纳洛酮对大鼠前脑缺血所致神经功能缺损的影响。

Naloxone effect on the neurological deficit induced by forebrain ischemia in rats.

作者信息

Capdeville C, Pruneau D, Allix M, Plotkine M, Boulu R G

出版信息

Life Sci. 1986 Feb 3;38(5):437-42. doi: 10.1016/0024-3205(86)90068-8.

Abstract

The effect of naloxone upon neurologic deficit was evaluated in a model of transient forebrain ischemia in rats. Awake male Wistar rats were subjected to a 30 minute ischemia by occluding both common carotid arteries 8 days after cauterizing vertebral arteries. Administration of naloxone 1 or 5 mg/kg iv 10 minutes after carotid occlusion or 1 mg/kg iv one hour after clamp removal failed to reduce immediate and tardive neurologic postischemic deficits. On the other hand, in rats treated by a dose of 1 mg/kg naloxone 10 minutes after carotid occlusion and perfused with an additional dose of 2 mg/kg/h for 80 minutes, neurologic score was improved one hour after ischemia. However mortality was not decreased whatever was the modality of naloxone administration. This result confirms previous data showing that naloxone exerts a protective effect when given at sufficiently high dosage.

摘要

在大鼠短暂性前脑缺血模型中评估了纳洛酮对神经功能缺损的影响。在烧灼椎动脉8天后，清醒雄性Wistar大鼠通过结扎双侧颈总动脉进行30分钟的缺血处理。在颈动脉闭塞后10分钟静脉注射1或5mg/kg纳洛酮，或在移除动脉夹1小时后静脉注射1mg/kg纳洛酮，均未能减轻缺血后即刻和延迟的神经功能缺损。另一方面，在颈动脉闭塞后10分钟给予1mg/kg纳洛酮治疗并额外以2mg/kg/h灌注80分钟的大鼠中，缺血1小时后神经评分有所改善。然而，无论纳洛酮的给药方式如何，死亡率均未降低。这一结果证实了先前的数据，即纳洛酮在给予足够高剂量时具有保护作用。