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1 ted by clinically relevant concentrations of inhaled anesthetics.
2 lly relevant targets for clinical actions of inhaled anesthetics.
3 els, which helps explain how closely related inhaled anesthetics achieve specific actions and suggest
4 ons may represent a fundamental mechanism of inhaled anesthetic action.
5 ecular volume is an important determinant of inhaled anesthetic activity at the GABA(A) receptor.
6 ments, T1 measurements obtained with several inhaled anesthetic agents and propofol dissolved in sali
7                All exposed children received inhaled anesthetic agents, and anesthesia duration range
8   Ligand-gated ion channels are a target for inhaled anesthetics and alcohols in the central nervous
9 specific or nonspecific interactions between inhaled anesthetics and proteins are more likely to unde
10 ther the weak molecular interactions between inhaled anesthetics and proteins, we studied the charact
11 inergic neurons, immobilizing actions of the inhaled anesthetics and sedative effects of halothane we
12                                              Inhaled anesthetics are a chemically diverse collection
13                                          The inhaled anesthetics are low affinity volatile compounds
14                        Physiologic sites for inhaled anesthetics are presumed to be cavities within t
15                                              Inhaled anesthetics are thought to alter the conformatio
16 chanism(s) and site(s) of action of volatile inhaled anesthetics are unknown in spite of the clinical
17 tance of aromatic residues as one feature of inhaled anesthetic binding sites.
18                            Here we show that inhaled anesthetics (chloroform and isoflurane) activate
19                                Halothane, an inhaled anesthetic, destabilizes the folded structure of
20 e molecular substrates for select actions of inhaled anesthetics; for immobilization, which is spinal
21 ein the location of the binding site for the inhaled anesthetic halothane at the amino acid residue l
22                                          The inhaled anesthetics halothane and isoflurane potentiate
23 nstrictors during concomitant exposure to an inhaled anesthetic (halothane); and b) to determine if e
24  nuclei, but causal investigations of potent inhaled anesthetics have not been conducted.
25 y was used to define the kinetics with which inhaled anesthetics interact with (Aalpha(2)-L1M/L38M)(2
26                               Similarly, the inhaled anesthetic isoflurane triggered a persistent inc
27 linically relevant concentrations of another inhaled anesthetic, isoflurane.
28                                  Halogenated inhaled anesthetics modulate voltage-gated ion channels
29 l membrane proteins are potential targets of inhaled anesthetics, most currently favored membrane pro
30                         Molecular targets of inhaled anesthetics must be represented in the group tha
31 ) M(-1), higher than any previously reported inhaled anesthetic-protein interaction.
32 rrent study investigated whether PreCon with inhaled anesthetic sevoflurane (SF-PreCon) remains cardi
33 led novel activation of K(v) channels by the inhaled anesthetic sevoflurane.
34  Previous work suggested that n-alcohols and inhaled anesthetics stabilize the closed state of the Sh
35                     Alkanols and halogenated inhaled anesthetics such as halothane and isoflurane inh
36 onstrate specific and discrete binding of an inhaled anesthetic to a mammalian-soluble protein, and f
37  is thought to involve the direct binding of inhaled anesthetics to ligand-gated ion channels.
38                 Saturable binding of various inhaled anesthetics to serum albumin has been shown with