目的　探讨在投射物侵彻撞击时产生的压力波作用下 ,血管内皮细胞肌醇磷脂信号通路的变化及其在继发损伤中的作用。　方法　以军用 7.6 2mm枪弹侵彻介质水所产生的强压力波作用于培养的血管内皮细胞 ,测定压力波作用后细胞内三磷酸肌醇 (IP3)、游离钙含量以及蛋白激酶C(PKC)、培养液中乳酸脱氢酶 (LDH)活性 ,并以特异的肌醇磷脂代谢阻断剂新霉素预作用于培养内皮细胞后 ,观察压力波作用后上述参数变化。　结果　压力波作用后 2h内IP3明显升高 ,游离钙水平和PKC活性在 4h内显著增加 ,培养液内升高的LDH活性与上述磷酸肌醇代谢激活一致。压力波作用前采用新霉素预作用培养内皮细胞可明显抑制肌醇磷脂代谢激活 ,细胞浆和LDH泄漏。　结论　血管内皮细胞肌醇磷脂信号通路可能是传导投射物侵彻撞击时压力波效应 ,启动继发损伤的重要化学信号通路。 Objective To investigate the changes of inositol phospholipid signaling pathway in vascular endothelial cells and its role in secondary injury under the pressure wave generated by projectile penetration and impact. Methods The vascular endothelial cells were cultured under intense pressure waves generated by penetration of medium with 7.6 2 mm bullets and the intracellular levels of inositol 1,4,5 - trisphosphate (IP3), free calcium and protein kinase C (PKC) The activity of lactate dehydrogenase (LDH) in the culture medium was determined. The changes of the above parameters were observed after the pretreatment of endothelial cells with neomycin, a specific inhibitor of inositol phospholipid metabolism. Results IP3 was significantly increased within 2 hours after pressure wave, and the level of free calcium and PKC activity increased significantly within 4 hours. The activity of LDH in culture broth was consistent with that of phosphoinositide metabolism. Pretreatment with neomycin prior to pressure wave treatment of endothelial cells significantly inhibited the activation of inositol phospholipid metabolism, cytosolic and LDH leakage. Conclusions The inositol phospholipid signaling pathway of vascular endothelial cells may be the pressure wave effect when the projectile penetrates and collides and starts the important chemical signal pathway of secondary injury.