Optically measured NADH concentrations are unaffected by propofol induced EEG silence during transient cerebral hypoperfusion in anesthetized rabbits.
Optically measured NADH concentrations are unaffected by propofol induced EEG silence during transient cerebral hypoperfusion in anesthetized rabbits.
复制标题
在麻醉兔子短暂脑灌注不足期间，光学测量的 NADH 浓度不受异丙酚诱导的 EEG 沉默的影响。
DOI：
10.1016/j.brainres.2011.04.002
复制
发表时间：
2011
期刊：
影响因子：
2.9
通讯作者：
Joshi,Shailendra
中科院分区：
文献类型：
--
作者：
Wang,Mei;Agarwal,Sachin;Mayevsky,Avraham;Joshi,Shailendra
术中麻醉的神经保护益处被广泛描述，并且常规目的是在预期短暂脑缺血时引起脑电图（EEG）沉默。先前的大鼠存活研究质疑在短暂性全脑灌注不足期间实现EEG沉默的额外益处。在氯胺酮-丙泊酚麻醉下，对12只新西兰白色家兔进行手术准备，包括放置颅骨螺钉用于双侧EEG监测，颅骨剃除用于激光多普勒探针，以及5 mm直径的右颞部颅骨切开术用于NADH探针。通过双侧颈内动脉阻断和经皮全身降压实现短暂性全脑低灌注。所有动物作为对照组，并在基线丙泊酚麻醉下进行脑灌注不足，并进行主动EEG。此后，将动物随机接受颈动脉内（3-5 mg）或静脉内（10-20 mg）推注1%丙泊酚，以创建EEG静默1-2 min。通过重复测量ANOVA和事后Bonferroni-Dunn检验分析在基线、峰值低灌注以及低灌注后5和10 min收集的数据。12只家兔中有11只完成了方案。所有动物的血流动力学和脑血流变化相当。与对照组相比，缺血期间NADH的增加不受静脉内或动脉内丙泊酚EEG沉默的影响。在短暂性全脑低灌注期间，我们未能观察到丙泊酚诱导的EEG沉默对NADH水平升高的任何显著额外衰减。这与先前的大鼠存活研究一致，该研究表明，硫喷妥钠麻醉的完全神经保护作用不需要EEG沉默。
The neuroprotective benefit of intra-operative anesthetics is widely described and routinely aimed to invoke electroencephalographic (EEG) silence in anticipation of transient cerebral ischemia. Previous rat survival studies have questioned an additional benefit from achieving EEG silence during transient global cerebral hypoperfusion. Surgical preparation on twelve New Zealand white rabbits under ketamine–propofol anesthesia, included placement of skull screws for bilateral EEG monitoring, skull shaving for laser Doppler probes, and a 5 mm diameter right temporal craniotomy for the NADH probe. Transient global cerebral hypoperfusion was achieved with bilateral internal carotid artery occlusion and pharmacologically induced systemic hypotension. All animals acted as controls, and had cerebral hypoperfusion under baseline propofol anesthesia with an active EEG. Thereafter, animals were randomized to receive bolus injection of intracarotid (3–5 mg) or intravenous (10–20 mg) 1% propofol to create EEG silence for 1–2 min. The data collected at baseline, peak hypoperfusion, and 5 and 10 min post hypoperfusion was analyzed by repeated measures ANOVA with post hoc Bonferroni–Dunn test. Eleven of the twelve rabbits completed the protocol. Hemodynamics and cerebral blood flow changes were comparable in all the animals. Compared to controls, the increase in NADH during ischemia was unaffected by EEG silence with either intravenous or intraarterial propofol. We failed to observe any significant additional attenuation of the elevation in NADH levels with propofol induced EEG silence during transient global cerebral hypoperfusion. This is consistent with previous rat survival studies showing that EEG silence was not required for full neuroprotective effects of pentothal anesthesia.