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1 centers mediating the antipruritic effect of butorphanol.
2 or agonist/antagonists such as naltrexone or butorphanol.
3                       Rats were administered butorphanol (26 nmol microl(-1) h(-1)) by continuous int
4 ndent by intracerebroventricular infusion of butorphanol (26 nmol microliter-1 h-1) via osmotic minip
5  been intracerebroventricularly infused with butorphanol (26 nmol/1 microl/h) or U-69,593 (26 nmol/10
6 imine (nor-BNI)-precipitated withdrawal from butorphanol, (5alpha,7alpha,8beta)-(+)-N-methyl-N-[7-(1-
7 NTI did not reduce the orexigenic effects of butorphanol, an agonist that binds to both kappa- and mu
8 t were involved in the inhibition of itch by butorphanol and could represent potential targets for th
9 rphine > DAMGO = beta-endorphin > morphine > butorphanol, and the affinity of DAMGO in alkaloid- but
10                                              Butorphanol (BT), a mixed kappa- and mu-opioid receptor
11 rphine, DAMGO, beta-endorphin, morphine, and butorphanol, DAMGO-stimulated GTP[gamma-35S] binding was
12 tem is more susceptible to alteration during butorphanol dependence than is the adenylate cyclase sys
13 evels of glutamate in the LC of morphine- or butorphanol-dependent rats measured by in vivo microdial
14 binge eating to control levels, and although butorphanol did not trigger chow binge eating, it enhanc
15                                   Similarly, butorphanol increased phospho-p38-ir in hKOR-expressing
16 re prominent by 7 h after discontinuation of butorphanol infusion and suggest that NMDA binding sites
17 died at 2, 7, and 24 h after withdrawal from butorphanol infusion.
18 e rat brain following 7 h of withdrawal from butorphanol infusion.
19 wal was initiated by abrupt cessation of the butorphanol infusion.
20 d at 2, 7, and 24 h after discontinuation of butorphanol infusion.
21 sed with 26 nmol/microliter/h of morphine or butorphanol intracerebroventricularly (i.c.v.) via osmot
22 ophen (moderate SOE), antiemetics (low SOE), butorphanol (low SOE), and tramadol in combination with
23 e examined the effect of mixed-action opioid butorphanol on histamine itch, cowhage itch, and heat pa
24   Influences of continuous administration of butorphanol on the autoradiography of [3H]glutamate bind
25 GNTI did not alter the orexigenic effects of butorphanol or NPY.
26 C mediate withdrawal in animals dependent on butorphanol or U-69,593, but not on morphine.
27 e levels in the LC markedly increased in the butorphanol- or U-69,593-dependent rats within 60 min fo
28  observed following nor-BNI challenge in the butorphanol- or U-69,593-infused rats, with only minimal
29 phine >> morphine > fentanyl = oxymorphine > butorphanol = oxycodone = nalbuphine.
30              In comparison with the placebo, butorphanol produced a bilateral deactivation of claustr
31            We found that both nalbuphine and butorphanol produced significantly greater analgesia in
32 tic and orexigenic responses to naloxone and butorphanol, respectively, and by testing the ability of
33                                              Butorphanol suppressed the itch induced experimentally w
34  respectively, and by testing the ability of butorphanol to elicit binge eating of chow when palatabl
35 vealed that the reduction in cowhage itch by butorphanol was correlated with changes in cerebral perf
36                            Like pentazocine, butorphanol was equally efficacious at activating ERK1/2
37         The suppression of histamine itch by butorphanol was paralleled by the activation of nucleus
38 ntly kappa-opioid analgesics, nalbuphine and butorphanol; was compared in males and females who under
39  results demonstrate that the development of butorphanol withdrawal is more prominent by 7 h after di
40 ng were investigated to study the effects of butorphanol withdrawal on NMDA receptors.
41 ay more important role in the development of butorphanol withdrawal than that of channel blocking sit