Back T, Hoehn-Berlage M, Kohno K, Hossmann K A
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.
Stroke. 1994 Feb;25(2):494-500. doi: 10.1161/01.str.25.2.494.
Diffusion-weighted nuclear magnetic resonance imaging has been shown to detect early ischemia-related alterations in experimental stroke. This raises the question of whether the observed increase in signal intensity is correlated with changes in cerebral metabolism. After middle cerebral artery occlusion, nuclear magnetic resonance diffusion images were recorded and compared with the regional concentration of cerebral metabolites and with histology of identical planes.
Seven anesthetized Fischer rats were subjected to permanent occlusion of the middle cerebral artery. T1, T2, and diffusion images (b factors ranging from 0 to 1500 s/mm2) were measured in three to five planes after 7 hours. Thereafter, brains were frozen in situ for histology and quantitative bioluminescence imaging of ATP, glucose, lactate, and for fluorescence imaging of tissue pH.
Seven hours after middle cerebral artery occlusion, the apparent diffusion coefficient was reduced from 615 +/- 97 x 10(-6).mm2.s-1 (contralateral brain) to 359 +/- 42 x 10(-6).mm2.s-1 (ischemic brain; mean +/- SD, P < .01). A precise topical coincidence was demonstrated between changes in nuclear magnetic resonance diffusion images, pattern of histological damage, ATP-depleted areas, and local tissue acidosis, the lesion area amounting to between 24.1% and 27.6% of the hemisphere at the level of the caudate-putamen. The area of elevated brain lactate clearly exceeded the acidic core of the infarct and included the slightly alkaline border zone.
The data demonstrate that after 7-hour middle cerebral artery occlusion, the reduction of the apparent diffusion coefficient in nuclear magnetic resonance diffusion images reflects precisely the region of histological injury, breakdown of energy metabolism, and tissue acidosis.
扩散加权核磁共振成像已被证明可在实验性中风中检测到早期缺血相关改变。这就引发了一个问题,即观察到的信号强度增加是否与脑代谢变化相关。大脑中动脉闭塞后,记录核磁共振扩散图像,并与脑代谢物的区域浓度以及相同平面的组织学进行比较。
对7只麻醉的Fischer大鼠进行大脑中动脉永久性闭塞。7小时后在三到五个平面测量T1、T2和扩散图像(b值范围为0至1500 s/mm²)。此后,将大脑原位冷冻以进行组织学检查以及ATP、葡萄糖、乳酸的定量生物发光成像和组织pH值的荧光成像。
大脑中动脉闭塞7小时后,表观扩散系数从615±97×10⁻⁶.mm².s⁻¹(对侧脑)降至359±42×10⁻⁶.mm².s⁻¹(缺血脑;平均值±标准差,P<.01)。核磁共振扩散图像的变化、组织学损伤模式、ATP耗竭区域和局部组织酸中毒之间显示出精确的局部一致性,在尾状核-壳核水平,病变面积占半球的24.1%至27.6%。脑乳酸升高的区域明显超过梗死灶的酸性核心,包括轻度碱性的边缘区。
数据表明,大脑中动脉闭塞7小时后,核磁共振扩散图像中表观扩散系数的降低精确反映了组织学损伤区域、能量代谢的破坏和组织酸中毒。