一些有害因素可引起钙平衡系统功能失调，钙分布紊乱，导致细胞内钙浓度异常性升高，即钙超载。钙超载15可引起线粒体内氧化磷酸化过程障碍，线粒体膜电位降低，组织ATP含量下降，以及胞浆内磷脂酶、蛋白酶等激活，可导致并促进细胞的不可逆性损伤。起始的钙蛋白酶激活导致胞外Ca2+经硝苯地平敏感的钙通道内流，接着转移到胞膜上，引起Cl-内流和细胞死亡。
已知钙超载(calcium overload)是心肌缺血-再灌注损伤的主要发病环节之一.本工作在离体灌流大鼠心脏缺血-再灌注损伤模型上,观察牛磺酸对心肌组织钙含量和心肌对...
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The Ca2+ fluorescence intensity of hippocampus neurons are increased in all time points after hypoxia compared with the control groups. Excessive Ca2+ influx is the key factor resulting in intracellular calcium overload in neurons.
4、缺氧后海马神经元内Ca2+荧光强度增加,Ca2+过度内流导致细胞内钙超载。
参考来源 - γThe protection may be related to the lowered expression of sarcoplasmic reticulum and membrane Ca~(2+)-ATPase which would lessen calcium overloading.
此保护作用与增加心肌细胞肌浆网和质膜钙离子ATP酶的表达，从而减少缺氧所致的细胞内钙超载有关。
参考来源 - 羟基红花黄色素A对缺氧心肌细胞的保护作用及其机制探讨Intracellular Ca2+ overload is considered as initiating agent of cell apoptosis.
细胞内钙超载被认为是细胞凋亡的始动因素。
参考来源 - 岩青兰黄酮的心肌保护作用及机制研究The Results indicated that Puerarin has protective action as to cerebral ischemia-reperfusion injury ,this study suggested the protect function mechanism is may be related to its resisting free radical damage, expanding brain blood vessel, resisting cell calcium overload,etc.
结果表明葛根素对脑缺血-再灌注损伤有保护作用，研究提示其保护作用机制与其抗自由基损伤、扩张脑血管、拮抗细胞内钙超载等有关。
参考来源 - 葛根素抗脑缺血—再灌注损伤的药理基础研究·2,447,543篇论文数据，部分数据来源于NoteExpress
目的：氟桂利嗪是通过血脑屏障的细胞钙超载阻滞剂。
AIM: Flunarizine is a blocker for calcium overload of cells, which could pass blood brain barrier.
结论：老龄大鼠脑缺血再灌注脑组织损伤与钙超载和自由基损伤有关。
Conclusion: the calcium overload and free radical injury were correlated with brain ischemia reperfusion injury in the aged rats.
正常情况下，NMDA受体活性较低从而保证神经细胞不会出现钙超载。
Under normal conditions, the activity of the NMDA receptors is tightly regulated to prevent nerve cells from becoming overloaded with calcium.
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