Shokunbi M T, Gelb A W, Wu X M, Miller D J
Division of Neurosurgery, University of Western Ontario, London, Canada.
Stroke. 1990 Jan;21(1):107-11. doi: 10.1161/01.str.21.1.107.
We measured somatosensory evoked potentials, infarct size, and cerebral blood flow in 20 cats subjected to occlusion of the middle cerebral artery for 3 hours, followed by an equal period of reperfusion. The cats were randomized into a treatment group that received a continuous infusion of 2 mg/kg lidocaine hydrochloride or a control group that received an equivalent volume of normal saline. All 10 treated cats retained measurable evoked potentials throughout the experiment. In five control cats, evoked potentials disappeared completely at some point during the occlusion (difference between groups significant at p less than 0.001). Mean amplitude of the major cortical wave in the nine treated cats with cerebral infarcts was higher than that of the nine corresponding controls (p less than 0.05). Lidocaine reduced the mean +/- SEM size of the infarcts from 30.1 +/- 6.0% in the control group to 14.7 +/- 4.9% in the treated group (p less than 0.05). As blood flow was reduced in the infarct and peri-infarct zones in the control but not the treated cats, our results suggest that the beneficial effects of lidocaine may be due to preservation of blood flow in the ischemic zone.
我们对20只猫进行了体感诱发电位、梗死灶大小和脑血流量的测量。这些猫先接受大脑中动脉闭塞3小时，随后再进行同等时长的再灌注。猫被随机分为两组，治疗组持续输注2mg/kg盐酸利多卡因，对照组输注等量生理盐水。在整个实验过程中，所有10只接受治疗的猫均保留了可测量的诱发电位。5只对照猫在闭塞过程中的某个时间点诱发电位完全消失（两组间差异在p<0.001时具有统计学意义）。9只患有脑梗死的治疗猫的主要皮质波平均振幅高于9只相应的对照猫（p<0.05）。利多卡因使梗死灶的平均±标准误大小从对照组的30.1±6.0%降至治疗组的14.7±4.9%（p<0.05）。由于对照组而非治疗组猫的梗死灶和梗死灶周围区域血流减少，我们的结果表明利多卡因的有益作用可能归因于缺血区血流的保留。
