EFFECT OF LIDOCAINE ON DYNAMIC CHANGES IN CORTICAL REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE FLUORESCENCE DURING TRANSIENT FOCAL CEREBRAL ISCHEMIA IN RATS
EFFECT OF LIDOCAINE ON DYNAMIC CHANGES IN CORTICAL REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE FLUORESCENCE DURING TRANSIENT FOCAL CEREBRAL ISCHEMIA IN RATS
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DOI：
10.1016/j.neuroscience.2013.01.010
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发表时间：
2013-04-03
期刊：
影响因子：
3.3
通讯作者：
Morita, K.
中科院分区：
文献类型：
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作者：
Naito, H.;Takeda, Y.;Morita, K.
结扎大鼠左侧大脑中动脉和双侧颈总动脉，造成局灶性脑缺血90min。通过测量直流电(DC)电位和紫外线照射下还原型烟酰胺腺嘌呤二核苷酸(NADH)的荧光强度，分析脑缺血区形成的动态变化。利多卡因组(n=10)，于缺血前30min静脉推注利多卡因1.5 mg/kg，然后以2 mg/kg/h持续输注150min。对照组(n=10)给予等量生理盐水。脑缺血后，两组大鼠大脑中动脉区均迅速形成高强度NADH荧光区，DC电位呈缺血型去极化。NADH荧光增强与DC去极化密切相关。两组边缘区血流量均有相似的下降。缺血5min后，利多卡因组NADH高强度荧光面积明显缩小(为对照组的67%，P=0.01)。这可能是由于利多卡因阻断电压依赖性钠通道而抑制了缺血去极化。虽然利多卡因不能减少缺血时心肌梗死侧的去极化数目，但利多卡因组在缺血结束时(对照组的78%；P=0.046)和24 h后(P=0.02)，高信号面积和梗死体积均明显小于对照组。Logistic回归分析表明，缺血去极化时间与组织学损伤之间存在关系，当去极化时间相同时，给予利多卡因并不能减轻神经元损伤。这些发现表明，利多卡因减少脑梗塞体积的机制主要是通过减少经历NADH荧光增强的大脑区域，这与去极化密切相关。(C)2013年IBRO。爱思唯尔有限公司出版。保留所有权利。
Rats were subjected to 90 min of focal ischemia by occluding the left middle cerebral and both common carotid arteries. The dynamic changes in the formation of brain ischemic areas were analyzed by measuring the direct current (DC) potential and reduced nicotinamide adenine dinucleotide (NADH) fluorescence with ultraviolet irradiation. In the lidocaine group (n = 10), 30 min before ischemia, an intravenous bolus (1.5 mg/kg) of lidocaine was administered, followed by a continuous infusion (2 mg/kg/h) for 150 min. In the control group (n = 10), an equivalent amount of saline was administered. Following the initiation of ischemia, an area of high-intensity NADH fluorescence rapidly developed in the middle cerebral artery territory in both groups and the DC potential in this area showed ischemic depolarization. An increase in NADH fluorescence closely correlated with the DC depolarization. The blood flow in the marginal zone of both groups showed a similar decrease. Five minutes after the onset of ischemia, the area of high-intensity NADH fluorescence was significantly smaller in the lidocaine group (67% of the control; P = 0.01). This was likely due to the suppression of ischemic depolarization by blockage of voltage-dependent sodium channels with lidocaine. Although lidocaine administration did not attenuate the number of pen-infarct depolarizations during ischemia, the high-intensity area and infarct volume were significantly smaller in the lidocaine group both at the end of ischemia (78% of the control; P = 0.046) and 24 h later (P = 0.02). A logistic regression analysis demonstrated a relationship between the duration of ischemic depolarization and histologic damage and revealed that lidocaine administration did not attenuate neuronal damage when the duration of depolarization was identical. These findings indicate that the mechanism by which lidocaine decreases infarct volume is primarily through a reduction of the brain area undergoing NADH fluorescence increases which closely correlates with depolarization. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.