Time-dependent alterations in functional and pharmacological arteriolar reactivity after subarachnoid hemorrhage
Time-dependent alterations in functional and pharmacological arteriolar reactivity after subarachnoid hemorrhage
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DOI：
10.1161/01.str.0000259853.43084.03
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发表时间：
2007-04-01
期刊：
影响因子：
8.3
通讯作者：
Ngai, Al C.
中科院分区：
文献类型：
--
作者：
Britz, Gavin W.;Meno, Joseph R.;Ngai, Al C.
背景和目的：除了大血管痉挛外，脑小动脉功能障碍可能是蛛网膜下腔出血后脑缺血的原因。本研究的目的是验证蛛网膜下腔出血改变脑微血管反应性的假说。方法-采用血管内细丝模型诱导氟烷麻醉的雄性SpragueDawley大鼠蛛网膜下腔出血。结果：在假手术大鼠中，坐骨神经刺激引起的小动脉直径增加23.5+/-1.8%，在蛛网膜下腔出血后24、48和72小时分别为13.7+/-0.9%、12.8+/-2.5%和18.8+/-2.9%(P<；0.05；N>；=7)。蛛网膜下腔出血后96小时和120小时，刺激引起的坐骨神经扩张恢复到假手术水平。蛛网膜下腔出血对体感诱发电位无明显影响。蛛网膜下腔出血后48h，脑膜血管对腺苷(10 mU/L)和硝普钠(1 mU/L)的扩张作用明显减弱，分别为47%和41%(P<；0.05；n=7)。结论：实验性蛛网膜下腔出血后2~3天，硬脑膜小动脉对皮质激活的反应减弱。
Background and Purpose-Disturbances in cerebral arteriolar function, in addition to large vessel vasospasm, may be responsible for ischemia after subarachnoid hemorrhage. The purpose of this study was to test the hypothesis that subarachnoid hemorrhage alters cerebral microvascular reactivity.Methods-An endovascular filament model was used to induce subarachnoid hemorrhage in halothane-anesthetized male Sprague-Dawley rats. We evaluated pial arteriolar responses to sciatic nerve stimulation, topically applied vasoactive agents (adenosine or sodium nitroprusside), and CO(2) inhalation in rats subjected to subarachnoid hemorrhage at 1 to 5 days after insult.Results-In sham-operated rats, sciatic nerve stimulation evoked a 23.5 +/- 1.8% increase in arteriolar diameter, which was significantly attenuated to 13.7 +/- 0.9%, 12.8 +/- 2.5%, and 18.8 +/- 2.9% at 24, 48, and 72 hours after subarachnoid hemorrhage, respectively (P < 0.05; n >= 7). At 96 and 120 hours after subarachnoid hemorrhage, sciatic nerve stimulation- induced dilation recovered to sham levels. Somatosensory-evoked potentials were unaltered by subarachnoid hemorrhage. Pial vasodilatation to adenosine (10 mu mol/L) and sodium nitroprusside (1 mu mol/L) were significantly impaired, by 47% and 41%, respectively, at 48 hours after subarachnoid hemorrhage (P < 0.05; n = 7). In contrast, CO(2) reactivity was unaffected by subarachnoid hemorrhage.Conclusions-Pial arteriolar responses to cortical activation may be decreased in the initial 2 to 3 days after experimental subarachnoid hemorrhage.