Koroleva V I, Vinogradova L V
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
Zh Vyssh Nerv Deiat Im I P Pavlova. 2000 Jul-Aug;50(4):612-23.
Cortical negative DC potential shifts were studied on two experimental models: focal cortical ischemia provoked by a photothrombotic occlusion of the distal part of the middle cerebral artery (dMCA) and a combination of systemic hypoxia induced by bilateral ligation of the common carotid arteries (temporary ligation of the left artery and permanent ligation of the right one) with breathing with 0.5% carbon monoxide (CO). The perifocal ischemic depolarization (ID) after the dMCA thrombosis was found to reach 28-33 mV and then gradually decline during 80 min to a certain residual level about 5 mV. Spontaneous depolarization didn't occur during hypoxia but it was easily provoked in one or both hemispheres by the waves of the cortical spreading depression (SD). The amplitude of hypoxic depolarization (HD) didn't exceed 20 mV, was remarkably stable during hypoxic condition (more than 60 min) and returned to the baseline level within 20-30 min after the cessation of CO breathing and releasing of the left carotid artery. Despite the similar durations of the ID and HD, their functional consequences differed greatly. The ID led to a damage of the nervous tissue as evidenced by a reduction of the SD amplitude (to 20-25%) and biphasic change in persistent negative potential (PNP) evoked by the SD wave alone. The 1.5-2-fold increase in the PNP amplitude in the perifocal region was the most prominent outcome of the ID. In contrast to the ID, the SD and PNP characteristics were unchanged after the HD. Such a discrepancy between the ID and HD can be related with their different origin. The results suggest that the HD is produced by blood-brain barrier processes associated with the intensive vasospasm and vasogenic edema. Besides these phenomena, the other well-known factors such as a disturbance of permeability of neuronal membranes, glutamatemediated exitotoxicity, and tissue destruction determine the ID noxious influences.
大脑中动脉远端光血栓闭塞诱发的局灶性皮质缺血（大脑中动脉远端闭塞，dMCA），以及双侧颈总动脉结扎（左侧动脉临时结扎，右侧动脉永久结扎）并吸入0.5%一氧化碳（CO）诱导的全身性缺氧。发现dMCA血栓形成后灶周缺血性去极化（ID）达到28 - 33 mV，然后在80分钟内逐渐下降至约5 mV的某个残余水平。缺氧期间未发生自发去极化，但皮质扩散性抑制（SD）波很容易在一个或两个半球诱发去极化。缺氧性去极化（HD）的幅度不超过20 mV，在缺氧状态下（超过60分钟）非常稳定，并且在停止吸入CO并松开左侧颈动脉后20 - 30分钟内恢复到基线水平。尽管ID和HD的持续时间相似，但它们的功能后果差异很大。ID导致神经组织损伤，表现为SD幅度降低（至20 - 25%）以及仅由SD波诱发的持续负电位（PNP）的双相变化。灶周区域PNP幅度增加1.5 - 2倍是ID最显著的结果。与ID相反，HD后SD和PNP特征未改变。ID和HD之间的这种差异可能与其不同的起源有关。结果表明，HD是由与强烈血管痉挛和血管源性水肿相关的血脑屏障过程产生的。除了这些现象外，其他众所周知的因素，如神经元膜通透性障碍、谷氨酸介导的兴奋性毒性和组织破坏，决定了ID的有害影响。
