EVOLVING FOCAL CEREBRAL-ISCHEMIA IN CATS - SPATIAL CORRELATION OF NUCLEAR MAGNETIC-RESONANCE IMAGING, CEREBRAL BLOOD-FLOW, TETRAZOLIUM STAINING, AND HISTOPATHOLOGY
EVOLVING FOCAL CEREBRAL-ISCHEMIA IN CATS - SPATIAL CORRELATION OF NUCLEAR MAGNETIC-RESONANCE IMAGING, CEREBRAL BLOOD-FLOW, TETRAZOLIUM STAINING, AND HISTOPATHOLOGY
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DOI：
10.1161/01.str.19.1.28
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发表时间：
1988-01-01
期刊：
影响因子：
8.3
通讯作者：
LITTLE, JR
中科院分区：
文献类型：
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作者：
BOSE, B;JONES, SC;LITTLE, JR
核磁共振成像（NMRI）和脑血流量（CBF）的空间相关性可能会提高我们识别缺血性脑病变的能力，并可能提供进一步了解早期脑缺血的病理生理学。11只戊巴比妥麻醉的成年猫通过经眶入路暴露双侧颈总动脉和右侧大脑中动脉。使用0.6 T场、0.4 cm层厚和表面线圈，通过单次自旋回波、多层技术获得基线NMRI图像。右侧大脑中动脉闭塞造成局灶性缺血，双侧颈总动脉结扎加重局灶性缺血。然后在1、2、4、6和12小时进行连续NMRI研究，或直至在2（n = 2）、4（n = 2）、6（n = 2）或12（n = 1）小时后使用[14 C]碘安替比林测定同一只猫的CBF。该方案允许NMRI和CBF的时空相关性。将交替的5-mm脑切片与1%氯化2，3，5-三苯基四唑（TTC）在37 - 41 ℃温育45分钟。C，并在液体氟利昂中冷冻，用于以后的放射自显影CBF测定。仅对4只猫进行了NMRI和TTC（非CBF）研究。评价了T2加权图像（重复时间2，000 msec，回波时间120 mesc）中观察到的NMRI信号强度增加区域、TTC活体染色、低CBF和常规组织学之间的相关性。在早期阶段（< 6小时），T2加权NMRI变化局限于中央缺血性灰质区域，如后期CBF图像中所定义的，不涉及白色物质。到第12小时，NMRI变化涉及整个缺血区域，包括灰质和白色物质。在T2加权NMRI上观察到的最初可见变化提示细胞水肿，后期变化为血管源性水肿的特征。与放射自显影CBF确定的缺血区域相比，NMRI变化的扩散与先前描述的缺血性损伤的双相演变一致。这些数据表明，T2加权NMRI可用于临床描绘急性缺血性卒中的区域。
The spatial correlation of nuclear magnetic resonance imaging (NMRI) and cerebral blood flow (CBF) may improve our ability to identify ischemic brain lesions and may provide further insight into the pathophysiology of early cerebral ischemia. Eleven pentobarbital-anesthetized adult cats underwent exposure of the common carotid arteries bilaterally and the right middle cerebral artery through a transorbital approach. Baseline NMRI images were obtained with a single spin-echo, multislice technique using a 0.6-T field, 0.4-cm slice thickness, and a surface coil. Focal ischemia was produced with right middle cerebral artery occlusion and potentiated with bilateral common carotid artery ligation. Sequential NMRI studies were then performed at 1, 2, 4, 6, and 12 hours or until CBF was determined in the same cats using [14C]iodoantipyrine at either 2 (n = 2), 4 (n = 2), 6 (n = 2), or 12 (n = 1) hours after the time of occlusion. This protocol allowed temporal and spatial correlation of NMRI and CBF. Alternate 5-mm brain slices were incubated with 1% 2,3,5-triphenyltetrazolium chloride (TTC) for 45 minutes at 37-41.degree. C and frozen in liquid Freon for later autoradiographic CBF determination. Four cats were studied only with NMRI and TTC (not CBF). The correlation between areas of increased NMRI signal intensity observed in T2-weighted images (repetition time 2,000 msec, echo time 120 mesc), vital staining with TTC, low CBF, and routine histology was evaluated. During the early phase (< 6 hours), T2-weighted NMRI changes were localized to the central ischemic gray matter areas, as defined in the later CBF images, with no involvement of the white matter. By the twelfth hour the NMRI changes involved the entire ischemic area including gray and white matter. The initial visible changes seen on T2-weighted NMRI are suggestive of cellular edema, and the later changes are characteristic of vasogenic edema. The spread of NMRI changes compared with the ischemic area determined from autoradiographic CBF is consistent with the previously described biphasic evolution of ischemic injury. These data suggest that T2-weighted NMRI could be used clinically to delineate areas of acute ischemic stroke.