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为什么是氯胺酮。

Why ketamine.

机构信息

Center for Orphan Drug Research, Department of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, MN, United States.

Department of Neurology, Massachusetts General Hospital, Boston, MA, United States.

出版信息

Epilepsy Behav. 2023 Apr;141:109066. doi: 10.1016/j.yebeh.2022.109066. Epub 2023 Jan 4.

Abstract

We present the rationale for testing ketamine as an add-on therapy for treating benzodiazepine refractory (established) status epilepticus. In animal studies, ketamine terminates benzodiazepine refractory status epilepticus by interfering with the pathophysiological mechanisms and is a neuroprotectant. Ketamine does not suppress respiration when used for sedation and anesthesia. A Series of reports suggest that ketamine can help terminate refractory and super refractory status epilepticus. We propose to use 1 or 3 mg/Kg ketamine intravenously based on animal-to-human conversion and pharmacokinetic studies. This paper was presented at the 8th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures held in September 2022.

摘要

我们提出了将氯胺酮作为附加治疗药物治疗苯二氮䓬类药物难治性(已确立)癫痫持续状态的理由。在动物研究中,氯胺酮通过干扰病理生理机制终止苯二氮䓬类药物难治性癫痫持续状态,并且是一种神经保护剂。氯胺酮在用于镇静和麻醉时不会抑制呼吸。一系列报告表明,氯胺酮可以帮助终止难治性和超难治性癫痫持续状态。我们建议根据动物到人转化和药代动力学研究,静脉内使用 1 或 3 mg/Kg 氯胺酮。本文于 2022 年 9 月在第八届伦敦因斯布鲁克癫痫持续状态和急性发作学术研讨会上发表。

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本文引用的文献

1
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