Changes of Cortical Perfusion in the Early Phase of Subarachnoid Bleeding in a Rat Model and the Role of Intracranial Hypertension
Changes of Cortical Perfusion in the Early Phase of Subarachnoid Bleeding in a Rat Model and the Role of Intracranial Hypertension
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DOI：
10.33549/physiolres.933795
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发表时间：
2017-01-01
影响因子：
2.1
通讯作者：
Pachl, J.
中科院分区：
文献类型：
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作者：
Kolar, M.;Nohejlova, K.;Pachl, J.
由于颅内高压和早期血管痉挛，蛛网膜下腔出血（SAH）后早期脑灌注减少。这两种机制的作用尚不清楚。通过在SAH大鼠模型中进行预防性去骨瓣减压术（DC），我们旨在研究颅内高压成分消除后的脑灌注。采用2 × 2析因设计，大鼠行去骨瓣减压术或假手术，视交叉前池注射250 μ l血液或生理盐水。用激光散斑对比分析法连续测定脑皮质灌注30 min，注血引起颅内压（ICP）突然升高，脑灌注下降，6 min内恢复到基线水平，DC有效地阻止了ICP的升高，但SAH后的脑灌注明显低于非SAH后，DC动物由于增加的脑血管阻力，这持续整个30分钟的实验期间。我们的研究结果表明颅内高压在SAH后极早期低灌注中起主导作用，而早期血管痉挛的作用较小。预防性DC有效地维持了脑灌注压，但由于血管阻力增加而使脑灌注恶化。
Brain perfusion is reduced early after subarachnoid hemorrhage (SAH) due to intracranial hypertension and early vasospasm. The contribution of these two mechanisms is unknown. By performing a prophylactic decompressive craniectomy (DC) in a rat model of SAH we aimed to study brain perfusion after the component of intracranial hypertension has been eliminated. We used 2x2 factorial design, where rats received either decompressive craniectomy or sham operation followed by injection of 250 mu l of blood or normal saline into prechiasmatic cistern. The cortical perfusion has been continually measured by laser speckle-contrast analysis for 30 min. Injection of blood caused a sudden increase of intracranial pressure (ICP) and drop of cerebral perfusion, which returned to baseline within 6 min. DC effectively prevented the rise of ICP, but brain perfusion after SAH was significantly lower and took longer to normalize compared to non-DC animals due to increased cerebral vascular resistance, which lasted throughout 30 min experimental period. Our findings suggest that intracranial hypertension plays dominant role in the very early hypoperfusion after SAH whilst the role of early vasospasm is only minor. Prophylactic DC effectively maintained cerebral perfusion pressure, but worsened cerebral perfusion by increased vascular resistance.