DIFFUSION IMAGING OF SPREADING DEPOLARIZATION: SUBARACHNOID HEMORRHAGE IN RATS

前言：磁共振弥散加权成像(DWI)可以检测到瞬变 表示表观扩散系数(ADC)的下降 扩散抑制(SD)相关的离子扰动 动态平衡和伴随的细胞外到细胞内的水分转移 梗死灶周围组织。我们研究了初始的动力学 高血糖大鼠和正常血糖大鼠的SD相关ADC瞬变 远端大脑中动脉闭塞(MCAO)验证假说 血糖水平升高会导致更快的 梗死灶周围组织中SD样瞬变的恢复。方法： 6只大鼠通过腹腔注射造成高血糖。注射用 局灶性脑缺血诱导前36小时链脲佐菌素 使用远程缝合模型。术中监测梗死区周围SD 远程诱导大脑中动脉后最初15分钟 大脑中动脉闭塞(MCAO)使用连续超快。每个ADC的数据 计算在16秒内完成。进行了灌注成像。 在DWI之后立即使用相同的多层EPI技术 静脉注射Gd-DTPA 0.3 mmol/kg。多个相邻的 感兴趣区在ADC图中定义。从MCAO到 ADC开始减少(LT)，即从ADC开始起的时间 减少到最大ADC下降(=T FADC)，从 ADC的起始值降低到ADC恢复和最大ADC 定义了变化(F ADC)以刻画时间 ADC的演变。结果：高血糖患者的缺血核心 与正常血糖相比，大鼠的LT显著延长 控制老鼠。此外，T-FADC显著增加。 高血糖大鼠的缺血核心。暂态ADC在以下过程中降低 两个实验组的梗死灶周围组织均可见SD。 高血糖大鼠表现出明显更快的短暂性脑缺血恢复 邻近缺血核心的ROI 2和3的ADC下降(5.610.6 最小。与10.111.6分钟对照组，p=0.03)。组织灌流做了 未显示两组间有显著差异。 结论：我们得出结论：高血糖延迟了终末期 缺血核心的去极化，并支持更快的 SD后严重灌流不良的脑影组织复极， 这反映了能源底物利用率的提高 高血糖状态。

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.