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1 when treated with indiplon, a GABAA receptor alpha1 agonist.
2 not after administration of beta1, beta2, or alpha1 agonists.
3       In this model, epinephrine through its alpha1-agonist action had adverse effects on cerebral mi
4 us noradrenaline release), phenylephrine (an alpha1 agonist) and clonidine (an alpha2 agonist) in 10
5 enous noradrenaline release), phenylephrine (alpha1-agonist) and clonidine (alpha2-agonist) were asse
6  noradrenaline (NA) release), phenylephrine (alpha1-agonist) and dexmedetomidine (alpha2-agonist) wer
7 genous NE release), phenylephrine (selective alpha1-agonist), and clonidine (alpha2-agonist) were det
8  survival is reduced following withdrawal of alpha1-agonist, and support the hypothesis that Tg/Galph
9                              Midodrine is an alpha1-agonist approved for orthostatic hypotension.
10 erestingly, LTD can be induced when M(1) and alpha1 agonists are coapplied at concentrations too low
11 er cells, LNCaP, to either quinazoline-based alpha1-agonist by androgens.
12                                           An alpha1-agonist could not substitute for epinephrine in p
13 noclonal antibody to Galphah/Tg reveals that alpha1-agonist deprivation during culture of VZ cells in
14 ntra-arterial infusion of phenylephrine (PE; alpha1 -agonist) during ATP or control vasodilatator inf
15      Methoxamine (10(-9) to 10(-5) mol/L, an alpha1-agonist) had no effect, whereas U44619, a thrombo
16 ulation combined with alpha2 antagonists and alpha1 agonists in a mixture to reinstate neonatal level
17 onstriction with different vasoconstrictors (alpha1-agonist methoxamine, endothelin [ET-1], phorbol e
18              The response of patients to the alpha1-agonist midodrine supports the hypothesis of part
19 -agonist) and phenylephrine (PE, a selective alpha1-agonist) on spontaneous and D,L-homocysteic acid
20 -agonist oxymetazoline (5 microM), while the alpha1-agonist phenylephrine (100 microM) caused only a
21 s) challenged with a dose-response using the alpha1-agonist phenylephrine (PE), with and without the
22 ulated during intraarterial infusions of the alpha1-agonist phenylephrine and the alpha2-agonist clon
23 entricular zone (VZ) germinal cells with the alpha1-agonist phenylephrine during development in vitro
24 ss sensitive to metabolic inhibition than an alpha1-agonist, phenylephrine (PE), in the exercising hu
25  NE, the beta-agonist, isoproterenol, or the alpha1-agonist, phenylephrine, were infused into the MPO
26 l dysautonomia and indicates that the use of alpha1-agonists to pharmacologically replace lower-extre