CORTICAL NEGATIVE DC DEFLECTIONS FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION AND KCL-INDUCED SPREADING DEPRESSION - EFFECT ON BLOOD-FLOW, TISSUE OXYGENATION, AND ELECTROENCEPHALOGRAM
CORTICAL NEGATIVE DC DEFLECTIONS FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION AND KCL-INDUCED SPREADING DEPRESSION - EFFECT ON BLOOD-FLOW, TISSUE OXYGENATION, AND ELECTROENCEPHALOGRAM
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DOI：
10.1038/jcbfm.1994.3
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发表时间：
1994-01-01
影响因子：
6.3
通讯作者：
HOSSMANN, KA
中科院分区：
文献类型：
--
作者：
BACK, T;KOHNO, K;HOSSMANN, KA
在缺血性脑损伤的外周，出现短暂的扩散性抑郁样直流电（DC）偏转，这可能对确定缺血性梗死体积具有病理生理学意义。这些偏转对脑血流量，组织氧分压，和电生理的影响进行了研究，在大鼠提交到大脑中动脉（MCA）的管腔内线闭塞，并与氯化钾（KCl）诱导的扩散性抑制的完整动物的变化进行了比较。MCA闭塞后，MCA区域周边的皮质激光多普勒血流（LDF）立即急剧下降至对照组的35 +/- 14%（平均值+/- SD; p < 0.05），组织PO 2从28 +/- 4下降至21 +/- 3 mm Hg（p < 0.05），EEG功率下降至与对照组相似的80%。在7小时的阻塞期间，以不规则的间隔发生3-11次DC偏转，平均持续时间为5.2 +/- 4.8分钟，并且EEG功率逐渐下降至对照的66 +/- 16%（p < 0.05）。在DC偏转的过程中，LDF没有变化，但PO 2进一步下降到19 +/- 4 mm Hg（p < 0.05）。KCl诱导的完整大鼠的去极化显著缩短（1.4 +/- 0.5 min; p < 0.05），并伴随着LDF增加43%（p < 0.05）和组织PO 2轻微但显著的增加，从22 +/- 4 mmHg增加到25 +/- 4 mmHg（p < 0.05）。梗死周围和KCl诱导的去极化的比较表明，氧需求不耦合到一个适当的流量响应在梗死周围区严重减少血流量。由此产生的相对缺氧事件可以解释以前记录的去极化次数和梗死体积之间的关系。
In the periphery of ischemic brain lesions, transient spreading depression-like direct current (DC) deflections occur that may be of pathophysiological importance for determining the volume of the ischemic infarct. The effect of these deflections on cerebral blood flow, tissue oxygen tension, and electrophysiology was studied in rats submitted to intraluminal thread occlusion of the middle cerebral artery (MCA) and compared with the changes following potassium chloride (KCl)-induced spreading depression of intact animals. Immediately after MCA occlusion, cortical laser-Doppler flow (LDF) in the periphery of the MCA territory sharply decreased to 35 +/- 14% of control (mean +/- SD; p < 0.05), tissue PO2, declined from 28 +/- 4 to 21 +/- 3 mm Hg (p < 0.05), and EEG power fell to similar to 80% of control. During 7-h occlusion, 3-11 DC deflections with a mean duration of 5.2 +/- 4.8 min occurred at irregular intervals, and EEG power gradually declined to 66 +/- 16% of control (p < 0.05). During the passage of DC deflections, LDF did not change, but PO2 further declined to 19 +/- 4 mm Hg (p < 0.05). KCl-induced depolarizations of intact rats were significantly shorter (1.4 +/- 0.5 min; p < 0.05) and were accompanied by a 43% increase in LDF (p < 0.05) and a slight but significant increase in tissue PO2, from 22 +/- 4 to 25 +/- 4 mm Hg (p < 0.05). The comparison of periinfarct and KCl-induced depolarizations demonstrates that oxygen requirements are not coupled to an appropriate flow response in the periinfarct zone with severely reduced blood flow. The resulting episodes of relative hypoxia could explain the previously documented relationship between the number of depolarizations and infarct volume.