Reicher D, Bhalla P, Rubinstein E H
Stroke. 1987 Mar-Apr;18(2):445-9. doi: 10.1161/01.str.18.2.445.
To analyze the mechanism of the cerebral vasodilator effect of ketamine in anesthetized rabbits, we measured the internal carotid blood flow with an electromagnetic flowmeter, the arterial pressure, intracranial pressure, end-tidal CO2, and the electroencephalogram. Ketamine injection (1 mg/kg) induced a significant cerebral vasodilatation that was blocked by scopolamine, a cholinergic antagonist. In contrast, the increase in cerebral blood flow after ketamine was additive to the cerebral vasodilator actions of inhaled CO2 and of physostigmine infusion, two procedures that activate cholinergic mechanisms. These observations suggest that in rabbits, ketamine activates a cholinergic cerebral vasodilator system.
为分析氯胺酮对麻醉兔脑的血管舒张作用机制，我们用电磁流量计测量颈内动脉血流量、动脉压、颅内压、呼气末二氧化碳分压及脑电图。注射氯胺酮（1毫克/千克）可引起显著的脑血管舒张，这一作用被胆碱能拮抗剂东莨菪碱所阻断。相反，氯胺酮引起的脑血流量增加与吸入二氧化碳和输注毒扁豆碱这两种激活胆碱能机制的脑舒张血管作用相加。这些观察结果表明，在兔体内，氯胺酮激活了胆碱能性脑血管舒张系统。
