A new rat model of thrombotic focal cerebral ischemia
A new rat model of thrombotic focal cerebral ischemia
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DOI：
10.1097/00004647-199702000-00001
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发表时间：
1997-02-01
影响因子：
6.3
通讯作者：
Chopp, M
中科院分区：
文献类型：
--
作者：
Zhang, AG;Zhang, RL;Chopp, M
我们建立了一种富含纤维蛋白的血栓性局灶性脑缺血模型，具有可重复性和可预测的梗死体积。在雄性Wistar大鼠（n = 77）中，通过放置在颈内动脉（ICA）颅内段的管腔内导管注射凝血酶，在大脑中动脉（MCA）的起源处诱导血栓。通过组织病理学分析和神经功能缺损评分，并通过使用激光多普勒血流仪（LDF），灌注加权成像（PWI）和弥散加权成像（DWI）测量脑血流（CBF）的变化来检查血栓诱导和随后的缺血性细胞损伤。组织学检查显示，富含纤维蛋白的血栓位于右侧MCA的起源处。在注射30 U凝血酶的大鼠（n = 10）中，注射凝血酶后右顶叶皮质的局部脑血流量（rCBF）减少了注射前水平的34-58%。磁共振成像（MRI）显示CBF减少，高信号DWI包括右侧MCA供血区。给予80 U凝血酶的大鼠的梗死体积在24 h时为对侧半球的31.29 +/- 12.9%（n = 13），在168 h时为对侧半球的34.7 +/- 16.4%（n = 6）。给予30 U凝血酶的大鼠在24 h和168 h的半球梗死体积分别为34.0 +/- 14.5%（n = 9）和29.7 +/- 13.9%（n = 8）。此外，血栓形成大鼠（n = 3）治疗重组组织型纤溶酶原激活剂（rt-PA）（10毫克/公斤）血栓形成后2小时显示，CBF迅速恢复到缺血前的PWI测量值。这种血栓性缺血模型与人类血栓栓塞性卒中相关，可能有助于记录溶栓干预的安全性和有效性，以及研究抗血栓治疗的补充疗法。
We developed a fibrin-rich thrombotic focal cerebral ischemic model with reproducible and predictable infarct volume in rats. In male Wistar rats (n = 77), a thrombus was induced at the origin of the middle cerebral artery (MCA) by injection of thrombin via an intraluminal catheter placed in the intracranial segment of the internal carotid artery (ICA). Thrombus induction and consequent ischemic cell damage were examined by histopathological analysis and neurological deficit scoring, and by measuring changes in cerebral blood how (CBF) using laser-Doppler flowmetery (LDF), perfusion-weighted imaging (PWI), and by diffusion weighted imaging (DWI). Histopathology revealed that a fibrin-rich thrombus localized to the origin of the right MCA. Regional cerebral blood flow (rCBF) in the right parietal cortex was reduced by 34-58% of preinjection levels after injection of thrombin in rats administered 30 U of thrombin (n = 10). Magnetic resonance imaging (MRI) showed a reduction in CBF and a hyperintensity DWI encompassing the territory supplied by the right MCA. The infarct volume in rats administered 80 U of thrombin was 31.29 +/- 12.9% of the contralateral hemisphere at 24 h (n = 13), and 34.7 +/- 16.4% of the contralateral hemisphere at 168 h (n = 6). Rats administered 30 U of thrombin exhibited a hemispheric infarct volume of 34.0 +/- 14.5% (n = 9) at 24 h and 29.7 +/- 13.9% (n = 8) at 168 h. In addition, thrombotic rats (n = 3) treated with recombinant tissue plasminogen activator (rt-PA) (10 mg/kg) 2 h after thrombosis showed that CBF rapidly returned towards preischemic values as measured by PWI. This model of thrombotic ischemia is relevant to thromboembolic stroke in humans and may be useful in documenting the safety and efficacy of thrombolytic intervention as well as for investigating therapies complementary to antithrombotic therapy.