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使用体内31P核磁共振波谱和1H磁共振成像对实验性脑缺血进行病理生理学研究。

Pathophysiological investigation of experimental cerebral ischaemia using in vivo 31P-NMR spectroscopy and 1H-MRI.

作者信息

Higuchi T, Naruse S, Horikawa Y, Tanaka C, Ebisu T, Yamamoto K, Hirakawa K

机构信息

Department of Neurosurgery, Kyoto Prefectural University of Medicine, Japan.

出版信息

Acta Neurochir Suppl (Wien). 1988;43:172-6. doi: 10.1007/978-3-7091-8978-8_37.

Abstract

The cerebral energy metabolism and brain oedema were investigated in three experimental cerebral ischaemia models using 31P-NMR spectroscopy (MRS) and 1H-NMR imaging (MRI) in the same subject animal. These measurements were performed also in experimental brain oedema models and the findings were compared with each other. 31P-MRS showed an ischaemic pattern in all of the cerebral ischaemia models, that is, ATP and PCr peaks decreased, and the Pi peak increased and shifted to a higher resonant frequency. However, 31P-MRS did not show any remarkable change in the brain oedema models. On the other hand, 1H-MRI clearly demonstrated brain oedema in the brain oedema model. In the cerebral ischaemia models, 1H-MRI findings differed depending upon the type of model, namely the most marked brain oedema was detected in the unilateral middle cerebral arterial occlusion model and no marked change was detected in the temporary four vessel occlusion model. It was thought that this difference depended on the severity of the ischaemic insult. Accordingly, the fundamental pathophysiological problem of cerebral ischaemia was the energy metabolism disturbance with the brain oedema being associated with this disturbance but occurring secondarily. However, in the brain oedema model the main pathological change was the increase in tissue water.

摘要

在同一实验动物身上,使用31P核磁共振波谱(MRS)和1H核磁共振成像(MRI),对三种实验性脑缺血模型的脑能量代谢和脑水肿进行了研究。在实验性脑水肿模型中也进行了这些测量,并将结果相互比较。31P-MRS在所有脑缺血模型中均显示出缺血模式,即ATP和磷酸肌酸(PCr)峰降低,无机磷(Pi)峰升高并向更高的共振频率偏移。然而,31P-MRS在脑水肿模型中未显示出任何显著变化。另一方面,1H-MRI在脑水肿模型中清晰地显示出脑水肿。在脑缺血模型中,1H-MRI的结果因模型类型而异,即在大脑中动脉单侧闭塞模型中检测到最明显的脑水肿,而在临时四动脉闭塞模型中未检测到明显变化。据认为,这种差异取决于缺血损伤的严重程度。因此,脑缺血的基本病理生理问题是能量代谢紊乱,脑水肿与这种紊乱相关但继发出现。然而,在脑水肿模型中,主要的病理变化是组织水分增加。

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