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首页> 外文期刊>American Journal of Neuroradiology >Acute Postischemic Renormalization of the Apparent Diffusion Coefficient of Water is not Associated with Reversal of Astrocytic Swelling and Neuronal Shrinkage in Rats
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Acute Postischemic Renormalization of the Apparent Diffusion Coefficient of Water is not Associated with Reversal of Astrocytic Swelling and Neuronal Shrinkage in Rats

机译：大鼠表观水扩散系数的急性缺血后恢复正常与大鼠星形胶质细胞肿胀和神经元收缩的逆转无关。

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摘要

BACKGROUND AND PURPOSE: Initially decreased apparent diffusion coefficient (ADC) values are reversible if reperfusion is rapidly performed after focal brain ischemia. We sought to determine if reperfusion-induced renormalization of initially abnormal values indicates reversal of cellular, morphologic changes that occur during acute ischemia. METHODS: Eighteen rats underwent 30 minutes of middle cerebral artery occlusion (MCAO) without reperfusion (group A, n = 6), with 1.5 hours of reperfusion (group B, n = 6), or with 12 hours of reperfusion (group C, n = 6). Diffusion- and perfusion-weighted MR images were obtained at the end of MCAO and 1.5 and 12 hours after reperfusion. Immediately after the final MR study, the brains were fixed by cardiac perfusion with 4% paraformaldehyde. Neuronal injury was evaluated on hematoxylin-eosin-stained slices, and astrocytic size was determined by the area of glial fibrillary acidic protein (GFAP) plus S-100 expression. RESULTS: In group A in which ADC values decreased significantly, 47 ± 12% of the neurons were slightly shrunken; astrocytes were moderately swollen, and the area expressing GFAP plus S-100 was larger than that in the contralateral hemisphere (117 µm2 ± 6 vs 89 µm2 ± 2; P < .001). In group B in which ADC had renormalized, most neurons were moderately shrunken, and the frequency of such neurons was greater in group B (92% ± 2) than in group A (P < .001); astrocytes were markedly swollen, and the area was larger than that in the contralateral hemisphere (123 µm2 ± 8 vs 85 µm2 ± 4, P < .001). In group C in which a secondary ADC decrease occurred, most neurons (94% ± 3) were severely shrunken, and some had eosinophilic cytoplasm; astrocytes were disintegrated, and the area of GFAP plus S-100 expression was reduced (78 µm2 ± 4 vs 90 µm2 ± 5, P < .001). CONCLUSION: Reperfusion-induced acute renormalization of ADC values is not associated with the reversal of neuronal shrinkage and astrocytic swelling that occur during ischemia. Conversely, the morphologic changes of astrocytes and neurons progressively worsen over time, although ADC values show a biphasic change.
机译：背景与目的：如果在局灶性脑缺血后迅速进行再灌注，则表观弥散系数（ADC）最初降低是可逆的。我们试图确定 是否由再灌注诱导的初始异常 值重新正常化指示了急性缺血期间发生的细胞形态变化的逆转。 方法：18只大鼠经过30分钟的中脑 动脉闭塞（MCAO），无再灌注（A组，n = 6）， ，再灌注1.5小时（A组，n = 6）。 B组，n = 6），或进行12小时的 再灌注（C组，n = 6）。在MCAO结束时以及再灌注后1.5和12小时 获得了弥散和灌注加权的 MR图像。在最后的MR研究后，立即通过4％多聚甲醛的心脏灌注来固定 大脑。 在苏木精-伊红染色的切片上评估神经损伤， 结果：A组中ADC值明显降低， 47±12％的神经元轻微收缩；星形胶质细胞 适度肿胀，表达GFAP和S-100 的区域比对侧半球大（117 µm 2 ±6 vs 89 µm 2 ±2； P <.001）。在ADC重新归一化的 B组中，大多数神经元呈中等程度的收缩，而 B组中此类神经元的频率更高（92％ ±2）比A组（P <.001）;星形胶质细胞 明显肿胀，面积大于对侧半球的面积（123 µm 2 ±8 vs 85 µm 2 ±4，P <.001）。在发生二次 ADC减少的C组中，大多数神经元（94％±3）严重 收缩，并且一些具有嗜酸性细胞质。星形胶质细胞 分解，GFAP + S-100表达的面积 减少（78 µm 2 ±4 vs 90 µm 2 ±5， P <.001）。 结论：再灌注引起的ADC 值的急性正常化与逆转无关缺血期间发生的神经元收缩 和星形细胞的肿胀。相反， 随着时间的推移，星形胶质细胞和神经元的形态变化逐渐变坏，尽管ADC值显示出双相变化。

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  • 来源
    《American Journal of Neuroradiology》 |2002年第2期|180-188|共9页
  • 作者

    Fuhai Li; Kai-Feng Liu; Matthew D. Silva; Xiangjun Meng; Tibo Gerriets; Karl G. Helmer; Joseph D. Fenstermacher; Christopher H. Sotak; Marc Fisher;

  • 作者单位

    Department of Neurology, UMass Memorial Health Care and University of Massachusetts Medical School, Worcester;

    Department of Pathology, Neuropathology Section, Henry Ford Hospital, Detroit, MI;

    Department of Biomedical Engineering, Worcester Polytechnic Institute, MA;

    Department of Neurology, UMass Memorial Health Care and University of Massachusetts Medical School, Worcester;

    Department of Neurology, UMass Memorial Health Care and University of Massachusetts Medical School, Worcester;

    Department of Biomedical Engineering, Worcester Polytechnic Institute, MA;

    Department of Anesthesiology, Henry Ford Hospital, Detroit, MI;

    Department of Radiology, UMass Memorial Health Care and University of Massachusetts Medical School, Worcester|Department of Biomedical Engineering, Worcester Polytechnic Institute, MA|Department of Chemistry and Biochemistry, Worcester Polytechnic Institute, MA;

    Department of Neurology, UMass Memorial Health Care and University of Massachusetts Medical School, Worcester|Department of Radiology, UMass Memorial Health Care and University of Massachusetts Medical School, Worcester;

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