Department of Biomedical Engineering, College of Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea.
Physiol Meas. 2010 Mar;31(3):439-50. doi: 10.1088/0967-3334/31/3/011. Epub 2010 Feb 11.
An increase in excitotoxic amino acid glutamate (GLU) concentration associated with neuronal damage might be the cause of the ischemic damage observed in stroke patients suffering from hyperglycemia. However, the effect has never been investigated by real-time in vivo monitoring. Therefore, this study examined the effects of the functional responses of ischemia-evoked electroencephalography (EEG), cerebral blood flow (%CBF) and DeltaGLU in hyperglycemia through real-time in vivo monitoring. Five Sprague-Dawley rats were treated with streptozocin (hyperglycemia) and five normal rats were used as the controls. Global ischemia was induced using an 11-vessel occlusion model. The experimental protocols consisting of 10 min pre-ischemic, 10 min ischemic and 40 min reperfusion periods were applied to both groups. Under these conditions, the responses of the ischemia-evoked EEG, %CBF and DeltaGLU were monitored in real time. The EEG showed flat patterns during ischemia followed by poor recovery during reperfusion. The peak reperfusion %CBF was decreased significantly in the hyperglycemia group compared to the control group (p < 0.05, n = 5). The extracellular DeltaGLU releases increased significantly during ischemia (p < 0.0001, n = 5) and reperfusion (p < 0.001, n = 5) in the hyperglycemia group compared to the control group. The decrease in reperfusion %CBF during short-term hyperglycemia might be related to the increased plasma osmolality, decreased adenosine levels and swollen endothelial cells with decreased vascular luminal diameters under hyperglycemic conditions. And, the increase in DeltaGLU during short-term hyperglycemia might be related to the neurotoxic effects of the high extracellular concentrations of DeltaGLU and the inhibition of GLU uptake.
与神经元损伤相关的兴奋性氨基酸谷氨酸 (GLU) 浓度增加可能是高血糖中风患者观察到的缺血损伤的原因。然而，这种影响从未通过实时体内监测进行过研究。因此，本研究通过实时体内监测，研究了高血糖对缺血性诱发脑电图 (EEG)、脑血流 (%CBF) 和 DeltaGLU 的功能反应的影响。将 5 只 Sprague-Dawley 大鼠用链脲佐菌素 (高血糖) 处理，将 5 只正常大鼠作为对照。使用 11 血管闭塞模型诱导全脑缺血。将 10 分钟缺血前、10 分钟缺血和 40 分钟再灌注期的实验方案应用于两组。在这些条件下，实时监测缺血性诱发 EEG、%CBF 和 DeltaGLU 的反应。EEG 在缺血期间呈平坦模式，随后再灌注期间恢复不良。与对照组相比，高血糖组在再灌注期间的峰值再灌注 %CBF 显著降低（p < 0.05，n = 5）。与对照组相比，高血糖组在缺血期间（p < 0.0001，n = 5）和再灌注期间（p < 0.001，n = 5）细胞外 DeltaGLU 释放显著增加。在高血糖条件下，短暂高血糖期间再灌注 %CBF 的降低可能与血浆渗透压升高、腺苷水平降低以及内皮细胞肿胀和血管腔直径减小有关。此外，短暂高血糖期间 DeltaGLU 的增加可能与高细胞外 DeltaGLU 浓度的神经毒性作用以及 GLU 摄取的抑制有关。
