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目的：探讨动脉粥样硬化（AS）的不同病理阶段中，中性白细胞变形性改变的分子机制。方法：动态检测兔AS前期、早期、中期和晚期的中性白细胞变形性、膜脂流动性、[Ca2＋]i和Na＋－K＋ATPase活性。结果：（1）中性白细胞膜脂流动性和Na＋－K＋ATPase活性降低始于AS前期，而中性白细胞变形性明显减退和[Ca2＋]i水平增高见于AS早期；（2）在AS进程中，中性白细胞变形性减退逐渐加重，与膜脂流动性和Na＋－K＋ATPase活性呈正相关，而与[Ca2＋]i呈负相关。结论：本研究结果表示中性白细胞的变形能力取决于膜脂流动性、Na＋－K＋ATPase活性及[Ca2＋]i水平，中性白细胞参与AS的发生和发展。
Objective: To investigate the molecular mechanism of neutrophil deformability in different pathological stages of atherosclerosis (AS). Methods: The neutrophil deformability, membrane lipid fluidity, [Ca2 +] i and Na + -K + ATPase activity in pre-early, early, mid-term and early stages of rabbit AS were detected dynamically. Results: (1) Neutrophil membrane fluidity and Na + -K + ATPase activity decreased from the pre-AS stage, while the degeneration of neutrophils and the increase of [Ca2 +] i level were seen in the early stage of AS. (2) Decreased neutrophil degeneration gradually aggravated, and membrane fluidity and Na + -K + ATPase activity was positively correlated with [Ca2 +] i was negatively correlated. CONCLUSIONS: The results of this study indicate that the deformability of neutrophils is dependent on membrane lipid fluidity, Na + -K + ATPase activity and [Ca2 +] i levels, and neutrophils are involved in the development and progression of AS.