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1 eams such as EMLA (Eutectic mixture of local anaesthetics).
2 ycine receptors by alcohols and two volatile anaesthetics.
3 t ML-based model solves electrode fouling of anaesthetics.
4 ctors of successful weaning from intravenous anaesthetics.
5 ability and the activation of the channel by anaesthetics.
6 soelectricity that can be induced by general anaesthetics.
7  individual variability in susceptibility to anaesthetics.
8 ients do not respond to treatment with local anaesthetics.
9 clear clinical advantages over other current anaesthetics.
10 he pH-sensitive current was blocked by local anaesthetics.
11 ribute to some important clinical effects of anaesthetics.
12 s, gastrointestinal hormone disruptions, and anaesthetics.
13 sitivity of the RYR to caffeine and volatile anaesthetics.
14 on dependent, but comparable between the two anaesthetics.
15 A receptors by structurally distinct general anaesthetics.
16 echanism of action of general (inhalational) anaesthetics.
17 ting of specific hypotheses of the action of anaesthetics.
18 linically relevant concentrations of inhaled anaesthetics.
19 sy, anxiety, depression and insomnia and for anaesthetics(1,2).
20 that are essential for responses to volatile anaesthetics(10), neurotransmitters(13) and G-protein-co
21 enges to antibiotics [40/44 (91%]) and local anaesthetics [41/44 (93%)].
22  rate of any maternal death was 9.8 per 1000 anaesthetics (5.2-15.7, I(2)=92%) when managed by non-ph
23 eep/wake cycles(8) and responses to volatile anaesthetics(8-11).
24                                    All three anaesthetics accelerated the rate of re-entrant excitati
25                           The discovery that anaesthetics affect a recently identified family of pota
26        Preclinical data suggest that general anaesthetics affect brain development.
27 bunits are required for direct activation by anaesthetics alone, and only one anaesthetic-sensitive s
28                Recent evidence suggests that anaesthetics also inhibit excitatory synaptic transmissi
29 glycine receptors is enhanced by a number of anaesthetics and alcohols, whereas activity of the relat
30 r basis for modulation of these receptors by anaesthetics and alcohols.
31                                While several anaesthetics and analgesics have been reported to alter
32                                        Local anaesthetics and anti-epileptic drugs can suppress hyper
33 ted by essential medicines including general anaesthetics and benzodiazepines(3).
34                                 Most general anaesthetics and classical benzodiazepine drugs act thro
35 ls on exposure to commonly used inhalational anaesthetics and depolarising muscle relaxants.
36 membrane stretch, arachidonic acid, volatile anaesthetics and heat.
37 the idea that TREK-1 is a target for general anaesthetics and neuroprotectants.
38 refractory status epilepticus), a variety of anaesthetics and nonpharmacological therapies can be adm
39 eptors that are contrastingly insensitive to anaesthetics and respond partially to several full GABA
40    Skin swabbing does not require the use of anaesthetics and triggers fewer changes in behaviour and
41                   Sodium channels bind local anaesthetics and various toxins.
42 erns about the neurotoxic potential of local anaesthetics and, in particular, of lignocaine.
43 ted signatures are observed across different anaesthetics, and they are reversed by electrical stimul
44 ible phenomena observed in higher organisms, anaesthetics antagonize high-pressure signalling mediate
45 e subcortical nucleus, energetic response to anaesthetics appears to be affected by changes in both c
46 ensitive, and its ability to be activated by anaesthetics, arachidonic acid and internal acidosis rem
47 this may be that the mechanisms of action of anaesthetics are not fully understood.
48                  All currently used volatile anaesthetics are ozone-depleting halogenated compounds.
49 ators, including benzodiazepines and general anaesthetics, are among the most successful drugs in cli
50 may be modulated by particular drugs such as anaesthetics, as well as by non-pharmacological factors
51                                         Both anaesthetics at each concentration also shifted the rela
52 ral information on the mechanisms of general anaesthetics at their physiological receptor sites is la
53 es of GABA(A) receptors bound to intravenous anaesthetics, benzodiazepines and inhibitory modulators.
54                                        Local anaesthetics block pain through non-specific actions at
55                                        These anaesthetics block sodium channels and thereby the excit
56                        Most barbiturates are anaesthetics but a few unexpectedly are convulsants.
57                        Most barbiturates are anaesthetics but unexpectedly a few are convulsants whos
58 lays an important role in the action of most anaesthetics, but is thought to be especially relevant i
59 hannel blockers (S1SCBs) act as potent local anaesthetics, but they can cause severe systemic toxicit
60                                     Volatile anaesthetics cause changes in the membrane resting poten
61 e depolarized potentials; on the other hand, anaesthetics decrease excitability by activating a TASK-
62  seems unlikely that the actions of volatile anaesthetics described here are involved in the state of
63 , time to perform the block, amount of local anaesthetics, duration of the block, need for supplement
64 s than 10% of the membrane patches, volatile anaesthetics either increased or decreased the mean open
65 n paired-pulse depression, but that volatile anaesthetics enhance paired-pulse depression by prolongi
66                       R-mTFD-MPPB, like most anaesthetics, enhanced receptor gating by rapidly bindin
67     These observations support the idea that anaesthetics exert a specific effect on these ion-channe
68 he mechanisms through which volatile general anaesthetics exert their behavioural effects remain uncl
69                   This extends to the use of anaesthetics for both scientific study, humane killing a
70 (>99+%) allows the use of the precious Xe as anaesthetics gas a viable general option in surgery.
71                                      General anaesthetics greatly impair thermoregulation, synchronou
72              The effects of the inhalational anaesthetics halothane and isoflurane on the high-voltag
73 (M314) upon allosteric regulation by general anaesthetics has been investigated.
74                                              Anaesthetics have been shown to exert both neurotoxic an
75       Although the molecular effects of many anaesthetics have been well characterized, a network-lev
76                                     Volatile anaesthetics have historically been considered to act in
77               Neurotransmitters and volatile anaesthetics have opposing effects on motoneuronal excit
78  conclusion, our data indicate that GABA and anaesthetics holistically activate the GABAA rho1 recept
79  to opioids, sedatives-hypnotics, or general anaesthetics in neonates (O-SH-GA).
80 tresses the importance of the choice of drug anaesthetics in order to avoid adverse effects on brain
81 little data exist to guide the withdrawal of anaesthetics in refractory status epilepticus.
82 inically relevant concentrations of volatile anaesthetics, including isoflurane.
83        A prominent in vivo effect of general anaesthetics, including volatile anaesthetics such as ha
84                                    All three anaesthetics increased the width of the tissue's vulnera
85 ce of seizures, whereas the prolonged use of anaesthetics increases the risk of treatment-associated
86 administration of adequate concentrations of anaesthetics is not always feasible.
87  midazolam, propofol, ketamine, inhalational anaesthetics (isoflurane, desflurane), antiepileptic dru
88 ciousness to unconsciousness under different anaesthetics (ketamine and propofol).
89           It is also not known whether local anaesthetics (LAs) transferred to the fetal systemic cir
90 laboratory animals, exposure to most general anaesthetics leads to neurotoxicity manifested by neuron
91 pecially relevant in the case of intravenous anaesthetics, like etomidate and propofol.
92 with members from neurology, neuroradiology, anaesthetics, neurosurgery and patient representatives.
93 nRT neurones by enflurane and other volatile anaesthetics occurs within concentrations that are relev
94               The overall effect of volatile anaesthetics on the [Ca2+]i profile is likely to be dete
95         We studied the effects of inhalation anaesthetics on the membrane properties of hypoglossal m
96 ents receiving either balanced with volatile anaesthetics or total intravenous anaesthesia were gener
97  pathway that permits the rapid diffusion of anaesthetics out of the Nav1.5 channel.
98 res of GABA(A) receptors in complex with the anaesthetics phenobarbital, etomidate and propofol revea
99                                          The anaesthetics preferentially affected the slow component
100 bition of NCX-mediated Ca2+ efflux, volatile anaesthetics produce myocardial depression.
101             The mechanisms by which volatile anaesthetics produce this effect were investigated in th
102  sought to determine whether the intravenous anaesthetics propofol and etomidate inhibit the release
103              Convergent effects also emerge: anaesthetics, psychedelics, and disorders of consciousne
104 Scottish Society of Anaesthetists, Edinburgh Anaesthetics Research and Education Fund.
105                      Premature withdrawal of anaesthetics risks the recurrence of seizures, whereas t
106 f a wide range of clinical agents, including anaesthetics, sedatives, hypnotics and antidepressants(1
107 ns acquired under the effects of the general anaesthetics sevoflurane and propofol to determine wheth
108  or that anaesthetic associates add value in anaesthetics; some evidence suggested that they do not.
109      The spikelets were inhibited by TTX and anaesthetics such as alpha-chloralose but not by the int
110  of general anaesthetics, including volatile anaesthetics such as halothane, is the prolonging of pai
111                                     Volatile anaesthetics such as halothane, isoflurane and sevoflura
112                                        Local anaesthetics such as lidocaine (lignocaine) interact wit
113 though sodium channels are targeted by local anaesthetics such as lidocaine (lignocaine), some patien
114 s riluzole) and volatile and gaseous general anaesthetics (such as halothane and nitrous oxide).
115 gly different sensitivities to high doses of anaesthetics that suggest a hierarchy governing how the
116 nct to reducing the usage of potent volatile anaesthetics, thereby improving their safety.
117 ptic GABA(A)Rs to ambient GABA, alcohols and anaesthetics, these receptors may present a critical sit
118  of GABA via orthosteric sites, the force of anaesthetics through allosteric sites may not propagate
119                                   Most local anaesthetics used clinically are relatively hydrophobic
120                                              Anaesthetics used during cancer surgery may influence tu
121 influence of the anaesthetic method (inhaled anaesthetics versus total-intravenous anaesthesia using
122 speed induction of anaesthesia with volatile anaesthetics, via a mechanism referred to as the "second
123 l ketamine or clonidine as adjuncts to local anaesthetics will grow.
124 iable data on alternative short-acting local anaesthetics with respect to transient neurological symp

 
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