CORRELATION OF DIFFUSION, BLOOD VOLUME & DC POTENTIAL CHANGES IN BRAIN: ISCHEMIA

MRI检测到的快速下降明显 认为脑缺血时脑组织的扩散系数(ADC) 是由于能量衰竭引起的细胞毒性水肿 血液流动停止。这项研究的目的是快速关联 使用直流电势采集ADC测量值(作为 细胞膜极化指示物)在全脑缺血期间 心脏骤停。方法：雄性SD大鼠麻醉。 加了氟烷。在大脑皮质上放置了一个氯化银电极 通过一个毛刺孔，测量大脑的直流电势。DC和MABP是 连续录制。磁共振成像在2.0T GE Omega系统上进行 使用回波平面成像。扩散加权和非扩散加权 图像交替显示，每6秒测量一次大脑的ADC值。 定义了三组动物：正常组、高血糖组和 降血糖。图像是在15岁之前连续采集的 静脉注射心脏骤停后几分钟。KCL注射剂。结果：MABP 在注射KCl5秒内降至零。ADC立即开始 缓慢下降，然后突然大幅下降，然后 保持不变或再次缓慢下降，直到扫描结束。 各组MABP下降与ADC快速下降之间的延迟 是(平均为1s.d。分钟)：正常1.4210.17(n=7)，高血糖 2.8510.83(n=5)，降血糖0.9410.39(n=5)。相应的值 DC下降：正常1.4210.8(n=5)，高血糖3.5010.76 降糖药0.6210.17(n=2)。结论：渐进式ADC MABP下降后立即开始下降，这可能是由于 瞬时跨膜水平移。随后的快速下降 ADC的发生与缺氧细胞膜去极化一致；两者 更改被超级或同时延迟或加速 低血糖症。

Introduction: The rapid decline in MRI detected apparent diffusion coefficient (ADC) of brain tissue during ischemia is thought to be due to cytotoxic edema following energy failure resulting from the cessation of blood flow. This study aims to correlate rapidly acquired ADC measurements with DC electrical potential (as an indicator of cell membrane polarization) during global ischemia by cardiac arrest. Methods: Male Sprague-Dawley rats were anesthetized with halothane. A chlorided silver electrode was placed on the cortex through a burr hole, to measure brain DC potentials. DC and MABP were recorded continuously. MRI was performed on a 2.0T GE Omega system using echo planar imaging. Diffusion and non-diffusion weighted images were alternated to measure ADC over the brain every 6 seconds. Three groups of animals were defined: normal, hyperglycemic and hypoglycemic. Images were acquired continuously before and up to 15 minutes after cardiac arrest by i.v. KCl injection. Results: MABP fell to zero within 5 seconds of KCl injection. ADC immediately began to decline slowly, followed by a sudden and large decline and then remained constant or declined slowly again until the end of the scan. The delay between MABP drop and the rapid ADC decline in each group was (mean1s.d. minutes): normal 1.4210.17 (n=7), hyperglycemic 2.8510.83 (n=5), hypoglycemic 0.9410.39 (n=5). Corresponding values for the DC drop were: normal 1.4210.8 (n=5), hyperglycemic 3.5010.76 (n=3), hypoglycemic 0.6210.17 (n=2). Conclusion: A gradual ADC decline begins immediately upon MABP decrease, which may be due to an instantaneous transmembrane water shift. A subsequent rapid drop in ADC occurs coincident with anoxic cell membrane depolarization; both changes were delayed or accelerated together by hyper- or hypoglycemia.