Ba Alyssa M, Guiou Michael, Pouratian Nader, Muthialu Arpitha, Rex David E, Cannestra Andrew F, Chen James W Y, Toga Arthur W
Laboratory of NeuroImaging, Department of Neurology, University of California, School of Medicine, Los Angeles, California 90024, USA.
J Neurophysiol. 2002 Nov;88(5):2726-35. doi: 10.1152/jn.00729.2001.
Cortical spreading depression (CSD) is an important disease model for migraine and cerebral ischemia. In this study, we exploit the high temporal and spatial resolution of optical imaging to characterize perfusion-dependent and -independent changes in response to CSD and to investigate the etiology of reflectance changes during CSD. In this experiment, we characterized the optical response to CSD at wavelengths that emphasize perfusion-related changes (610 and 550 nm), and we compared these results with 850 nm and blood volume data. Blood volume changes during CSD were recorded using an intravascular fluorescent dye, Texas Red dextran. We observed triphasic optical signals at 850 and 550 nm characterized by spreading waves of increased, decreased, then increased reflectance (Fig. 1) which expanded at a rate of approximately 3-5 mm/min. The signal at 610 nm had a similar initial phase, but the phase 2 response was slightly more complex, with a parenchymal decrease in reflectance but a vascular increase in reflectance. Reflectance values decreased in phase three. Blood volume signals were delayed relative to the optical intrinsic signals and corresponded temporally to phases 2 and 3. This is the first study to characterize optical imaging of intrinsic signal responses to CSD, in vivo, at multiple wavelengths. The data presented here suggest that changes in light scattering precede perfusion responses, the blood volume increase (phase 2) is accompanied by a reduction in deoxyhemoglobin, and the blood volume decrease (phase 3) is accompanied by an increase in deoxyhemoglobin. Previous studies have suggested the oligemia of spreading depression was a result of decreased metabolic demand. This study suggests that during the oligemic period there is a greater reduction in oxygen delivery than in demand.
皮层扩散性抑制（CSD）是偏头痛和脑缺血的重要疾病模型。在本研究中，我们利用光学成像的高时间和空间分辨率来表征对CSD的灌注依赖性和非依赖性变化，并研究CSD期间反射率变化的病因。在本实验中，我们在强调灌注相关变化的波长（610和550nm）下表征了对CSD的光学响应，并将这些结果与850nm和血容量数据进行了比较。使用血管内荧光染料德克萨斯红葡聚糖记录CSD期间的血容量变化。我们在850和550nm处观察到三相光学信号，其特征是反射率先增加、然后降低、再增加的扩散波（图1），以约3-5mm/分钟的速度扩展。610nm处的信号有类似的初始阶段，但第二阶段的响应稍复杂一些，实质反射率降低但血管反射率增加。第三阶段反射率值降低。血容量信号相对于光学固有信号延迟，并且在时间上与第二和第三阶段相对应。这是第一项在体内多个波长下表征对CSD的固有信号响应的光学成像的研究。此处呈现的数据表明，光散射变化先于灌注响应，血容量增加（第二阶段）伴随着脱氧血红蛋白减少，血容量减少（第三阶段）伴随着脱氧血红蛋白增加。先前的研究表明，扩散性抑制的低血是代谢需求降低的结果。本研究表明，在低血期，氧输送的减少比需求的减少更大。
