ライフサイエンスコーパス: anaesthetics

1 individual variability in susceptibility to anaesthetics.

2 ients do not respond to treatment with local anaesthetics.

3 clear clinical advantages over other current anaesthetics.

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

5 ribute to some important clinical effects of anaesthetics.

6 s, gastrointestinal hormone disruptions, and anaesthetics.

7 sitivity of the RYR to caffeine and volatile anaesthetics.

8 on dependent, but comparable between the two anaesthetics.

9 A receptors by structurally distinct general anaesthetics.

10 echanism of action of general (inhalational) anaesthetics.

11 ting of specific hypotheses of the action of anaesthetics.

12 linically relevant concentrations of inhaled anaesthetics.

13 ycine receptors by alcohols and two volatile anaesthetics.

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

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

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

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

18 Preclinical data suggest that general anaesthetics affect brain development.

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

20 Recent evidence suggests that anaesthetics also inhibit excitatory synaptic transmissi

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

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

23 While several anaesthetics and analgesics have been reported to alter

24 Local anaesthetics and anti-epileptic drugs can suppress hyper

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

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

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

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

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

30 Sodium channels bind local anaesthetics and various toxins.

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

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

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

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

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

36 Both anaesthetics at each concentration also shifted the rela

37 Local anaesthetics block pain through non-specific actions at

38 These anaesthetics block sodium channels and thereby the excit

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

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

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

42 Volatile anaesthetics cause changes in the membrane resting poten

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

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

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

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

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

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

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

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

51 General anaesthetics greatly impair thermoregulation, synchronou

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

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

54 Anaesthetics have been shown to exert both neurotoxic an

55 Volatile anaesthetics have historically been considered to act in

56 Neurotransmitters and volatile anaesthetics have opposing effects on motoneuronal excit

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

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

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

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

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

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

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

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

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

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

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

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

69 The anaesthetics preferentially affected the slow component

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

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

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

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

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

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

76 Volatile anaesthetics such as halothane, isoflurane and sevoflura

77 Local anaesthetics such as lidocaine (lignocaine) interact wit

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

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

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

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

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

83 Most local anaesthetics used clinically are relatively hydrophobic

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

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

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