extracellular entrance was observed upon isoflurane binding.

147 Isoflurane-binding sites in beta2 and alpha7 were found

148 modulate etomidate binding to the GABA(A)R: isoflurane binds directly to the site with millimolar af

149 This study suggested that isoflurane binds to both the alphaI and betaI domains al

150 Isoflurane bound to several locations within GLIC, inclu

151 An orientation preference was observed for isoflurane bound to T189 and S208, but not to S129 and L

152 The inhalation anesthetic isoflurane, but not desflurane, has been shown to induce

153 Here we show that isoflurane, but not desflurane, induces opening of mitoc

154 animals to the general anesthetic effects of isoflurane, but that the sedation produced by VLPO neuro

155 Isoflurane can impair cognitive functions of animals und

156 Furthermore, we find that isoflurane causes a sustained increase in activity in th

157 e have also observed (unpublished data) that isoflurane causes apoptosis of cellular profiles in the

158 Here, we show that isoflurane causes robust activation of CO(2)/pH-sensitiv

159 ues in the S5, S6, and the first pore helix; isoflurane competitively disrupts A-967079 antagonism, a

160 Isoflurane concentrations that anesthetize only Ndufs4(K

161 20-month-old) rats prior to a 3h exposure to isoflurane, control, propofol, or 10% intralipid.

162 store righting or produce EEG changes during isoflurane CSSGA in 5/5 mice.

163 Thus, propofol and isoflurane decrease force development by directly depres

164 ntact and skinned preparations, propofol and isoflurane depressed maximum Ca(2+)-activated force and

165 In contrast, several volatile (isoflurane, desflurane) and i.v. (propofol) general anes

166 opofol, ketamine, inhalational anaesthetics (isoflurane, desflurane), antiepileptic drugs (topiramate

167 n-response of TASK-3 to several anesthetics (isoflurane, desflurane, sevoflurane, halothane, alpha-ch

168 he VLPO of a mouse lightly anesthetized with isoflurane, dexmedetomidine increased behavioral arousal

169 However, isoflurane did not affect the cognitive functions of IL-

170 General anesthetics, such as chloroform, isoflurane, diethyl ether, xenon, and propofol, disrupt

171 Brains exposed to isoflurane displayed significant apoptosis in both the w

172 Isoflurane disrupted the quaternary structure of GLIC, a

173 We conclude that isoflurane disrupts the development of hippocampal neuro

174 Both propofol and isoflurane dose dependently depressed force from low dos

175 ence time (r=0.54); an interaction-effect of isoflurane dose was observed (burst-suppression ratio: p

176 This isoflurane effect was attenuated by lidocaine, a local a

177 IL-1beta may play an important role in this isoflurane effect.

178 We measured isoflurane effects on time to loss of righting reflex, o

179 Isoflurane-exposed rats had reduced freezing behavior du

180 Isoflurane exposure after IRI led to significant attenua

181 Finally, isoflurane exposure led to increased TGF-beta1 levels in

182 ial learning and memory that are impaired by isoflurane exposure.

183 with non-injurious hypoxia or the anesthetic isoflurane express different genes but are equally prote

184 ated by exposing the neuronal cultures to 2% isoflurane for 1h at various times after the onset of th

185 10-week old mice were exposed to 1.2 or 1.4% isoflurane for 2 h.

186 posure of the infant rhesus macaque brain to isoflurane for 5 hours is sufficient to cause widespread

187 xposure of 6-day-old (P6) rhesus macaques to isoflurane for 5 hours triggers a robust neuroapoptosis

188 smission alone can affect the emergence from isoflurane general anesthesia.

189 We aimed to determine whether isoflurane, given after intestinal ischemia, protects ag

190 Volatile anesthetics, including isoflurane, have anti-inflammatory effects.

191 We conclude that combined isoflurane-hypoxia preconditioning augments neuroprotect

192 Our studies showed that isoflurane impaired the cognitive functions of the rats

193 Our results suggest that isoflurane impairs the learning but may not affect the r

194 strong decreases in the source entropy under isoflurane in area V1 and the prefrontal cortex (PFC)-as

195 tials in two ferrets after administration of isoflurane in concentrations of 0.0%, 0.5%, and 1.0%.

196 ble to inhibition by the volatile anesthetic isoflurane in electrophysiology measurements.

197 atory neurotransmission is hypersensitive to isoflurane in Ndufs4(KO) mice due to the inhibition of p

198 ation with propofol and during sedation with isoflurane in patients with severe subarachnoid hemorrha

199 Here, we induced burst suppression with isoflurane in rodents and then created a neocortical acu

200 reversed the VLPO depolarization induced by isoflurane in slices in vitro.

201 Structures of ELIC co-crystallized with isoflurane in the absence or presence of an agonist reve

202 side are disconnected, we observe binding of isoflurane in the central cavity.

203 We also found that isoflurane increased activity of the parvalbumin interne

204 Both propofol and isoflurane increased autophagy induction (P < 0.05) in a

205 Isoflurane increased the expression of interleukin 1beta

206 Isoflurane increases regional cerebral blood flow in com

207 sitive RTN neurons was strongly increased by isoflurane, independent of prevailing pH conditions.

208 Nitrous oxide together with isoflurane induced a statistically significant decrease

209 Discrete photostimulations under isoflurane-induced anesthesia from an optical probe posi

210 ("shaker") channels: reduced sensitivity to isoflurane-induced anesthesia.

211 Isoflurane-induced autophagy in mice lacking the SPK1 is

212 ced autophagy, and SPK2 inhibitors abolished isoflurane-induced disruption of the Beclin 1/Bcl-2 asso

213 Isoflurane-induced hypnosis following injections of TTA-

214 VLPO neurons produces an acute resistance to isoflurane-induced hypnosis.

215 ine A, a blocker of mPTP opening, attenuates isoflurane-induced mPTP opening, caspase 3 activation, a

216 be additive to the potential consequences of isoflurane-induced neuroapoptosis.

217 urthermore, we found that TTA-P2 facilitated isoflurane induction of hypnosis in the Ca(V)3.3 KO mice

218 ts suggest that volatile anesthetics such as isoflurane inhibit NaV by stabilizing the inactivated st

219 ed inhaled anesthetics such as halothane and isoflurane inhibit the archetypical voltage-gated Kv3 ch

220 Anaesthesia (inhaled isoflurane) inhibited the cardiac reflexes evoked by inh

221 istent with allosteric interactions, whereas isoflurane inhibition was nearly complete, apparently co

222 dence for a direct pore-binding mechanism of isoflurane inhibition, which has a general implication f

223 e notion that binding at these sites renders isoflurane inhibition.

224 We conclude that isoflurane inhibits NaChBac by two distinct mechanisms:

225 However, it remains to be determined how isoflurane interacts with the full ectodomain LFA-1 and

226 Isoflurane is a volatile anesthetic that has a vasodilat

227 Given that isoflurane is a widely used volatile anesthetic, and is

228 Immobility induced by another VA, isoflurane, is not affected by these treatments, thereby

229 he halogenated ethers sevoflurane (SEVO) and isoflurane (ISO), using UV-Vis spectroscopy, time depend

230 e pups to a prototypical general anesthetic, isoflurane (ISO, 1.5% for 3 hr), at three early postnata

231 MRI recordings under isoflurane, ketamine/xylazine, ketamine/isoflurane, and

232 Finally, isoflurane may induce the opening of mPTP via increasing

233 hippocampus and cortex of rats treated with isoflurane/ N(2)O anesthesia at 18-months-old, leading t

234 igs in each experimental group): thiopental, isoflurane, nitrous oxide and isoflurane plus nitrous ox

235 ce or presence of an agonist revealed double isoflurane occupancies inside the pore near T237(6') and

236 rousal and reduced the depressant effects of isoflurane on barrel cortex somatosensory-evoked potenti

237 assess the effects of chloroform or the VGA isoflurane on TRP channel activation.

238 fects of the most common general anesthetic, isoflurane, on time perception and the circadian clock u

239 did not induce behavioral hyperactivity and isoflurane only caused behavioral hyperactivity with bor

240 dazolam and barbiturates have failed, use of isoflurane or ketamine anesthesia has been tried at a me

241 Here, we demonstrate that isoflurane or propofol anesthesia decreases hippocampal

242 Isoflurane or propofol did not affect new cell prolifera

243 Furthermore, isoflurane or propofol may prevent or reverse TXA-induce

244 99% expression of InsP3R-1 were treated with isoflurane or propofol.

245 Isoflurane or sevoflurane administered after the ischemi

246 ng IV propofol (n = 74) or inhaled volatile (isoflurane or sevoflurane) anesthetic agent (n = 67).

247 Ten-day-old mice received 2% sevoflurane, 1% isoflurane, or 6% desflurane for 10 minutes.

248 We found that exposure to either isoflurane (p=0.017) or propofol (p=0.006) decreased hip

249 ): thiopental, isoflurane, nitrous oxide and isoflurane plus nitrous oxide.

250 Our findings demonstrate that isoflurane post-conditioning protects against small inte

251 not better than NMDA receptor inhibition or isoflurane postconditioning alone for neuroprotection.

252 r activation, isoflurane preconditioning, or isoflurane postconditioning alone.

253 on with either isoflurane preconditioning or isoflurane postconditioning induced a better neuroprotec

254 Isoflurane preconditioning and isoflurane postconditioning may involve CaMKII inhibitio

255 combination of NMDA receptor inhibition and isoflurane postconditioning was not better than NMDA rec

256 fter the onset of the simulated reperfusion (isoflurane postconditioning).

257 Isoflurane posttreatment delays the development of posts

258 We examined whether isoflurane posttreatment is protective against early bra

259 tive effect than NMDA receptor inhibition or isoflurane preconditioning alone.

260 Isoflurane preconditioning and isoflurane postconditioni

261 The combination of isoflurane preconditioning and postconditioning induced

262 ongly indicate that autophagy is involved in isoflurane preconditioning both in vivo and in vitro and

263 combination of NMDA receptor inhibition and isoflurane preconditioning caused a better neuroprotecti

264 denosine A2A receptor activation with either isoflurane preconditioning or isoflurane postconditionin

265 fect than adenosine A2A receptor activation, isoflurane preconditioning, or isoflurane postconditioni

266 e Sprague-Dawley rats were anesthetized with isoflurane, prepared for parasagittal fluid percussion i

267 Moreover, in the latter model, isoflurane prevented BBB dysfunction and neurodegenerati

268 steady-state general anesthesia (CSSGA) with isoflurane produced behavioral and EEG evidence of arous

269 B dysfunction and neurodegeneration, whereas isoflurane reduced neuroinflammation in the kainate mode

270 The addition of N(2)O to isoflurane reduced the time to loss of the righting refl

271 The significance of isoflurane's effect was assessed in both intracellular a

272 ld affect the onset, depth, or recovery from isoflurane's general anesthetic effects.

273 e 1 phosphate receptor inhibitor VPC23019 on isoflurane's protective action against postsubarachnoid

274 Isoflurane sedation was changed to midazolam in two nons

275 Isoflurane sedation with the AnaConDa during 24 hours th

276 Thus, changes in information transfer under isoflurane seem to be a consequence of changes in local

277 Different from volatile anesthetic isoflurane, sevoflurane exposure significantly improved

278 on the uptake of the inhalation anesthetics isoflurane, sevoflurane, and desflurane when used in rou

279 Isoflurane significantly decreased the number of maturin

280 Isoflurane significantly improved neurobehavioral functi

281 In the absence of isoflurane, spontaneous recurrent seizures were common i

282 tivation-sensitive antibodies suggested that isoflurane stabilized LFA-1 in the closed conformation.

283 n mouse brain in the awake and anesthetized (isoflurane) states.

284 We previously demonstrated that isoflurane targets lymphocyte function-associated antige

285 we utilize a photoaffinity analog of the VA isoflurane to identify a VA-binding site in the TREK1 K2

286 In these animals, isoflurane transiently enhanced activity of the respirat

287 nerated in the forebrain white matter of the isoflurane-treated group was 6.3% of the total populatio

288 Similarly, the inhaled anesthetic isoflurane triggered a persistent increase in tonic curr

289 When isoflurane was administered during kainate injection, du

290 Isoflurane was either administered during (kainate) or a

291 eneral anesthetics (etomidate, propofol, and isoflurane) was greater at negative membrane potentials.

292 The beneficial effects of isoflurane were abolished by N, N-dimethylsphingosine an

293 Furthermore, the protective effects of isoflurane were abolished by treatment with a TGF-beta1

294 Rats anesthetized with isoflurane were given intravenous infusions (9 mL/kg ove

295 The effects of isoflurane were investigated in two rat models of SE-ind

296 The effects of isoflurane were similar on evoked field excitatory posts

297 gnificantly shorter in patients sedated with isoflurane when compared with IV sedation although no di

298 re, it has been shown in animal studies that isoflurane, when used as a preconditioning agent, has ne

299 We report novel preclinical findings with isoflurane, which exerts various nonanesthetic effects t

300 spectroscopy showed a strong interaction of isoflurane with S129, T189, and S208; relatively weakly