Effects of cortical spreading depression on cortical blood flow, impedance, DC potential, and infarct size in a rat venous infarct model

被引:31
|
作者
Otsuka, H [1 ]
Ueda, K [1 ]
Heimann, A [1 ]
Kempski, O [1 ]
机构
[1] Univ Mainz, Inst Neurosurg Pathophysiol, D-55101 Mainz, Germany
关键词
spreading depression; cerebral blood flow; venous infarct; laser Doppler flowmetry; photochemical thrombotic technique; impedance; penumbra; rat;
D O I
10.1006/exnr.1999.7326
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A cortical venous infarction model has been evaluated as to the degree of regional flow reduction and by studying effects of cortical spreading depression (CSD). Two adjacent cortical veins were occluded photochemically with rose bengal and fiberoptic illumination. Seven rats served to demonstrate effects on regional cortical blood flow using laser Doppler scanning. In 36 rats local CBF, DC potential, and brain tissue impedance were measured continuously for 75 min after vein occlusion, No, 3, or 10 CSD waves were induced by potassium chloride injection during the initial 75 min, Rats were compared for spontaneous CSDs; baseline local CBF, CBF, and impedance response to CSD; and infarct volume. Seventy-five minutes after vein occlusion regional cortical flow in a 3.5 x 7-mm window was reduced to 34.3 +/- 13.2%. At 45% of the 840 measured locations in 7 rats flow was <40% baseline and at 27.3% <30%, indicating a widespread penumbra territory. During the initial 75 min 2.1 +/- 1.1 spontaneous CSDs were observed. There was a positive correlation between the number of spontaneous CSDs seen acutely and infarction volume after 5 days. Moreover, brain injury was significantly increased in the group with 10 KCl-induced CSDs. A reduced 1CBF response and an overshooting tissue impedance change during CSD were predictors of ischemic damage. This study demonstrates a CSD-related growth of the venous infarct. Second, the data indicate that flow after two-vein occlusion resembles that seen under penumbra conditions, allowing for studies of damage mechanisms responsible for infarct growth. (C) 2000 Academic Press.
引用
收藏
页码:201 / 214
页数:14
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