ライフサイエンスコーパス: anaesthetic

1 expulsion without the need for a surgeon or anaesthetic.

2 vagus nerve by topical application of local anaesthetic.

3 the prolongation of mIPSCs produced by this anaesthetic.

4 viours and fish should not seek to avoid the anaesthetic.

5 anorectal physiology, and examination under anaesthetic.

6 the treatment of varicose veins under local anaesthetic.

7 y invasive varicose vein surgery under local anaesthetic.

8 ective even when patients were under general anaesthetic.

9 dergo multiparametric MRI and have a general anaesthetic.

10 ients do not respond to treatment with local anaesthetics.

11 clear clinical advantages over other current anaesthetics.

12 he pH-sensitive current was blocked by local anaesthetics.

13 ribute to some important clinical effects of anaesthetics.

14 s, gastrointestinal hormone disruptions, and anaesthetics.

15 sitivity of the RYR to caffeine and volatile anaesthetics.

16 on dependent, but comparable between the two anaesthetics.

17 A receptors by structurally distinct general anaesthetics.

18 echanism of action of general (inhalational) anaesthetics.

19 ting of specific hypotheses of the action of anaesthetics.

20 linically relevant concentrations of inhaled anaesthetics.

21 ycine receptors by alcohols and two volatile anaesthetics.

22 individual variability in susceptibility to anaesthetics.

23 66-0.93; p=0.005), and spinal versus general anaesthetic (0.85, 0.74-0.97; p=0.019).

24 The anaesthetic 2,6-diisopropylphenol (propofol, 3 microM) a

25 xposure to intraluminal application of local anaesthetic (2 % Xylocaine).

26 enges to antibiotics [40/44 (91%]) and local anaesthetics [41/44 (93%)].

27 rate of any maternal death was 9.8 per 1000 anaesthetics (5.2-15.7, I(2)=92%) when managed by non-ph

28 All three anaesthetics accelerated the rate of re-entrant excitati

29 and neurophysiological analyses of volatile anaesthetic action in Drosophila, and suggest candidate

30 The mechanism of general anaesthetic action is only partially understood.

31 echanistic basis for the genetic analysis of anaesthetic action, by analysing the neurophysiological

32 These data suggest that anaesthetic actions resulting from effects on either TAS

33 The discovery that anaesthetics affect a recently identified family of pota

34 Preclinical data suggest that general anaesthetics affect brain development.

35 A modified technique for estimating local anaesthetic affinity of inactivated channels was develop

36 s available to facilitate a humane choice of anaesthetic agent for fish despite over 100 years of use

37 No one anaesthetic agent has emerged as best.

38 Propofol is primarily an anaesthetic agent, but its use in a sedative capacity ha

39 aesthesia with halothane and the alternative anaesthetic agent, sevoflurane.

40 anxiolytics, antidepressants, beta-blockers, anaesthetic agents and analgesics; length of sedation an

41 ity in a large series involving a variety of anaesthetic agents and techniques.

42 The approach of early escalation to anaesthetic agents for refractory generalised convulsive

43 respiratory dysfunction, differences between anaesthetic agents have emerged in systemic inflammation

44 that the sensitivity of GABA(A) receptors to anaesthetic agents is heterogeneous, the structural basi

45 A common feature of general anaesthetic agents is their ability to potentiate neuron

46 nts confirm the above and also indicate that anaesthetic agents may offer some protection against the

47 tudy was to evaluate the impact of different anaesthetic agents on EGG in experimental pigs.

48 First, the cerebrovascular effects of anaesthetic agents used for neurological surgery are con

49 equipment, safer and more easily titratable anaesthetic agents, and possibly the practice of subspec

50 llowing treatments was critically evaluated: anaesthetic agents, anti-epileptic drugs, magnesium infu

51 the laboratory, exposed to three widely used anaesthetic agents.

52 ensitivities to CO(2), lung inflation and/or anaesthetic agents.

53 y to the potentiating effects of intravenous anaesthetic agents.

54 demonstrated for the potentiating effects of anaesthetic agents.

55 ticity and cell death, and responsiveness to anaesthetic agents.

56 bunits are required for direct activation by anaesthetics alone, and only one anaesthetic-sensitive s

57 Recent evidence suggests that anaesthetics also inhibit excitatory synaptic transmissi

58 n, focusing on three topics: choice of local anaesthetic and adjunct drugs, technical aspects and com

59 xide (N2O, laughing gas) has been used as an anaesthetic and analgesic for almost two centuries, but

60 ction in the radiology suite with obstetric, anaesthetic and neonatal teams in attendance.

61 e use of specialized assistants to undertake anaesthetic and peri-anaesthetic tasks.

62 odulate the inflammatory response, surgical, anaesthetic and pharmacological, may enhance recovery wi

63 glycine receptors is enhanced by a number of anaesthetics and alcohols, whereas activity of the relat

64 r basis for modulation of these receptors by anaesthetics and alcohols.

65 While several anaesthetics and analgesics have been reported to alter

66 Local anaesthetics and anti-epileptic drugs can suppress hyper

67 ls on exposure to commonly used inhalational anaesthetics and depolarising muscle relaxants.

68 membrane stretch, arachidonic acid, volatile anaesthetics and heat.

69 the idea that TREK-1 is a target for general anaesthetics and neuroprotectants.

70 refractory status epilepticus), a variety of anaesthetics and nonpharmacological therapies can be adm

71 eptors that are contrastingly insensitive to anaesthetics and respond partially to several full GABA

72 Sodium channels bind local anaesthetics and various toxins.

73 erns about the neurotoxic potential of local anaesthetics and, in particular, of lignocaine.

74 ible phenomena observed in higher organisms, anaesthetics antagonize high-pressure signalling mediate

75 uch as antioxidant, anti-inflammatory, local anaesthetic, antinociceptive, cicatrizing, antiseptic, a

76 e subcortical nucleus, energetic response to anaesthetics appears to be affected by changes in both c

77 ensitive, and its ability to be activated by anaesthetics, arachidonic acid and internal acidosis rem

78 this may be that the mechanisms of action of anaesthetics are not fully understood.

79 homomeric HCN1 channels is mediated through anaesthetic association with the membrane embedded chann

80 Both anaesthetics at each concentration also shifted the rela

81 ceptors (GABAA Rs) by photolabelling with an anaesthetic barbiturate.

82 The method involves application of the anaesthetic benzocaine and intubation to maintain ventil

83 We found that the anaesthetic benzocaine at 50 mg l(-1) was an effective a

84 mutation (N395K) that lies within the local anaesthetic binding site of the channel.

85 signal transduction or as a component of an anaesthetic binding site per se is discussed.

86 a mutation (F216S), not located in the local anaesthetic binding site, had no effect on lidocaine inh

87 ping to fatigue before and after acute local anaesthetic block of the sympathetic nerves (stellate ga

88 e (F1579) in domain IV-S6, critical in local anaesthetic block, to alanine in QQQ (QQQ-F1579A) disabl

89 Local anaesthetics block pain through non-specific actions at

90 These anaesthetics block sodium channels and thereby the excit

91 responses to mental stress after unilateral anaesthetic blockade of the stellate ganglion, alone or

92 Most barbiturates are anaesthetics but a few unexpectedly are convulsants.

93 Most barbiturates are anaesthetics but unexpectedly a few are convulsants whos

94 lays an important role in the action of most anaesthetics, but is thought to be especially relevant i

95 anaesthesia and rural setting for improving anaesthetic care in pregnant women.

96 r titles or abstracts mentioning surgical or anaesthetic care provision by associate clinicians or no

97 doscopy procedures performed under monitored anaesthetic care using propofol as a sedative agent can

98 d in patients receiving nitrous oxide as the anaesthetic carrier gas compared with those receiving ni

99 nts (approximately 1 aspiration/3000 general anaesthetic cases), gastric volume and pH have been used

100 Volatile anaesthetics cause changes in the membrane resting poten

101 RECENT FINDINGS: As well as the immediate 'anaesthetic' complications of pain, nausea and vomiting

102 Anaesthetic concentrations in solution were determined u

103 arge movements, at micromolar and millimolar anaesthetic concentrations, respectively.

104 ere told that they may or may not receive an anaesthetic cream on one arm.

105 e assessment sites was anaesthetised with an anaesthetic creme.

106 e depolarized potentials; on the other hand, anaesthetics decrease excitability by activating a TASK-

107 ensitive subunit is sufficient to confer the anaesthetic-dependent potentiation to the GABA current.

108 al benefits of intra-operative monitoring of anaesthetic depth and cerebral oxygenation as a pragmati

109 Control of anaesthetic depth has been reported using the median fre

110 Recently, the monitoring of anaesthetic depth using the bispectral index or auditory

111 ith action potentials blocked with the local anaesthetic derivative, QX-314.

112 seems unlikely that the actions of volatile anaesthetics described here are involved in the state of

113 High concentrations of either anaesthetic directly activated alpha6beta3gamma2L, but n

114 about risk and dealing with the aftermath of anaesthetic disasters are also reviewed specifically.

115 In contrast, no study showed an effect of anaesthetic doses (>100 mg kg(-1)) of ketamine on dopami

116 dies of the acute effects of ketamine at sub-anaesthetic doses for meta-analysis.

117 mined following application of different sub-anaesthetic doses of Ket.

118 ll as what can be achieved without access to anaesthetic drugs at all.

119 n domains III and IV) was required for local anaesthetic drugs to modify Na+ channel gating currents,

120 ved with subanaesthetic doses of traditional anaesthetic drugs, as well as what can be achieved witho

121 hile reducing the administration and cost of anaesthetic drugs.

122 transmitter release sites, thereby bypassing anaesthetic effects on channels and receptors in order t

123 e effects; transmitter action prevailed over anaesthetic effects on TASK channels, but not over effec

124 on channels and receptors in order to allow anaesthetic effects on the neurotransmitter release mach

125 s than 10% of the membrane patches, volatile anaesthetics either increased or decreased the mean open

126 The halogenated volatile anaesthetic enflurane blocked both currents, but only th

127 n paired-pulse depression, but that volatile anaesthetics enhance paired-pulse depression by prolongi

128 R-mTFD-MPPB, like most anaesthetics, enhanced receptor gating by rapidly bindin

129 These observations support the idea that anaesthetics exert a specific effect on these ion-channe

130 he mechanisms through which volatile general anaesthetics exert their behavioural effects remain uncl

131 Simulated anaesthetic exposure reduced APD and ERP in both epicard

132 further gains in our understanding of local anaesthetic eye blocks and the management of patients un

133 travenous bolus) or saline adjunctive to the anaesthetic for the duration of their ECT course.

134 This extends to the use of anaesthetics for both scientific study, humane killing a

135 flurane resulted in a ten-fold difference in anaesthetic gas emissions between hospitals.

136 its high cost because it is an almost ideal anaesthetic gas.

137 Anaesthetic gases and energy consumption were the larges

138 General anaesthetics greatly impair thermoregulation, synchronou

139 The general anaesthetic halothane (1.5%) increased the oxygen-sensit

140 The effects of the inhalational anaesthetics halothane and isoflurane on the high-voltag

141 otonin (5-HT) and noradrenaline (NA)) and an anaesthetic (halothane) indeed compete for modulation of

142 (M314) upon allosteric regulation by general anaesthetics has been investigated.

143 Anaesthetics have been shown to exert both neurotoxic an

144 Volatile anaesthetics have historically been considered to act in

145 Neurotransmitters and volatile anaesthetics have opposing effects on motoneuronal excit

146 conclusion, our data indicate that GABA and anaesthetics holistically activate the GABAA rho1 recept

147 to opioids, sedatives-hypnotics, or general anaesthetics in neonates (O-SH-GA).

148 tresses the importance of the choice of drug anaesthetics in order to avoid adverse effects on brain

149 A prominent in vivo effect of general anaesthetics, including volatile anaesthetics such as ha

150 All three anaesthetics increased the width of the tissue's vulnera

151 information on factors contributing to local anaesthetic induced neurotoxicity: adrenaline significan

152 re used to simulate the functional impact of anaesthetic-induced blockade of membrane currents on APD

153 Anaesthetic-induced changes in the membrane potential we

154 We hypothesised that a volatile anaesthetic-induced decrease in myocardial contractility

155 and fast exponential components, revealed an anaesthetic-induced increase in the duration of the slow

156 nder current clamp conditions, 5-HT reversed anaesthetic-induced membrane hyperpolarization and incre

157 Propofol has been an immensely successful anaesthetic induction agent but there is an increasing n

158 receive either methylprednisolone (250 mg at anaesthetic induction and 250 mg at initiation of cardio

159 ol, i.e. no injection) and between subjects (anaesthetic injection vs. saline injection).

160 ated the effectiveness of an intra-operative anaesthetic intervention in reducing post-operative cogn

161 ew describes the radiological, obstetric and anaesthetic interventions which are often carried out in

162 Measuring the direct drug costs of an anaesthetic is relatively easy, but assessing increased

163 administration of adequate concentrations of anaesthetics is not always feasible.

164 Etomidate, an intravenous imidazole general anaesthetic, is thought to produce anaesthesia by modula

165 e neurophysiological effects of the volatile anaesthetic isoflurane on axonal and synaptic function i

166 midazolam, propofol, ketamine, inhalational anaesthetics (isoflurane, desflurane), antiepileptic dru

167 The antidepressant and anaesthetic ketamine (Ket) and four Ket metabolites were

168 e VTD receptor aligns closely with the local anaesthetic (LA) receptor, which resides at D1S6, D3S6 a

169 g studies have shown that lidocaine, a local anaesthetic (LA) that elicits depolarization-dependent (

170 is present in anaesthetized monkeys even at anaesthetic levels known to induce profound loss of cons

171 intestinal mucosal application of the local anaesthetic lidocaine (lignocaine) or administration of

172 n extensive mutagenesis data, that the local anaesthetic lidocaine docks eccentrically below the sele

173 The hypothesis that a local anaesthetic, lidocaine (lignocaine), binds primarily to

174 pecially relevant in the case of intravenous anaesthetics, like etomidate and propofol.

175 ew randomized studies are available to guide anaesthetic management but anaesthetists should aim to a

176 There is emerging evidence that anaesthetic management influences outcome.

177 To review the current anaesthetic management of patients undergoing transthora

178 s review is to outline the priorities in the anaesthetic management of the child with facial abnormal

179 Anaesthetic molecules act on synaptic transmission via t

180 VSTX1, small hydrophobic poisons and anaesthetic molecules reveal a common theme of voltage s

181 uvenile hair cells, unlike the commonly used anaesthetic MS-222, which reduces the size of basolatera

182 Strikingly, either anaesthetic now activated the receptor, an effect confir

183 nRT neurones by enflurane and other volatile anaesthetics occurs within concentrations that are relev

184 nsating animals through superfusion of local anaesthetic on the round window.

185 The overall effect of volatile anaesthetics on the [Ca2+]i profile is likely to be dete

186 We studied the effects of inhalation anaesthetics on the membrane properties of hypoglossal m

187 ing and breathing were made within subjects (anaesthetic or saline injection vs. control, i.e. no inj

188 pathway that permits the rapid diffusion of anaesthetics out of the Nav1.5 channel.

189 He was completely anaesthetic over the entire left trigeminal distribution

190 od incorporating a miniature respiratory and anaesthetic perfusion set-up for live adult zebrafish, a

191 mechanism that governs internal QX and local anaesthetic pore block of voltage-gated Na+ channels and

192 This is a challenging area of anaesthetic practice but the use of a structured approac

193 ion, and training have had a major effect on anaesthetic practice, so that anaesthesia is increasingl

194 surgical patient is an integral part of good anaesthetic practice.

195 Anaesthetic preconditioning occurs when a volatile anaes

196 The anaesthetics preferentially affected the slow component

197 ween April 1, 2014, and Jan 31, 2015, 31 127 anaesthetic procedures in 30 874 children with a mean ag

198 associate clinicians undertook surgical and anaesthetic procedures without supervision (100% for sur

199 bition of NCX-mediated Ca2+ efflux, volatile anaesthetics produce myocardial depression.

200 The mechanisms by which volatile anaesthetics produce this effect were investigated in th

201 nits is inhibited by the intravenous general anaesthetic propofol (2,6-diisopropylphenol).

202 tations of the conserved M1 proline, and the anaesthetic propofol, increase a rate constant for desen

203 sought to determine whether the intravenous anaesthetics propofol and etomidate inhibit the release

204 The time needed to train new surgical and anaesthetic providers was estimated with average length

205 forts to bridge the gap between surgical and anaesthetic providers.

206 d world, alternative indicators of obstetric anaesthetic quality are required.

207 ervice) investigates suspected perioperative anaesthetic reactions using serial tryptase, urinary met

208 Instead, the anaesthetic reduced channel open probability to the same

209 or tactile stimuli and under four different anaesthetic regimens.

210 As anaesthetic-related maternal mortality reduces in the de

211 Anaesthetic research has the potential to further improv

212 Scottish Society of Anaesthetists, Edinburgh Anaesthetics Research and Education Fund.

213 nal excitability and are implicated in pain, anaesthetic responses, thermosensation, neuroprotection,

214 d influence pain, temperature perception and anaesthetic responses.

215 HCN1 channels in the absence and presence of anaesthetic reveals that (1) gating is best described by

216 ype and the mutated rho1 subunits, which are anaesthetic-sensitive and respond with full efficacy to

217 hen demonstrate that, in the pentamer, three anaesthetic-sensitive rho1 subunits are needed to impart

218 tivation by anaesthetics alone, and only one anaesthetic-sensitive subunit is sufficient to confer th

219 By contrast, five anaesthetic-sensitive subunits are required for direct a

220 An anaesthetic should not induce negative behaviours and fi

221 We recently located the anaesthetic sites on GABAA receptors (GABAA Rs) by photo

222 m its negligible affinity for the enhancing, anaesthetic sites.

223 nded cortical representation of adjacent non-anaesthetic skin does not influence the cortical process

224 st to adults, neuraxial blockade using local anaesthetic solutions is associated with stable cardiova

225 pidural space (which may mimic that of local anaesthetic solutions) appears to be highly variable, al

226 lpha-2-agonists have long been known to have anaesthetic-sparing, sedative and analgesic properties w

227 propofol can be recommended for use without anaesthetic staff.

228 Nitrous oxide is by far the oldest anaesthetic still in routine use and its continued use i

229 go the procedure and two had missing data on anaesthetic strategy), 236 (30%) of 797 patients who had

230 The spikelets were inhibited by TTX and anaesthetics such as alpha-chloralose but not by the int

231 of general anaesthetics, including volatile anaesthetics such as halothane, is the prolonging of pai

232 Volatile anaesthetics such as halothane, isoflurane and sevoflura

233 Local anaesthetics such as lidocaine (lignocaine) interact wit

234 though sodium channels are targeted by local anaesthetics such as lidocaine (lignocaine), some patien

235 s riluzole) and volatile and gaseous general anaesthetics (such as halothane and nitrous oxide).

236 hetic preconditioning occurs when a volatile anaesthetic, such as sevoflurane, is administered before

237 action in Drosophila, and suggest candidate anaesthetic target molecules.

238 ttractive model system for identification of anaesthetic targets.

239 Although surgical and anaesthetic task shifting has been described in many cou

240 global distribution and use of surgical and anaesthetic task shifting is needed to strengthen strate

241 Anaesthetic task shifting occured in 108 (65%) of 165 co

242 assistants to undertake anaesthetic and peri-anaesthetic tasks.

243 There are many different ways of organizing anaesthetic teams, in particular because the role of non

244 were randomised in the operating theatre and anaesthetic technique and pain-control methods were stan

245 advancements and innovations in surgical and anaesthetic technique have allowed us to offer surgical

246 tation with the patient, should decide which anaesthetic technique to use on an individual basis.

247 est managed by utilizing a total intravenous anaesthetic technique with propofol, the avoidance of ni

248 reoperative risk assessment and surgical and anaesthetic techniques have resulted in a significant de

249 terized as PONV, at the very least, avoid an anaesthetic that may make PONV/PDNV worse and be aggress

250 gly different sensitivities to high doses of anaesthetics that suggest a hierarchy governing how the

251 and the number of cases reported for all non-anaesthetic therapies is low.

252 es or recurs 24 h or more after the onset of anaesthetic therapy, including those cases where status

253 ptic GABA(A)Rs to ambient GABA, alcohols and anaesthetics, these receptors may present a critical sit

254 of GABA via orthosteric sites, the force of anaesthetics through allosteric sites may not propagate

255 ury by injecting rhesus monkeys with a local anaesthetic to block the median and ulnar nerves at the

256 ced in the presence or absence of a volatile anaesthetic to selectively promote Ca2+ efflux via NCX.

257 ine at 50 mg l(-1) was an effective and safe anaesthetic to use on juvenile zebrafish.

258 mental effects of nitrous oxide derived from anaesthetic use are negligible and there is no convincin

259 Most local anaesthetics used clinically are relatively hydrophobic

260 olutions were equilibrated with inhalational anaesthetic vapour delivered from a calibrated vaporizer

261 and reflexology is a useful adjunct to local anaesthetic varicose vein surgery, with participants in

262 speed induction of anaesthesia with volatile anaesthetics, via a mechanism referred to as the "second

263 l ketamine or clonidine as adjuncts to local anaesthetics will grow.

264 iable data on alternative short-acting local anaesthetics with respect to transient neurological symp