DIFFUSION IMAGING OF SPREADING DEPOLARIZATION: SUBARACHNOID HEMORRHAGE IN RATS

扩散去极化的扩散成像：大鼠蛛网膜下腔出血

• 批准号: 6123020
• 负责人: CHRISTIAN BEAULIEU
• 金额: $ 1.75万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-01-01 至 2000-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6123020
• 关键词: Mammalia; bioimaging /biomedical imaging; biomedical resource; magnetic resonance imaging; technology /technique

Introduction: Diffusion-weighted MRI (DWI) can detect transient declines of the apparent diffusion coefficient (ADC) that represent spreading depression (SD) associated disturbances of the ion homeostasis and the concomitant extra- to intracellular water shift in the periinfarct tissue. We investigated the dynamics of the initial SD-related ADC transients in hyper- and normoglycemic rats after remote middle cerebral artery occlusion (MCAO) to test the hypothesis that an increased blood glucose level should result in a faster recovery of SD like transients in the periinfarct tissue. Methods: Six rats were rendered hyperglycemic by i.p. injection of streptozotocin 36 hours before induction of focal cerebral ischemia using the remote suture model. Periinfarct SD was monitored during the initial 15 minutes after remotely induced middle cerebral artery occlusion (MCAO) using serial ultrafast. Data for each ADC calculation was acquired in 16s. Perfusion imaging was performed immediately after the DWI using the same multi-slice EPI technique to follow a bolus injection of 0.3 mmol/kg Gd-DTPA. Multiple adjacent ROIs were defined in the ADC maps. The latency time from MCAO to the onset of the ADC decrease (LT), the time from the start of the ADC decrease to the maximal ADC decline (= T FADC), the time from the start of the ADC decrease to the ADC recovery and the maximal ADC change (F ADC) were defined in order to characterize the temporal evolution of the ADC. Results: The ischemic core in hyperglycemic rats had a significant prolongation of LT as compared to normoglycemic control rats. Furthermore, T FADC was significantly increased in the ischemic core of hyperglycemic rats. Transient ADC decreases during SD occurred in the periinfarct tissue of both experimental groups. Hyperglycemic rats showed a significantly faster recovery of transient ADC declines in ROIs 2 and 3 adjacent to the ischemic core (5.610.6 min. vs. 10.111.6 min. in controls, p=0.03). Tissue perfusion did not reveal significant differences between the two groups. Conclusion: We conclude that hyperglycemia delays the terminal depolarization in the ischemic core and supports a faster repolarization in severely mal-perfused pen-umbral tissue after SD, which reflects the increased availability of energy substrate in the state of hyper-glycemia.

简介：弥散加权MRI（DWI）可以检测瞬态 表观扩散系数（ADC）的下降， 扩散抑制（SD）相关的离子干扰 体内平衡和伴随的细胞外水转移， 梗死周围组织 我们研究了最初的动力学 高血糖和正常血糖大鼠中SD相关ADC瞬变， 远端大脑中动脉闭塞（MCAO）来检验这一假设 血糖水平升高会导致 梗死周围组织中SD样瞬变的恢复。 研究方法： 通过腹膜内注射 链脲佐菌素在诱导局灶性脑缺血前36小时 使用远程缝合模型。 在治疗期间监测梗死周围SD 远程诱导大脑中动脉后的最初15分钟 闭塞（MCAO）使用串行超快。 每个ADC的数据 计算时间为16 s。 进行灌注成像 DWI后立即使用相同的多切片EPI技术， 然后静脉注射0.3mmol/kg Gd-DTPA。 多个相邻 在ADC图中定义ROI。 从MCAO到 ADC降低开始（LT），即从ADC开始的时间 降低至最大ADC下降（= T FADC）的时间， ADC开始降低至ADC恢复和最大ADC 定义变化（F ADC）以表征时间特征 ADC的发展。 结果：高血糖组缺血核心区 与血糖正常的大鼠相比， 对照组大鼠。 此外，T FADC显著增加， 高血糖大鼠的缺血核心。 瞬态ADC降低， SD发生在两个实验组的梗死周围组织。 高血糖大鼠表现出明显更快的短暂恢复， 邻近缺血核心的ROI 2和ROI 3的ADC下降（5.6 ± 10.6 分钟 对照组为10.111.6 min，p=0.03）。 组织灌注 两组之间没有显着差异。 结论：高血糖可延迟终末期胰腺癌的发生， 在缺血核心去极化，并支持更快的 SD后严重灌注不良的半暗带组织中的复极， 这反映了能源基板的可用性增加， 超临界状态