A photothrombotic 'ring' model of rat stroke-in-evolution displaying putative penumbral inversion.
A photothrombotic 'ring' model of rat stroke-in-evolution displaying putative penumbral inversion.
复制标题
大鼠中风进化的光血栓“环”模型显示假定的半影反转。
DOI：
10.1161/01.str.26.3.444
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发表时间：
1995
期刊：
影响因子：
8.3
通讯作者：
Dietrich,WD
中科院分区：
文献类型：
--
作者：
Wester,P;Watson,BD;Prado,R;Dietrich,WD
背景和目的为了促进对具有侵犯性缺血损伤风险的组织区域的可重复和严格的研究，我们提出了一种新的模型，其中潜在受损组织位于缺血部位内而不是周围。周边的“危险区”是由photothrombotically产生的皮质病变的形状的环形（或“环”）。MethodsThe暴露的颅骨赤藓红B注射大鼠照射514.5 nm的激光束，配置为5 mm直径的环，产生一个环形病变引起的光化学诱导的血小板闭塞的皮质血管。通过碳黑灌注揭示了内部区域的灌注缺陷。结果注射赤藓红B 17 mg/kg，以0.92 W/cm 2的环形束照射2 min后，大鼠脑缺血再灌注损伤明显减轻（P <0.05），脑缺血再灌注损伤明显减轻（P <0.05），脑缺血再灌注损伤明显减轻（P <0.05），脑缺血再灌注损伤明显减轻（P <0.05），脑缺血再灌注损伤明显减轻（P <0.05）（65 mW的射束功率），炭黑输注时间长达4小时，显示出环绕完全开放的危险区的浅皮质环损伤，其在24小时时表明基本上完全灌注不足。在长达24小时的时间内，大脑中动脉和大脑前动脉的远端分支穿透软脑膜表面的环形病变。基于立体定位的组织病理学评估显示，到24小时，病变跨越皮质厚度。照射后4 - 24小时，病灶体积从14.5±8.0 mm 3（平均值±SD）（n=8）增加至46.2±15.6 mm 3（n=8（P<0.01），但前后病变直径在4小时之间无显著变化（6.00±1.03 mm; n=9）和24小时（6.75±1.15）mm; n=9）.结论目前的模型缓慢发展，但不可避免的皮层组织死亡在隔离区应促进更精确的观察组织代谢反应的演变，从缺血的即将发生到不可逆损伤的阈值。该系统可能被证明是有效的评估治疗旨在挽救半影区。
Background and PurposeTo facilitate reproducible and rigorous study of a tissue zone at risk of encroaching ischemic damage, we propose a new model in which the potentially compromised tissue lies within rather than perifocal to an ischemic locus. The perimeter of the “zone at risk” is defined by a photothrombotically produced cortical lesion in the shape of a toroid (or “ring”).MethodsThe exposed crania of erythrosin B–injected rats were irradiated with a 514.5-nm laser beam, configured as a 5-mm-diameter ring, to yield a ring-shaped lesion caused by photochemically induced platelet occlusion of cortical vasculature. Developing perfusion deficits in the interior region were revealed by carbon black infusion. Tissue damage and infarct volumes were assessed by light and electron microscopy, and blood-brain barrier integrity was assessed with Evans blue dye and horseradish peroxidase as tracers.ResultsFor rats injected with 17 mg/kg erythrosin B and irradiated for 2 minutes with a ring beam intensity of 0.92 W/cm2(beam power of 65 mW), carbon black infusion at times up to 4 hours demonstrated a shallow cortical ring lesion encircling a fully patent zone at risk, which by 24 hours evinced an essentially complete perfusion deficit. At times up to 24 hours, the ring lesion was penetrated at the pial surface by distal branches of the middle cerebral and anterior cerebral arteries. Stereotaxically based histopathological assessment showed that by 24 hours the lesion spanned the cortical thickness. Lesion volume increased from 14.5±8.0 mm3(mean±SD) (n=8) to 46.2±15.6 mm3(n=8) between 4 and 24 hours after irradiation (P<.01), but the anteroposterior lesion diameter did not change significantly between 4 hours (6.00±1.03 mm; n=9) and 24 hours (6.75±1.15 mm; n=9).ConclusionsThe present model of slowly developing but inevitable cortical tissue death in a sequestered area should facilitate more precise observations of the evolution of tissue metabolic responses, from the impending onset of ischemia to the threshold of irreversible damage. This system may prove efficient for evaluating treatments intended to salvage a penumbral region.