Kass I S, Abramowicz A E, Cottrell J E, Amorim P, Chambers G
Department of Anesthesiology and Pharmacology, State University of New York Health Science Center, Brooklyn 11203.
Brain Res. 1994 Jan 7;633(1-2):262-6. doi: 10.1016/0006-8993(94)91547-4.
Veratridine-induced depolarization caused a large increase in Ca uptake in the rat hippocampal slice (30.2 vs. 9.0 nM/mg dry weight). This uptake was reduced to 18.4 nM/mg when veratridine was combined with anoxia. When compared with veratridine exposure alone, the combination of anoxia and veratridine increased intracellular Na (460 vs. 380 microM/g), decreased intracellular K (30 vs. 40 microM/g) and decreased ATP levels (0.1 vs. 0.8 nM/mg). The changes in Na, K, and ATP should enhance net Ca uptake, yet Ca uptake was reduced. This suggests an effect of anoxia to block Ca channels. In summary anoxia attenuates depolarization-induced Ca uptake. This may represent a mechanism by which neurons are partially protected against anoxic damage which could be more severe if depolarization-induced Ca uptake was not limited.
藜芦定诱导的去极化使大鼠海马切片中的钙摄取大幅增加（30.2对9.0纳摩尔/毫克干重）。当藜芦定与缺氧联合时，这种摄取减少至18.4纳摩尔/毫克。与单独暴露于藜芦定相比，缺氧和藜芦定联合使细胞内钠增加（460对380微摩尔/克），细胞内钾减少（30对40微摩尔/克），ATP水平降低（0.1对0.8纳摩尔/毫克）。钠、钾和ATP的变化应会增强净钙摄取，但钙摄取却减少了。这表明缺氧对钙通道有阻断作用。总之，缺氧减弱了去极化诱导的钙摄取。这可能代表了一种神经元部分免受缺氧损伤的机制，如果去极化诱导的钙摄取不受限制，缺氧损伤可能会更严重。
