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1 gonists, such as yohimbine, rauwolscine, and atipamezole.
2 ect which was prevented by pretreatment with atipamezole.
3 ter than those following dexmedetomidine and atipamezole.
4                            Pretreatment with atipamezole (0.25 mg/kg, IV) fully blocked the hypoxic e
5                                              Atipamezole (1 mg/kg, s.c.) or vehicle (sterile saline)
6 of the specific alpha2-adrenergic antagonist atipamezole (1.5 mg/kg i.p.) after chronic treatment wit
7          Apparent K(b) values calculated for atipamezole (1.7 nM), MK-912 (4.8 nM), BRL-44408 (15 nM)
8 rmined for the selective alphaAR antagonists atipamezole (8.79), rauwolscine (7.75), 2-(2,6-dimethoxy
9                                              Atipamezole, a selective alpha-2 adrenergic antagonist,
10 ore the treatment potential of naloxone plus atipamezole, a selective alpha2-adrenoceptor antagonist,
11  increasing central noradrenergic tone using atipamezole, an alpha-2 adrenoceptor antagonist, could i
12 ors was demonstrated in rats pretreated with atipamezole, an alpha2 adrenoceptor antagonist.
13                      In rats pretreated with atipamezole and in alpha2AC KO mice, (11)C tracer bindin
14 The anesthetic was immediately reversed with atipamezole, and the animals quickly recovered.
15  selective alpha(2)-adrenoceptor antagonist, atipamezole (ATZ).
16 d initial brain hypoxia, but only naloxone + atipamezole decreased the prolonged weaker hypoxia.
17                 Both naloxone and naloxone + atipamezole, delivered at the peak of brain hypoxia (3 m
18 followed by atipamezole injection (clonidine-atipamezole) demonstrated dramatic behavioral effects in
19 of the thoracic spinal cord in the clonidine-atipamezole group compared to a sham-operated atipamezol
20 ells was elevated 8-10-fold in the clonidine-atipamezole group compared to the other groups.
21                  The brains of the clonidine-atipamezole group showed massive c-Fos expression (espec
22 se over background in selected areas (saline-atipamezole group).
23 NE or of the alpha2-adrenoceptor antagonist, atipamezole, in the mouse amygdala produces localized ex
24                                              Atipamezole injected 10 min after a single injection of
25 tipamezole group compared to a sham-operated atipamezole-injected group.
26 eated chronically with clonidine followed by atipamezole injection (clonidine-atipamezole) demonstrat
27 te that combined treatment with naloxone and atipamezole is more effective than naloxone alone in rev
28                            Pretreatment with atipamezole + naloxone was more potent than naloxone alo
29 sedative dexmedetomidine, and its antagonist atipamezole, on spontaneous brain dynamics and auditory
30 e or absence of a2 adrenoceptor antagonists, atipamezole or yohimbine, or an a2A adrenoceptor antagon
31                            Animals receiving atipamezole plus rehabilitation exhibited significantly
32 ptor antagonists (propranolol, prazosin, and atipamezole: PPA), enhanced glymphatic flow and effectiv
33 nists of alpha(1)- (terazosin) or alpha(2)- (atipamezole) receptors or of either the partial alpha(1)
34 a 2-AR-selective antagonists, rauwolscine or atipamezole, reversed the functional effects of dexmedet
35  (saline-saline, clonidine-saline and saline-atipamezole) showed no overt unusual behavioral effects
36 istration of the selective alpha2-antagonist atipamezole to rats chronically treated with the alpha2-
37  receptor-like immunoreactivity in clonidine-atipamezole treated (withdrawing) rats.
38                                   Naloxone + atipamezole treatment should be considered in preventing
39 y were abolished by alpha(2) -AR antagonist (atipamezole), which was partly reversed by the PI3K agon
40             Interestingly, animals receiving atipamezole without rehabilitation exhibited a significa
41       Intracerebroventricular application of atipamezole, yohimbine or BRL-44408 blocked the protecti