ライフサイエンスコーパス: sumatriptan

1 lood-brain barrier-permeable 5-HT1BR agonist sumatriptan.

2 he RVM did not block the effects of systemic sumatriptan.

3 ation persisted after pain was controlled by sumatriptan.

4 novascular neurons are directly inhibited by sumatriptan.

5 nitially decreased after IS, increased after sumatriptan.

6 itially dropped after IS, remained low after sumatriptan.

7 f after treatment with the antimigraine drug sumatriptan.

8 t continued to have an excellent response to sumatriptan.

9 ished by tonabersat pre-treatment but not by sumatriptan.

10 eurons by the serotonergic antimigraine drug sumatriptan.

11 on into clinical use of the 5HT1B/1D agonist sumatriptan.

12 which predicts the antimigraine efficacy of sumatriptan.

13 urned to normal by a 5-HT1 receptor agonist, sumatriptan.

14 The same held true for sumatriptan (0.7 mumol/kg) and GTI (0.6 mumol/kg).

15 receptor subtype, since the 5-HT1D agonist, sumatriptan (1 microM), was effective.

16 s inhibited by CP 93129 (1 nM-10 microM) and sumatriptan (1 nM-1 microM), agonists at 5-HT1B and 5-HT

17 Sumatriptan 100 mg orally and 6 mg subcutaneously aborte

18 y iontophoresis of ergometrine (9/10 cells), sumatriptan (2/3 cells) and zolmitriptan (9/15 cells) bu

19 Following pre-treatment with vehicle (n=3), sumatriptan (300 microg kg(-1) i.v, n=3) or tonabersat (

20 The effects of sumatriptan (300 microg/kg i.v.) on central sensitizatio

21 Coejection of sumatriptan, 4991W93, or ergometrine resulted in a signi

22 triptan, 85 mg, and naproxen sodium, 500 mg; sumatriptan, 85 mg (monotherapy); naproxen sodium, 500 m

23 ratio to receive a single tablet containing sumatriptan, 85 mg, and naproxen sodium, 500 mg; sumatri

24 Sumatriptan, 85 mg, plus naproxen sodium, 500 mg, as a s

25 The current study examines the effect of sumatriptan, a 5-HT(1B/1D) agonist and effective antimig

26 over, this study also examined the effect of sumatriptan, a clinically effective antimigraine agent,

27 In the presence of sumatriptan, a decrease below baseline in cortical rCBF(

28 Sumatriptan, a drug commonly used to treat headaches, bl

29 tration of 5HT1(B/D) antagonists on systemic sumatriptan action and (2) determining whether RVM appli

30 ficacy, the cellular target and mechanism of sumatriptan action are not well understood beyond the ph

31 tase inhibitor okadaic acid, suggesting that sumatriptan action is mediated by calcium-recruited phos

32 ed by using the ionophore ionomycin to mimic sumatriptan action.

33 Sumatriptan administered into the RVM similarly produced

34 fective migraine drugs, the 5-HT1B/D agonist sumatriptan and a CGRP-blocking monoclonal antibody, att

35 We first demonstrate that sumatriptan and another 5-HT1 agonist, CGS 12066A (CGS),

36 antagonists blocked the repression caused by sumatriptan and eletriptan.

37 Oral sumatriptan and naratriptan are effective as short-term

38 These results suggest that CP-93,129, sumatriptan, and GTI exert their effects via 5-HT1B (5-H

39 Sumatriptan appears to decrease the amplitude of nitric

40 Sumatriptan blunted the increase in blood flow following

41 RP gene expression during migraine, and that sumatriptan can diametrically oppose that activation via

42 tured trigeminal neurons to demonstrate that sumatriptan can directly repress CGRP secretion from sen

43 Here we examined whether the drug sumatriptan can prevent and/or suppress peripheral and c

44 y of the 5-HT1B autoreceptor but shifted the sumatriptan concentration-response curve to the right (P

45 The potency of sumatriptan, CP-122,288, CP-93,129, and 5-CT in wild-typ

46 Systemic sumatriptan did not alter pain relief-induced CPP in rat

47 y effective antimigraine 5-HT(1B/1D) agonist sumatriptan did not inhibit forskolin-stimulated CGRP re

48 Unexpectedly, sumatriptan did not lower cAMP levels, in contrast to th

49 gered by nitroglycerin and was unaffected by sumatriptan, dihydroergotamine and ergotamine.

50 ion was established in both types of neuron, sumatriptan effectively normalized intracranial mechanic

51 We found that sumatriptan effectively prevented the induction of sensi

52 (1B/D) agonists, including the triptan drugs sumatriptan, eletriptan, and rizatriptan that are used f

53 Systemic sumatriptan elicited a dose- and time-related blockade o

54 Sumatriptan had no effect on the number of depolarisatio

55 The most widely used 5-HT1D agonist is sumatriptan; however, this agent reportedly displays lit

56 ation of saline or the antimigraine compound sumatriptan in chloralose-anesthetized cats.

57 Late sumatriptan intervention counteracted two aspects of cen

58 On the other hand, late sumatriptan intervention did not reverse other aspects o

59 Early sumatriptan intervention effectively blocked the develop

60 The mechanism for this action of sumatriptan is unknown but may include; modulation of ce

61 Sumatriptan is used specifically to relieve headache pai

62 and 23% in studies 1 and 2, respectively) to sumatriptan monotherapy (16% and 14% in studies 1 and 2)

63 ilar between sumatriptan-naproxen sodium and sumatriptan monotherapy.

64 Pretreatment with sumatriptan (n = 9) produced a highly significant reduct

65 ally in the treatment of migraine, including sumatriptan, naproxen, and a calcitonin gene-related pep

66 ain-free response for the comparison between sumatriptan-naproxen sodium and each monotherapy.

67 of absence of nausea did not differ between sumatriptan-naproxen sodium and placebo (65% vs 64%; P =

68 absence of nausea for the comparison between sumatriptan-naproxen sodium and placebo, and the percent

69 idence of adverse events was similar between sumatriptan-naproxen sodium and sumatriptan monotherapy.

70 nausea 2 hours after dosing was higher with sumatriptan-naproxen sodium than placebo in study 1 (71%

71 Sumatriptan-naproxen sodium was more effective than plac

72 2- to 24-hour sustained pain-free response, sumatriptan-naproxen sodium was superior at P<.01 (25% a

73 rison with known antimigraine agents such as sumatriptan, naratriptan, rizatriptan, and VML-251.

74 th an initial trial of ibuprofen followed by sumatriptan nasal spray for children over 12 years of ag

75 f migraine are ibuprofen, acetaminophen, and sumatriptan nasal spray, all of which have shown safety

76 superoxide concentrations and the effect of sumatriptan on each variable.

77 The effects of systemic sumatriptan on referred hypersensitivity were tested in

78 esion of the rACC or treatment with systemic sumatriptan or alphaCGRP(8-37) abolished RVM lidocaine-i

79 Co-administration of NXN-323 with sumatriptan over several days prevented the expression o

80 Following initiation of SD, sumatriptan pretreatment (300 microg kg(-1) i.v., 15 min

81 Sumatriptan regulation of CGRP gene expression did not c

82 Treatment with sumatriptan repressed NGF- and MAPK-stimulated CGRP prom

83 d (2) determining whether RVM application of sumatriptan reproduced the actions of systemic drug admi

84 increased after IS, remained elevated after sumatriptan; response threshold to heating of the skin,

85 Treatment with the drug sumatriptan returns CGRP levels to normal coincident wit

86 -4-yl)pyrrolo[3,2-b]pyrid-5-one (CP-93,129), sumatriptan, serotonin-5-O-carboxymethyl-glycyl -tyrosin

87 Sumatriptan significantly (Students t-test, P<0.05, two

88 and safety of a fixed-dose tablet containing sumatriptan succinate and naproxen sodium relative to ef

89 We analyzed data for sumatriptan succinate nasal spray and zolmitriptan, elet

90 Our findings suggest that sumatriptan suppresses either inflammatory or noninflamm

91 Sumatriptan treatment blocked NAc dopamine release in IM

92 The possible efficacy of sumatriptan was investigated in 2 models of visceral pai

93 Effects of sumatriptan within the rostral ventromedial medulla (RVM