ライフサイエンスコーパス: ondansetron

1 ydroxytryptamine receptor antagonist such as ondansetron.

2 f blocking the excitatory 5HT3 receptor with ondansetron.

3 iness and abnormal vision were reported with ondansetron.

4 anges were recorded with both dolasetron and ondansetron.

5 g/kg dolasetron base, respectively) or 32 mg ondansetron.

6 ea with either dolasetron dose compared with ondansetron.

7 ered intravenous fluids did not receive oral ondansetron.

8 ng alcoholics receiving the 5-HT3 antagonist ondansetron.

9 e function and binding of 5-HT3 receptors to ondansetron.

10 come of treatment of alcohol dependence with ondansetron.

11 s blocked with the 5-HT3-receptor antagonist ondansetron.

12 charge, but this effect was not inhibited by ondansetron.

13 competitive 'setron' antagonists typified by ondansetron.

14 response to the 5-HT(3) receptor antagonist, ondansetron.

15 l injection of the 5-HT3 receptor antagonist ondansetron.

16 ed by capsaicin pretreatment, and blunted by ondansetron.

17 with a two-drug regimen of dexamethasone and ondansetron.

18 lled in the trial received dexamethasone and ondansetron.

19 ganglia with the 5-HT(3) receptor antagonist ondansetron (0.4 microm) alone completely and irreversib

20 ean log CDT ratio between those who received ondansetron (1 and 4 microg/kg twice per day) compared w

21 hypothesis, we counted Fos-LI in the DVC of ondansetron (1 mg/kg; 5-HT3 receptor antagonist) and veh

22 Intrathecal ondansetron (1, 3, 10, 30, and 100microg) produced no ef

23 nts with early-onset alcoholism who received ondansetron (1, 4, and 16 microg/kg twice per day) compa

24 Ondansetron (1.0 and 2.0 microg/100 nl) delivered into t

25 signed to receive 11 weeks of treatment with ondansetron, 1 microg/kg (n = 67), 4 microg/kg (n = 77),

26 tigated the effects of spinally administered ondansetron (10, 50 and 100 microg) on the responses of

27 ourth ventricular (i.c.v.) administration of ondansetron (10.0 microg/3.0 microl) significantly atten

28 66 patients were included: 37 had parenteral ondansetron, 14 were treated with traditional therapy, a

29 83); however, the proportion was higher with ondansetron (16/111) than with placebo (6/111; 3.30, 1.0

30 , patients were randomly assigned placebo or ondansetron (24 mg daily) for a further 4 weeks.

31 1 hour before chemotherapy (n = 534) or i.v. ondansetron (32 mg) 30 minutes before chemotherapy (n =

32 l antiemetic control when compared with i.v. ondansetron (32 mg) in patients who received highly emet

33 Single-dose oral granisetron (2 mg) and I.V. ondansetron (32 mg) resulted in equivalent levels of tot

34 lent levels of antiemetic protection as I.V. ondansetron (32 mg).

35 ere 283 European Americans who received oral ondansetron (4 mg/kg of body weight twice daily) or plac

36 Participants received either ondansetron (4 mug/kg twice daily) or placebo for 11 wee

37 Ondansetron, 4 microg/kg twice per day, was superior to

38 served in hexamethonium, but were blocked by ondansetron (5-HT(3) antagonist), suggesting Dogiel Type

39 ingle-dose oral granisetron (54.7%) and i.v. ondansetron (58.3%) (95% confidence interval [CI], -9.6

40 M 5-HT and this response is blocked by 1 muM ondansetron, a 5-HT3 antagonist, and mimicked by applica

41 iously shown that systemic administration of ondansetron, a selective serotonin type-3 (5-HT3) recept

42 sk of adverse fetal outcomes associated with ondansetron administered during pregnancy.

43 Acute ondansetron administration at the lowest dose (0.1 mg/kg

44 Ondansetron administration attenuated DVC Fos-LI by CCK

45 Furthermore, ondansetron administration attenuated the overall DVC en

46 The presence or absence of oral ondansetron administration was identified for each patie

47 Ondansetron alone had no effect on sucrose intake at any

48 e improvement in auditory gating produced by ondansetron alone.

49 Ondansetron also conferred no significantly increased ri

50 GR113808A) or 5-HT(3)-selective antagonists (ondansetron and 0.3 microM tropisetron).

51 4) or an aprepitant regimen (aprepitant plus ondansetron and dexamethasone on day 1; aprepitant and d

52 rst time were given either standard therapy (ondansetron and dexamethasone on day 1; dexamethasone on

53 rokinin-1 receptor antagonist (NK1RA), to an ondansetron and dexamethasone regimen improves preventio

54 n >/= 70 mg/m(2) for the first time received ondansetron and dexamethasone with a standard aprepitant

55 Given with ondansetron and dexamethasone, single-dose intravenous f

56 as compared in cases who received parenteral ondansetron and in cases who received traditional therap

57 t blocked by the 5-HT(3) receptor antagonist ondansetron and mimicked by the 5-HT(3) receptor agonist

58 mulation of vagal afferent fibres, and since ondansetron and other 5-HT3 antagonists decrease afferen

59 significant overall mean difference between ondansetron and placebo in drinks per drinking day (22.5

60 e role of adjunctive therapies, particularly ondansetron and probiotics in improving AGE outcomes.

61 Ondansetron and probiotics may improve patient outcomes

62 ancies in Denmark, women who were exposed to ondansetron and those who were not exposed were included

63 against postoperative vomiting compared with ondansetron, and the same appears to be true for other d

64 Other agents such as ramosetron and ondansetron are still in use and have not been associate

65 The 5-HT(3) antagonists, granisetron and ondansetron, are useful in combating the nausea associat

66 Likewise, ondansetron attenuated Fos-LI by gastric distension in t

67 ctivation of vagal afferents inhibited using ondansetron, before repeating experiments using water or

68 ta-erythroidine, with the 0.33 mg/kg dose of ondansetron blocked the improvement in auditory gating p

69 Ondansetron by itself was similar to naltrexone and the

70 tation with the aid of an antiemetic such as ondansetron can be as effective and efficient as intrave

71 tion of nicotinic acetylcholine receptors by ondansetron can improve auditory gating parameters in DB

72 001), and in 45 of 109 patients who received ondansetron compared with 65 of 108 allocated placebo (0

73 Nineteen percentage of children treated with ondansetron continued vomiting after the administration

74 trexone with (P = .02) or without (P = .049) ondansetron decreased alcohol cue-induced activation of

75 s whether a three-drug antiemetic regimen of ondansetron, dexamethasone, and the neurokinin-1-recepto

76 However, in the presence of CO, ondansetron did not block LTP.

77 uding dexamethasone, digoxin, cyclosporin A, ondansetron, domperidone, and loperamide.

78 e, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) either in combination with selective seroto

79 r mild symptoms), pyridoxine-doxylamine, and ondansetron (for moderate symptoms) were associated with

80 ree in the granisetron group (55.4%) and the ondansetron group (59%) (95% CI, -9.6 to 2.4).

81 2% in the granisetron group and 67.1% in the ondansetron group (95% CI, -11.7 to -0.1).

82 cebo group, versus 6.5 per week (3.9) in the ondansetron group (estimated difference 6.8 [95% CI 4.0-

83 , trend in vomiting scores was better in the ondansetron group (P = .042).

84 LL individuals in the ondansetron group also had a lower number of drinks per

85 The ondansetron group also showed significant improvement, c

86 cebo, and 14 ondansetron; one patient in the ondansetron group dropped out owing to accidental injury

87 LL/TT individuals in the ondansetron group had a lower number of drinks per drink

88 ng episodes without vomiting per week in the ondansetron group, compared with 0.2 in the placebo grou

89 ecreased on average by 7.6 h per week in the ondansetron group, compared with 2.3 h in the placebo gr

90 ndividuals with the LL genotype who received ondansetron had a lower mean number of drinks per drinki

91 Ondansetron has been suggested as an adjunctive treatmen

92 a pronociceptive role in the spinal cord and ondansetron has previously been shown to produce antinoc

93 The 5-HT(3) receptor antagonist, ondansetron, has been shown to correct the auditory gati

94 iemetics, such as serotonin antagonists like ondansetron, have demonstrated efficacy in relief of vom

95 ith 50 mg of naltrexone (n = 23), 0.50 mg of ondansetron hydrochloride (n = 23), the combination of t

96 Ondansetron hydrochloride use in children with gastroent

97 ere blocked by the 5-HT3 receptor antagonist ondansetron (IC50 = 103 pM) and by the non-selective age

98 setron were compared with intravenous (I.V.) ondansetron in chemotherapy-naive patients who received

99 ty and efficacy to a single 32-mg IV dose of ondansetron in patients receiving cisplatin chemotherapy

100 o test this, we acutely injected intrathecal ondansetron in rats between 14 and 30 days after SNL and

101 egies are needed to optimally integrate oral ondansetron into clinical practice to maximize its poten

102 Administration of ondansetron into the medial NTS completely reversed supp

103 e intake in response to direct injections of ondansetron into various sites of the dorsal hindbrain.

104 Ondansetron is a peripherally active antagonist of the s

105 Single-dose oral ondansetron is effective and safe in reducing hospital a

106 Ondansetron is frequently used to treat nausea and vomit

107 Parenteral ondansetron is significantly more effective than traditi

108 ional ondansetron use: low (<5% administered ondansetron), medium (5%-25%), or high (>25%).

109 ve either oral granisetron (n = 542) or I.V. ondansetron (n = 543).

110 Ondansetron, naltrexone, topiramate, and baclofen are ex

111 The combination of pergolide and ondansetron normalized not only behavioral sensitization

112 attenuation of distension-induced Fos-LI by ondansetron occurred in the NTS, particularly in the med

113 s of both acute and chronically administered ondansetron on auditory gating in DBA/2 mice.

114 We investigated the effects of ondansetron on bulimic behaviours in patients with sever

115 <12 years) on days 2 and 3, or placebo plus ondansetron on day 1 followed by placebo on days 2 and 3

116 125 mg for ages 6 months to <12 years) plus ondansetron on day 1, followed by aprepitant (80 mg for

117 equired to observe the inhibitory effects of ondansetron on spinal neuronal excitability and behavior

118 stration of the 5-HT(3) receptor antagonist, ondansetron (OND), to the posterior IC impaired the esta

119 12 patients were assigned placebo, and 14 ondansetron; one patient in the ondansetron group droppe

120 Children who received ondansetron or no therapy were less likely to require an

121 NTS by either the chronic administration of ondansetron or the genetic inactivation of Tph2 in cauda

122 Dolasetron, granisetron, ondansetron, palonosetron, and tropisetron have similar

123 Our results suggest that ondansetron (particularly the 4 microg/kg twice per day

124 In contrast, ondansetron, pentazocine, and dimenhydrinate may be usef

125 th 59,450 of 334,264 (17.8%) during the high ondansetron period (adjusted percentage change = -0.33%;

126 3 of 232,706 children (18.7%) during the low ondansetron period compared with 59,450 of 334,264 (17.8

127 dified protocol, with or without intravenous ondansetron pretreatment (4 mg).

128 Ondansetron produced less marked effects on thermal resp

129 Ondansetron produced little effect on the electrically e

130 Among ondansetron recipients, the number of drinks per drinkin

131 l data that suggest that both naltrexone and ondansetron reduce alcohol-stimulated dopamine output in

132 (5-hydroxytryptamine-3) receptor antagonist ondansetron reduced the amplitude of the CMMC, the propu

133 olasetron mesylate 1.8 mg/kg, 2.4 mg/kg, and ondansetron, respectively, were 49.2%, 45.6%, and 50.4%

134 f casopitant mesylate plus dexamethasone and ondansetron significantly reduced CINV events in patient

135 Ondansetron taken during pregnancy was not associated wi

136 ight the need to focus efforts to administer ondansetron to children at greatest risk for oral rehydr

137 propose a new pharmacogenetic approach using ondansetron to treat severe drinking and improve abstine

138 s study, they explored additional markers of ondansetron treatment response in alcoholics by examinin

139 decrease in binge-eating and vomiting under ondansetron treatment was not achieved by compensatory c

140 l-level analyses of the associations between ondansetron use and 3 outcomes: intravenous rehydration

141 outcomes varied widely between low and high ondansetron use categories at an institutional level.

142 Ondansetron use has increased significantly; however, 'r

143 Although ondansetron use increased during the study period, intra

144 Oral ondansetron use increased from a median institutional ra

145 During the transition from low to high ondansetron use, we observed no change in the hospitaliz

146 sits were categorized based on institutional ondansetron use: low (<5% administered ondansetron), med

147 analog scale [VAS] score, 4.1 [SD, 2.9] for ondansetron vs 5.7 [SD, 2.3] for metoclopramide [P = .02

148 he parenteral (intravenous or intramuscular) ondansetron vs traditional therapy to resolve the sympto

149 Ondansetron was associated with improvement for a range

150 One RCT (n = 83) found that ondansetron was associated with lower nausea scores on d

151 Ondansetron was dosed per the product label for paediatr

152 Receipt of ondansetron was not associated with a significantly incr

153 Oral ondansetron was provided to 13.5% (95% CI, 13.3% to 13.7

154 colon; and (9) the 5-HT3 receptor antagonist ondansetron, which reduced CMMCs and blocked their propa

155 Addition of aprepitant to ondansetron with or without dexamethasone is effective f