ライフサイエンスコーパス: sumatriptan

1 ients responded to treatment with aspirin or sumatriptan.

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

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

4 ation persisted after pain was controlled by sumatriptan.

5 novascular neurons are directly inhibited by sumatriptan.

6 nitially decreased after IS, increased after sumatriptan.

7 itially dropped after IS, remained low after sumatriptan.

8 f after treatment with the antimigraine drug sumatriptan.

9 t continued to have an excellent response to sumatriptan.

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

11 eurons by the serotonergic antimigraine drug sumatriptan.

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

13 which predicts the antimigraine efficacy of sumatriptan.

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

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

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

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

18 1.59 (1.18 to 2.17) to 2.44 (1.75 to 3.45)), sumatriptan (1.35 (1.03 to 1.75) to 2.04 (1.49 to 2.86))

19 Sumatriptan 100 mg orally and 6 mg subcutaneously aborte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 Sumatriptan administered into the RVM similarly produced

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

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

38 antagonists blocked the repression caused by sumatriptan and eletriptan.

39 Oral sumatriptan and naratriptan are effective as short-term

40 s, including drugs like morphine, metformin, sumatriptan, and fenoterol.

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

42 Overall, eletriptan, rizatriptan, sumatriptan, and zolmitriptan had the best profiles and

43 e events, and certain triptans (rizatriptan, sumatriptan, and zolmitriptan) were also associated with

44 Sumatriptan appears to decrease the amplitude of nitric

45 Sumatriptan blunted the increase in blood flow following

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

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

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

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

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

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

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

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

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

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

56 We found that sumatriptan effectively prevented the induction of sensi

57 (1B/D) agonists, including the triptan drugs sumatriptan, eletriptan, and rizatriptan that are used f

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

59 Sumatriptan had no effect on the number of depolarisatio

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

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

62 Late sumatriptan intervention counteracted two aspects of cen

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

64 Early sumatriptan intervention effectively blocked the develop

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

66 Sumatriptan is used specifically to relieve headache pai

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

68 ilar between sumatriptan-naproxen sodium and sumatriptan monotherapy.

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

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

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

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

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

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

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

76 Sumatriptan-naproxen sodium was more effective than plac

77 2- to 24-hour sustained pain-free response, sumatriptan-naproxen sodium was superior at P<.01 (25% a

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

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

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

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

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

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

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

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

86 Sumatriptan prevented periorbital allodynia when adminis

87 Sumatriptan regulation of CGRP gene expression did not c

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

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

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

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

92 -4-yl)pyrrolo[3,2-b]pyrid-5-one (CP-93,129), sumatriptan, serotonin-5-O-carboxymethyl-glycyl -tyrosin

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

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

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

96 Our findings suggest that sumatriptan suppresses either inflammatory or noninflamm

97 Sumatriptan treatment blocked NAc dopamine release in IM

98 scriptomic data revealed pathways related to sumatriptan treatment, i.e. '5HT1 type receptor mediated

99 ucturally diverse substrates like metformin, sumatriptan, trospium, and fenoterol.

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

101 Effects of sumatriptan within the rostral ventromedial medulla (RVM