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炎症在实验性脑血管痉挛中的作用。

The role of inflammation in experimental cerebral vasospasm.

作者信息

Peterson J W, Kwun B D, Hackett J D, Zervas N T

机构信息

Laboratory for Cerebrovascular Biophysics, Massachusetts General Hospital, Boston.

出版信息

J Neurosurg. 1990 May;72(5):767-74. doi: 10.3171/jns.1990.72.5.0767.

DOI:10.3171/jns.1990.72.5.0767
PMID:2182792
Abstract

The short-term (less than or equal to 72-hour) cerebral vascular reaction to subarachnoid injectates of various specific blood components was determined by angiography in a canine model of cerebral vasospasm. Cell-free subarachnoid clots of autologous plasma in the basal cistern were found to produce no significant reaction of the basilar artery, while whole-blood clots induced a small (15%) chronic constriction after 24 hours. Because the plasma clots were not well retained in the basal cistern, however, small beads (dextran or latex) were added to stabilize them. Injection of beads and plasma led to moderate-to-severe chronic vasoconstriction (35% to 40%) with rapid onset. Control experiments demonstrated that these foreign bodies (beads) alone induced this vascular reaction. Histological examination showed that severe inflammation followed the introduction of subarachnoid beads. The experiments demonstrate that inflammation alone, in the absence of other processes associated with subarachnoid hemorrhage, may induce persistent and severe cerebroarterial constriction and raises the possibility that inflammation in response to subarachnoid blood may play a role in clinical vasospasm.

摘要

在犬脑血管痉挛模型中,通过血管造影术测定了各种特定血液成分蛛网膜下腔注射后的短期(小于或等于72小时)脑血管反应。发现基底池内无细胞的自体血浆蛛网膜下腔血凝块对基底动脉无明显反应,而全血血凝块在24小时后引起轻微(15%)的慢性收缩。然而,由于血浆血凝块不能很好地保留在基底池中,因此添加了小珠子(右旋糖酐或乳胶)来使其稳定。注射珠子和血浆导致中度至重度慢性血管收缩(35%至40%),且起效迅速。对照实验表明,仅这些异物(珠子)就能诱发这种血管反应。组织学检查显示,蛛网膜下腔珠子引入后会出现严重炎症。这些实验表明,在没有与蛛网膜下腔出血相关的其他过程的情况下,仅炎症就可能诱发持续性和严重的脑动脉收缩,并增加了蛛网膜下腔血液引发的炎症可能在临床血管痉挛中起作用的可能性。

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