ライフサイエンスコーパス: flumazenil

1 trazepam), negative (Ro15-4513), or neutral (flumazenil).

2 steric mechanism for anaesthetic reversal by flumazenil.

3 dations, and adverse effects of naloxone and flumazenil.

4 empiric administration of both naloxone and flumazenil.

5 ment with the benzodiazepine site antagonist flumazenil.

6 e, as did the benzodiazepine site antagonist flumazenil.

7 tivity is affected by tricaine, diazepam and flumazenil.

8 ta2gamma2 GABAA receptors was not blocked by flumazenil.

9 g), and returned to control levels following flumazenil.

10 ; its effects are reversed by the antagonist flumazenil.

11 The sleep-inducing effect was blocked by flumazenil.

12 augmentation by diazepam which is blocked by flumazenil.

13 with the benzodiazepine receptor antagonist, flumazenil.

14 umazenil, and a full antagonism at 10 microM flumazenil.

15 The benzodiazepine antagonist flumazenil (0.1-10 microM) unexpectedly potentiated alph

16 behavior and CNS neurons were antagonized by flumazenil (10 mg/kg in vivo; 10 muM in vitro), the benz

17 Intraseptal infusion of the BDZ antagonist, flumazenil (10 nmol), enhanced the amplitude of the dent

18 itron emission tomography (PET) with [(11) C]flumazenil ([(11) C]FMZ), an antagonist of the central b

19 l (18)F-labeled radiopharmaceuticals ([(18)F]Flumazenil, [(18)F]PBR06, [(18)F]Fallypride, and [(18)F]

20 ancement produced by zolpidem was reduced by flumazenil (-31 +/- 13 %, relative to the AHP HW during

21 different amounts of isotopically unmodified flumazenil (4, 20, 100, or 400 mug) to cover a wide rang

22 The administration of flumazenil, a benzodiazepine (BZ) antagonist, is effecti

23 which functions upstream of Abp1, plus (iii) flumazenil, a benzodiazepine antagonist that binds to GA

24 Flumazenil, a benzodiazepine antagonist, blocked the dia

25 n at 10 pM was fully antagonised by 1 microM flumazenil, a benzodiazepine receptor antagonist.

26 The binding of [(11)C]flumazenil, a benzodiazepine-specific PET radiotracer, w

27 The transport of flumazenil across the blood-brain barrier and the bindin

28 -constant infusion method was used for (11)C-flumazenil administration.

29 This concentration of flumazenil also antagonised the decrease in firing rate

30 Intraseptal flumazenil also significantly enhanced the magnitude of

31 Although the density and affinity of [3H]flumazenil and [3H]imidazenil binding failed to change i

32 ant alpha4beta3delta receptors is blocked by flumazenil and beta-carboline-ethyl ester (beta-CCE).

33 ptors bind the imidazo-benzodiazepines (BZs) flumazenil and Ro15-4513 with high affinity (K(d) < 10 n

34 [3H]Ro15-4513 was displaced by Ro15-4513, flumazenil and Ro19-4603, but not by RU34347.

35 The relative potencies of flumazenil and zolpidem in blocking convulsions induced

36 sm of the peak effect was seen with 1 microM flumazenil, and a full antagonism at 10 microM flumazeni

37 hough the benzodiazepine ligands flurazepam, flumazenil, and methyl-6,7-dimethoxy-4 ethyl-beta-carbol

38 acid A-benzodiazepine receptor ligand, (11)C-flumazenil, and the reconstructed images were compared w

39 serious adverse events including the use of flumazenil, assisted ventilation, permanent injury or de

40 in P-glycoprotein (P-gp)-mediated efflux of flumazenil at the blood-brain barrier may confound inter

41 ioral alcohol antagonism of Ro15-4513 (i.e., flumazenil, beta-carbolinecarboxylate ethyl ester (beta-

42 sociation between decreases in cortical [11C]flumazenil binding and revised ALS functional rating sca

43 al association between reduced cortical [11C]flumazenil binding and the ALSFRS-R, rather than the UMN

44 D90A subjects, a small focus of reduced [11C]flumazenil binding at the left fronto-temporal junction

45 ons of cerebral cortex with disproportionate flumazenil binding compared with local grey matter volum

46 in the distribution of reduced cortical [11C]flumazenil binding in homD90A compared with sALS patient

47 included regions not found to have abnormal flumazenil binding on analysis of the PET data alone.

48 We hypothesized that (11)C-flumazenil binding potential (BPND) would be higher in i

49 Flumazenil binding was decreased in some MCDs with incre

50 m of the present study was to investigate if flumazenil blood-brain barrier transport and binding to

51 There was close agreement in (11)C-flumazenil BPND values between awake and anesthetized co

52 EtOH effect, and that Ro15-4513 differs from flumazenil by only a single group in the molecule (an az

53 Naloxone and flumazenil can be used as diagnostic as well as therapeu

54 The fact that only Ro15-4513, but not flumazenil, can inhibit the EtOH effect, and that Ro15-4

55 Flumazenil caused a modest increase in total sleep, and

56 In this subgroup, [(11)C]flumazenil DeltaVT in the medial temporal lobe was corre

57 roup but not the schizophrenia group, [(11)C]flumazenil DeltaVT was positively associated with gamma-

58 ocedure: after injection of 20 mCi of [(11)C]flumazenil, dynamic emission images of the brain were ac

59 In contrast, the promnestic BDZ ligand, flumazenil, enhances dentate granule cell responsivity,

60 itron emission tomography was used with [11C]flumazenil (FMZ) and [18F]fluorodeoxyglucose to study GA

61 hy (PET) study using the BZR antagonist [11C]flumazenil (FMZ) found two- to threefold greater cerebra

62 [11C]flumazenil (FMZ) imaged with PET allows the computation

63 [(11)C]Flumazenil (FMZ) PET images most subtypes of GABA(A) rec

64 [(11)C]Flumazenil (FMZ) PET images the majority of GABA(A) rece

65 Studies report that (11)C-flumazenil (FMZ) PET more specifically localizes the epi

66 sing statistical parametric mapping and [11C]flumazenil (FMZ) PET we have previously shown reduction

67 imaging was performed using the tracer [11C]flumazenil (FMZ), a ligand that binds to alpha subunits

68 ) perfusion and follow-up quantitative (11)C-flumazenil (FMZ)-PET to map SNL in the non-infarcted tis

69 10 nM flumazenil fully antagonised the second, declining, phas

70 Flumazenil given by itself had no significant effects on

71 mmune antibody fragments, electrical pacing, flumazenil, glucagon, hemodialysis, hydroxocobalamin, hy

72 At a dose of 0.76 microg, flumazenil had no effect on sleep when given alone, and

73 The GABA(A) receptor PET ligand [11C]flumazenil has demonstrated motor and extra-motor cortic

74 treatment increased brain concentrations of flumazenil in both groups, but B(max) estimates were not

75 vo positron emission tomography marker (11)C-flumazenil in humans.

76 Although the empiric use of naloxone and flumazenil in the comatose adult patient who presents to

77 Decreases in the binding of [11C]flumazenil in the sALS group were found within premotor

78 with the benzodiazepine receptor antagonist flumazenil, into the MPA.

79 ion with the benzodiazepine receptor blocker flumazenil, into the MPA.

80 raphy and the benzodiazepine receptor ligand flumazenil labeled with carbon 11 to assess the regional

81 compromise was defined as use of naloxone or flumazenil, nonmechanical or cardiopulmonary resuscitati

82 The CGS 8216, but neither flumazenil nor ZK 93426, reliably reversed the RO19-4603

83 but not by microinjection of 5 micrograms of flumazenil or 200 ng of PK 11195.

84 barrier may confound interpretation of (11)C-flumazenil PET in epilepsy.

85 sALS) and 10 homD90A patients underwent [11C]flumazenil PET of the brain.

86 total, 29 rats underwent 2 consecutive (11)C-flumazenil PET scans, each one lasting 30 min.

87 Previous MRI and [11C]flumazenil PET studies have demonstrated widespread stru

88 In this study, we used [11C]flumazenil PET to explore differences in the pattern of

89 of neuronal integrity measured with [(18)F] flumazenil PET.

90 Using [11C]flumazenil-PET and statistical parametric mapping (SPM),

91 normal control high-resolution MRI and [11C]flumazenil-PET image using a novel technique.

92 l GABA(A) receptor densities by using [(18)F]flumazenil positron emission tomography ([(18)F]FMZ-PET)

93 obe the right or left hemisphere), and (11)C-flumazenil positron emission tomography generating bindi

94 Acute/subacute flumazenil positron emission tomography studies are bein

95 By using [11C]flumazenil-positron emission tomography ([11C]FMZ-PET),

96 on of the benzodiazepine receptor antagonist flumazenil, resulted in a dose-dependent recovery of sup

97 [(3)H]-flumazenil revealed no significant effects.

98 Positron emission tomography with [11C]flumazenil revealed normal benzodiazepine receptor distr

99 This anticonflict effect is blocked by flumazenil (Ro 15-1788), indicating that like benzodiaze

100 nce of flurazepam or the BZD-site antagonist flumazenil (Ro15-1788) decreased the rate of modificatio

101 s were not influenced, suggesting that (11)C-flumazenil scanning is not confounded by alterations in

102 e ligands, detected as an increase in [(11)C]flumazenil tissue distribution volume (VT).

103 up-regulated; and (iii) the binding of [(3)H]flumazenil to hippocampal synaptic membranes is decrease

104 of a5GABA(A) receptors (a5GABA(A)R), [(3)H]-flumazenil to quantify a1-3;5GABA(A)R, and [(3)H]-MK801

105 a5GABA(A) receptors (alpha5GABA(A)R), [(3)H]-flumazenil to quantify alpha1-3;5GABA(A)R, and [(3)H]-MK

106 ed the benzodiazepine GABA(A) marker [(11)C] flumazenil to study cerebral dysfunction in amyotrophic

107 There was no difference in flumazenil transport across the blood-brain barrier betw

108 Tariquidar treatment also decreased flumazenil transport out of the brain by 73%, increased

109 e A (GABAA)-benzodiazepine radiotracer (11)C-flumazenil under anesthetized and awake conditions.

110 esence of amitriptyline that is increased by flumazenil, unlike augmentation by diazepam which is blo

111 We calculated [(11)C]flumazenil volume of distribution ([(11)C]FMZ-V(d)) afte

112 were derived to localize changes in regional flumazenil volumes of distribution (FMZVD), which correl

113 Flumazenil voxelwise binding potential relative to nondi

114 with positive symptoms, and baseline [(11)C]flumazenil VT in the medial temporal lobe was negatively

115 [(11)C]Flumazenil VT was significantly increased across all cor

116 tion in the blood-brain barrier transport of flumazenil was observed.

117 with the benzodiazepine receptor antagonist flumazenil, which has no effects on membrane fluidity or

118 ombination with the BDZ receptor antagonists flumazenil, ZK 93426, and CGS 8216 (20 mg/kg) in selecti