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1 ripheral nerve block or spinal clonidine, an alpha2-adrenergic agonist.
2 o assess anesthetic depth in the presence of alpha2-adrenergic agonists.
3 Stimulated release was inhibited by alpha(2)-adrenergic agonists.
5 ta-blockers, 4.01 (CrI, 0.48 to 7.43); 1995: alpha2-adrenergic agonists, 5.64 (CrI, 1.73 to 9.50); 19
9 as to investigate the effects of a selective alpha2-adrenergic agonist, alpha-methylnorepinephrine (a
12 that Muller cells are unique in response to alpha2-adrenergic agonists and imply a role for Muller c
13 0 microM NE or 62% by 2 microM UK-14,304, an alpha2-adrenergic agonist, and reduced 63% by 10 microM
16 romoter (Thy1-CFP mice) to determine how the alpha2-adrenergic agonist brimonidine influences loss of
18 mg/kg i.p.) after chronic treatment with the alpha2-adrenergic agonist clonidine (200 microg/kg per d
19 We therefore examined the effects of the alpha2-adrenergic agonist clonidine on mean arterial pre
20 amezole to rats chronically treated with the alpha2-adrenergic agonist clonidine triggers a powerful
21 onist, phenylephrine (PHE; 0.5 mg/kg BW), an alpha2-adrenergic agonist, clonidine (CLON; 0.6 mg/kg BW
22 pha2-adrenergic receptors because a specific alpha2-adrenergic agonist could substitute for epinephri
23 inoimidazolidines including analogues of the alpha2 adrenergic agonist drug clonidine is elaborated.
24 nd atomoxetine than for the extended-release alpha2-adrenergic agonists guanfacine or clonidine (no s
27 ntageous for treating hypertension over pure alpha(2)-adrenergic agonists (i.e., guanabenz) due to it
28 necrosis factor-alpha (TNF) as well as to an alpha(2)-adrenergic agonist in an area of the central ne
29 gonists and imply a role for Muller cells in alpha2-adrenergic agonist-induced photoreceptor protecti
31 es of this work were to study the effects of alpha2-adrenergic agonists on the inflammatory response
33 i.m. treatment with xylazine or UK14304, two alpha2-adrenergic agonists, reduced neutrophil migration
34 ults indicate that systemically administered alpha2-adrenergic agonists selectively activate ERKs in
36 xhibited similar sensitivity to the specific alpha(2)-adrenergic agonist UK 14,304, to serotonin, and
37 raarterial hindlimb infusion of the specific alpha2-adrenergic agonist UK 14,304 during KATP channel
38 ate the role and mechanisms of action of the alpha(2)-adrenergic agonist UK14,304 in the regulation o
42 l trauma, and systemic administration of the alpha(2)-adrenergic agonist xylazine, all of which have
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