Higuchi T, Fernandez E J, Maudsley A A, Shimizu H, Weiner M W, Weinstein P R
Magnetic Resonance Unit, Department of Veterans Affairs Medical Center, San Francisco, California, USA.
Neurosurgery. 1996 Jan;38(1):121-9; discussion 129-30. doi: 10.1097/00006123-199601000-00030.
The time course, anatomic distribution, and extent of changes in cerebral lactate, N-acetyl-L-aspartate (NAA), and other metabolite levels determined by three-dimensional in vivo 1H magnetic resonance spectroscopy and single-voxel spectral analysis after middle cerebral artery occlusion in rats. Increased lactate was detected in the central ischemic region within 1.3 hours after the onset of permanent occlusion (n = 22) or 0.5 hour after the onset of 1 hour of temporary occlusion and then reperfusion (n = 8). Permanent occlusion resulted in persistent lactate elevation and a 25.4 +/- 4.1% reduction in the NAA peak after 1.3 hours; NAA was almost completely depleted after 24 hours. Results also demonstrated delayed depletion of all other magnetic resonance spectroscopy-visible 1H metabolites, including creatine, choline, and glutamate, after permanent occlusion. After 1 hour of temporary focal ischemia, lactate returned to nearly normal levels within 0.4 hour after the onset of reperfusion; at 72 hours, a recurrent increase in lactate and a new decrease in NAA were observed, suggesting delayed tissue injury. Histological analysis, performed in 10 rats, demonstrated infarcts that corresponded in distribution to regions of NAA depletion at 72 hours. These findings indicate that lactate elevation is a sensitive early marker of ischemia; however, temporary recovery of lactate accumulation after reperfusion did not predict sustained metabolic recovery. In contrast, NAA depletion within 1.3 hours after the onset of ischemia identified central ischemic regions that were destined for infarction. Potential clinical applications include selection and monitoring of therapeutic intervention, as well as prediction of outcome, in patients with acute stroke.
通过三维活体¹H磁共振波谱和单体素频谱分析，测定大鼠大脑中动脉闭塞后大脑乳酸、N-乙酰-L-天冬氨酸（NAA）及其他代谢物水平变化的时间进程、解剖分布和程度。在永久性闭塞开始后1.3小时内（n = 22）或短暂闭塞1小时后再灌注开始后0.5小时（n = 8），在中央缺血区域检测到乳酸增加。永久性闭塞导致乳酸持续升高，1.3小时后NAA峰降低25.4±4.1%；24小时后NAA几乎完全耗尽。结果还表明，永久性闭塞后，所有其他磁共振波谱可见的¹H代谢物，包括肌酸、胆碱和谷氨酸，均出现延迟消耗。短暂局灶性缺血1小时后，再灌注开始后0.4小时内乳酸恢复到接近正常水平；在72小时时，观察到乳酸再次升高和NAA再次降低，提示延迟性组织损伤。对10只大鼠进行的组织学分析显示，梗死灶的分布与72小时时NAA耗竭区域相对应。这些发现表明，乳酸升高是缺血的敏感早期标志物；然而，再灌注后乳酸积累的短暂恢复并不能预测代谢的持续恢复。相比之下，缺血开始后1.3小时内NAA的耗竭可确定注定会发生梗死的中央缺血区域。潜在的临床应用包括急性中风患者治疗干预的选择和监测以及预后预测。
