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本实验用激光扫描共聚焦技术发现肿瘤坏死因子（１ＭＩＵ·Ｌ－１）使培养的单个血管内皮细胞胞浆区和核区Ｃａ２＋皆呈现一过性升高，而且核区上升幅度大，下降缓慢。同等剂量的肿瘤坏死因子没有引起单个白细胞Ｃａ２＋水平的明显变化。蛋白激酶Ｃ的活化剂佛波醇酯（３．５ｎｍｏｌ·Ｌ－１）可引起两类细胞Ｃａ２＋水平皆迅速升高，随后下降，低于原水平，最后，内皮细胞核区Ｃａ２＋完全被排空，而白细胞核区仍残留Ｃａ２＋。结果提示肿瘤坏死因子对不同的靶细胞的刺激效应不同；细胞不同区的Ｃａ２＋水平变化效应也不同；蛋白激酶Ｃ的作用主要是排出细胞内Ｃａ２＋。观察单个细胞Ｃａ２＋变化有助于研究Ｃａ２＋参与动脉粥样硬化发病机制。
In this experiment, we found that the tumor necrosis factor (1MIU · L-1) increased transiently in the cytoplasm and nucleus Ca2 + of cultured single vascular endothelial cells by laser scanning confocal technique, and the nuclear region increased greatly and decreased slowly . The same dose of tumor necrosis factor did not cause a significant change in the level of Ca2 + in a single leukocyte. Phorbol ester (3.5 nmol·L-1), an activator of protein kinase C, caused the levels of Ca2 + in both cell types to rapidly increase, and then decreased to a level lower than the original level. Finally, Ca2 + in the endothelial cell nucleus was completely evacuated, The leucocyte nucleus is still residual Ca2 +. The results suggest that tumor necrosis factor has different stimulation effect on different target cells; Ca2 + level changes in different regions of cells are also different; and protein kinase C mainly excretes intracellular Ca2 +. To observe the changes of Ca2 + in single cells is helpful to study the pathogenesis of Ca2 + involved in atherosclerosis.