Correlation between tissue depolarizations and damage in focal ischemic rat brain
Correlation between tissue depolarizations and damage in focal ischemic rat brain
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DOI：
10.1016/s0006-8993(99)01769-2
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发表时间：
1999-09-04
期刊：
影响因子：
2.9
通讯作者：
Nicolay, K
中科院分区：
文献类型：
--
作者：
Dijkhuizen, RM;Beekwilder, JP;Nicolay, K
缺血诱导的去极化可能在脑缺血损伤的发生发展中起关键作用。我们的目标是评估局灶性缺血中组织去极化和组织损伤之间的关系。我们进行了多电极皮层直流（DC）电位记录，随后在i）皮层应用KCl和ii）大鼠永久性和短暂性大脑中动脉（MCA）闭塞后，对大鼠进行了弥散加权和T-2加权磁共振成像（MRI）。皮质KCl应用在同侧半球上每小时诱导10.0 +/-2.2次瞬时负DC电位偏移（即皮质扩散性抑制）（n = 4）。在6小时的永久性MCA闭塞（n = 9）1-10直流电位的变化，观察到依赖于大脑的位置。缺血中心出现缺氧性去极化。缺血区以外的DC电位变化类似于皮层扩散性抑制。皮层缺血边缘区的去极化也是短暂的，但通常是持久的。MCA闭塞后1（n = 5）或3 h（n = 6）诱导的再灌注导致2.9 +/-15 min的复极。7 h后的缺血病变体积（根据弥散加权和T-2加权MRI图像计算）与皮质病灶周围区的总去极化时间显著相关（R = 0.741，p < 0.05），但与去极化次数无关。从水扩散系数和T-2的变化测量的缺血性损伤的程度也与去极化的总时间显著相关（R分别为0.762和0.738，p < 0.01）。我们得出结论，早期缺血性组织损伤与组织去极化的总持续时间有关，而与去极化的频率无关。(C)1999 Elsevier Science B. V.保留所有权利。
Ischemia-induced depolarizations may play a key role in the development of cerebral ischemic injury. Our goal was to assess the relationship between tissue depolarizations and tissue damage in focal ischemia. We performed multi-electrode cortical direct current (DC) potential recording and, subsequently, diffusion-weighted and T-2-weighted magnetic resonance imaging (MRI) in rats after i) cortical application of KCI, and ii) permanent and transient middle cerebral artery (MCA)-occlusion in rats. Cortical KCI application induced 10.0 +/- 2.2 transient negative DC potential shifts per h on the ipsilateral hemisphere (i.e. cortical spreading depressions) (n = 4). During 6 h of permanent MCA-occlusion (n = 9) 1-10 DC potential shifts were observed, dependent on the brain location. Anoxic depolarization developed in the ischemic core. Outside ischemic areas DC potential shifts resembled cortical spreading depressions. Depolarizations in cortical ischemic borderzones were also transient, but generally long-lasting. Reperfusion induced 1 (n = 5) or 3 h (n = 6) after MCA-occlusion resulted in repolarization in 2.9 +/- 1 5 min. Ischemic lesion volumes after 7 h, calculated from diffusion-weighted and T-2-weighted MR images, correlated significantly with total depolarization time in cortical perifocal zones (R = 0.741, p < 0.05), but not with the number of depolarizations. The extent of ischemic damage, as measured from alterations in the water diffusion coefficient and T-2, was also significantly related to the total time of depolarization (R = 0.762 and 0.738, respectively, p < 0.01). We conclude that early ischemic tissue injury is related to the total duration of tissue depolarization and not to the frequency of depolarizations. (C) 1999 Elsevier Science B.V. All rights reserved.