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首页> 外文期刊>Acute pain: international journal of acute pain management >Intranasal ketamine for acute pain
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Intranasal ketamine for acute pain

机译：鼻内氯胺酮治疗急性疼痛

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The physiology of the nasal mucosa makes it an ideal environment for rapid, non-invasive delivery of systemic drugs. Its large surface area, uniform temperature, high permeability and extensive vascularisationfacilitate rapid absorption of drugs into the bloodstream. A number of drugs in current clinical use are effective when administered intranasally. An extensive body of literature beginning soon after the approval of ketamine in the 1970s documents its effectiveness as an analgesic when given in low, subanesthetic doses. The drug has a rapid onset of action after intramuscular (IM), intravenous (IV) as well as intranasal (IN) dosing, the latter observations being based upon the presenter's clinical studies. IN ketamine is in development as a sole analgesic agent for acute pain, and also as an add-on to opioids for the treatment of cancer breakthrough pain. Ketamine's preservation of blood pressure and respiratory drive in hypovolemic, opioid-naive patients makes it a potentially attractive alternative to morphine or other opioids in civilian emergency, mass casualty or military settings. Practical IN ketamine analgesia requires a metered dose delivery system and drug formulation to provide a plasma concentration of 50-150 ng/ml. This range allows analgesia with relatively few serious psychological effects. An appropriate formulation can minimise neurotoxicityobserved in animal models in response to various NMDA antagonists including conventionally formulated ketamine.
机译：鼻粘膜的生理特性使其成为快速无创递送全身性药物的理想环境。其表面积大，温度均匀，通透性高和广泛的血管形成有助于药物快速吸收到血液中。鼻内给药目前在临床上使用的许多药物都是有效的。在1970年代氯胺酮获得批准后不久，大量文献开始报道，低剂量的亚麻醉剂给予氯胺酮作为止痛药是有效的。该药物在肌内（IM），静脉内（IV）和鼻内（IN）给药后起效迅速，后者的观察结果基于发表者的临床研究。 IN氯胺酮正在发展成为急性疼痛的唯一止痛药，并且是阿片类药物的附加药物，用于治疗癌症突破性疼痛。氯胺酮在低血容量，未使用阿片类药物的患者中可保持血压和呼吸驱动力，使其成为民用紧急情况，大规模伤亡或军事场合中吗啡或其他阿片类药物的潜在诱人替代品。实用的IN氯胺酮镇痛药需要定量给药系统和药物制剂，以提供50-150 ng / ml的血浆浓度。该范围允许镇痛相对较少的严重心理影响。适当的制剂可以最小化在动物模型中对各种NMDA拮抗剂（包括常规配制的氯胺酮）的反应所产生的神经毒性。

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