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1 n and cardiovascular and airway effects with desflurane.
2  [161-176]) > sevoflurane (164% [150-177]) > desflurane (119% [109-129]).
3  during stepwise reduction of the anesthetic desflurane (6%, 4%, 2%, and 0%).
4 hy were enhanced by surgery as compared with desflurane alone.
5 matched 3xTgAD and WT mice exposed to air or desflurane alone.
6 However, treatment with a combination of 12% desflurane and hypoxia (18% O(2)) (desflurane/hypoxia) f
7    Here, we set out to assess the effects of desflurane and hypoxia on caspase activation, amyloid pr
8  the favorable binding enthalpy observed for desflurane and isoflurane, with an opposing increase of
9  reduction strategies including avoidance of desflurane and occupancy-based ventilation have the pote
10                         Rapid recovery after desflurane and single-breath inductions with sevoflurane
11   In contrast, several volatile (isoflurane, desflurane) and i.v. (propofol) general anesthetics exci
12                               Recovery after desflurane anesthesia is more rapid than with the other
13 r disease (3xTgAD) and C57BL/6 WT mice under desflurane anesthesia.
14 mine, inhalational anaesthetics (isoflurane, desflurane), antiepileptic drugs (topiramate, lacosamide
15 ional agents, usage costs of sevoflurane and desflurane are 10 and 25 times, respectively, that of is
16  of emergence delirium after sevoflurane and desflurane are discussed.
17 tile anesthetics isoflurane, sevoflurane and desflurane at clinically relevant concentrations did not
18 ession systems, sevoflurane, isoflurane, and desflurane at subsurgical concentrations potentiated del
19                                  In summary, desflurane can induce Abeta production and caspase activ
20                              Sevoflurane and desflurane continue to challenge our abilities to anesth
21  that underwent surgery compared with air or desflurane controls persisted to at least 14 weeks after
22  INTERPRETATION: These findings suggest that desflurane could be a safer anesthetic for AD patients a
23                                              Desflurane did not induce behavioral hyperactivity and i
24                      Finally, the anesthetic desflurane does not induce activation of mitochondrial p
25 eceived 2% sevoflurane, 1% isoflurane, or 6% desflurane for 10 minutes.
26 librium association constants (K(a) values): desflurane > isoflurane approximately enflurane > haloth
27 he inhalation anesthetic isoflurane, but not desflurane, has been shown to induce caspase activation
28                              Sevoflurane and desflurane have important advantages over isoflurane and
29                                 Propofol and desflurane have reliable anticonvulsant effects, whereas
30                                              Desflurane/hypoxia also increased levels of beta-site AP
31 on of 12% desflurane and hypoxia (18% O(2)) (desflurane/hypoxia) for 6 h induced caspase-3 activation
32                                 In addition, desflurane/hypoxia-induced Abeta generation could be red
33 8 attenuated caspase-3 activation induced by desflurane/hypoxia.
34 ual cortex of rodents during anesthesia with desflurane in vivo.
35        Here we show that isoflurane, but not desflurane, induces opening of mitochondrial permeabilit
36                                              Desflurane is one of the most commonly used inhalation a
37 on of closely related anesthetic haloethers (desflurane, isoflurane, enflurane, and sevoflurane), a h
38                                  Neither 12% desflurane nor hypoxia (18% O(2)) alone affected caspase
39                      However, the effects of desflurane on AD neuropathogenesis have not been previou
40  out to assess the effects of isoflurane and desflurane on mitochondrial function, cytotoxicity, lear
41 tions of isoflurane, halothane, sevoflurane, desflurane or the nonimmobilizer 1,2-dichlorohexafluoroc
42 ents (isoflurane (IF), sevoflurane (SF), and desflurane) or MF were added to rat proximal tubular seg
43 ly nondefluorinated inhalational anesthetic (desflurane) or with a nonfluorinated anesthetic (pentoba
44 omparative account of three key anesthetics (desflurane, propofol, and ketamine) when used under iden
45                          Preferential use of desflurane resulted in a ten-fold difference in anaesthe
46                     Molecular simulations of desflurane reveal a binding pathway to GLIC via a membra
47 s of isoflurane, sevoflurane, enflurane, and desflurane sensitize TRPV1 to capsaicin and protons and
48 f TASK-3 to several anesthetics (isoflurane, desflurane, sevoflurane, halothane, alpha-chloralose, 2,
49 t comparable tubular necrosis, resulted with desflurane use.
50 ced by isoflurane, halothane, sevoflurane or desflurane was 221, 173, 184 and 929 microM, respectivel
51 ion anesthetics isoflurane, sevoflurane, and desflurane when used in routine clinical practice.
52 n studies using sevoflurane, isoflurane, and desflurane, which poorly quench tryptophan fluorescence,
53 ple entropy, and EMG activity occurred in 6% desflurane with 40.0% frequency.
54  expensive than administering sevoflurane or desflurane with premedication using antiemetics.