Chan J, Greenberg D A
Department of Neurology, University of California, San Francisco.
Neurosci Lett. 1991 Jan 2;121(1-2):34-6. doi: 10.1016/0304-3940(91)90642-7.
Hyperglycemia has been reported to alter outcome following experimental and clinical cerebral ischemia, but the mechanisms involved are incompletely understood. Since glucose influences the function of dihydropyridine-sensitive, voltage-gated Ca2+ channels in some non-neural cells, and since cellular Ca2+ overload has been implicated in the pathogenesis of ischemic neuronal injury, we examined whether glucose regulates Ca2+ channel function in a cultured neural cell line. Physiologic concentrations of glucose had no effect on free intracellular Ca2+ levels in PC12 cells, but 4-fold elevation of glucose above physiologic levels reduced the dihydropyridine-sensitive, depolarization-induced increase in Ca2+. This effect would not account for exacerbation of ischemic brain injury by hyperglycemia, but may contribute to attenuation of ischemic injury by glucose in certain settings.
据报道，高血糖会改变实验性和临床脑缺血后的预后，但其中涉及的机制尚不完全清楚。由于葡萄糖会影响一些非神经细胞中对二氢吡啶敏感的电压门控Ca2+通道的功能，并且由于细胞内Ca2+过载与缺血性神经元损伤的发病机制有关，我们研究了葡萄糖是否调节培养的神经细胞系中的Ca2+通道功能。生理浓度的葡萄糖对PC12细胞内游离Ca2+水平没有影响，但葡萄糖浓度比生理水平升高4倍会降低对二氢吡啶敏感的、去极化诱导的Ca2+增加。这种效应并不能解释高血糖对缺血性脑损伤的加重作用，但在某些情况下可能有助于葡萄糖减轻缺血性损伤。
