Talk:Etomidate: Difference between revisions

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Etomidate is an imidazole-derived, non-barbiturate, short-acting intravenous anesthetic. The etomidate distribution model conforms to the three-compartment drug distribution model, and the distribution volume is 2.2-4.5L/kg. Because of its high binding capacity to serum proteins and rapid drug metabolism, the time-dose-related half-life does not extend significantly with continuous infusion. It is not only suitable for single administration during induction, but also for intraoperative maintenance. The site of action of intravenous anesthetics is generally related to gamma-aminobutyric acid, and the important target of etomidate's molecular mechanism of action is the GABA-A receptor.
Etomidate is an imidazole-derived, non-barbiturate, short-acting intravenous anesthetic. The etomidate distribution model conforms to the three-compartment drug distribution model, and the distribution volume is 2.2-4.5L/kg. Because of its high binding capacity to serum proteins and rapid drug metabolism, the time-dose-related half-life does not extend significantly with continuous infusion. It is not only suitable for single administration during induction, but also for intraoperative maintenance. The site of action of intravenous anesthetics is generally related to gamma-aminobutyric acid, and the important target of etomidate's molecular mechanism of action is the GABA-A receptor.


Forman found in experimental studies that different concentrations of etomidate act on GABA-A receptors in different ways. Commonly used doses of etomidate are similar to GABA-A receptor agonists, prolonging the decay time of postsynaptic inhibitory currents, lengthening the duration of inhibition, and also activating extrasynaptic GABA receptors. Excessive doses of etomidate act directly on GABA-A receptors and are similar to GABA allosteric activators. Studies have found that etomidate not only acts on GABA receptors, but also on α-2β adrenergic receptors, thereby causing vasoconstriction and maintaining hemodynamic stability.
Forman found in experimental studies that different concentrations of etomidate act on GABA-A receptors in different ways. Commonly used doses of etomidate are similar to GABA-A receptor agonists, prolonging the decay time of postsynaptic inhibitory currents, lengthening the duration of inhibition, and also activating extrasynaptic GABA receptors. Excessive doses of etomidate act directly on GABA-A receptors and are similar to GABA allosteric activators. Studies have found that etomidate not only acts on GABA receptors, but also on α-2β adrenergic receptors, thereby causing vasoconstriction and maintaining hemodynamic stability.<ref>[https://www.sohu.com/a/343157114_668064#google_vignette 依托咪酯持续输注在临床中的应用], additional text.</ref>
==Subjective effects==
==Subjective effects==
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