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目的和方法：以高速枪弹压力波致伤培养细胞为实验模型，以特异的Ｇ蛋白和肌醇磷脂代谢抑制剂作用培养内皮细胞，力图从分子创伤学角度探讨压力波调控ＥＴ－１的信号通路。结果：磷脂酶Ｃ抑制剂ｎｅｏｍｙｃｉｎ作用内皮细胞，明显消除压力波对ＥＴ－１释放及表达的刺激作用。Ｇ蛋白抑制剂ＧＤＰ－β－Ｓ则无明显作用。蛋白激酶Ｃ抑制剂ｓｌａｕｒｏｓｐｏｒｉｎｅ对压力波作用后ＥＴ－１基因表达增强有较强的抑制作用。结论：高速枪弹压力波对内皮细胞ＥＴ－１的调控可能通过某种直接途径（而非Ｇ蛋白介导）激活肌醇磷脂代谢，从而生成ＩＰ３和二酰基甘油。ＩＰ３可能参与早期ＥＴ－１释放，二酰基甘油对ＰＫＣ的激活参与了ＥＴ－１基因表达的调控。
OBJECTIVE: To investigate the effect of pressure wave on ET-1 signaling pathway in vitro and in vivo.Methods: Endothelial cells were cultured with high-speed bullet pressure wave and cultured in vitro with specific G protein and inositol phospholipid metabolism inhibitors . Results: Neomycin, a phospholipase C inhibitor, significantly inhibited the release of ET-1 and its stimulation by pressure wave. G-protein inhibitor GDP-β-S had no significant effect. The protein kinase C inhibitor, slaurosporine, has a strong inhibitory effect on the expression of ET-1 gene after pressure wave. CONCLUSION: The regulation of ET-1 by endothelial progenitor cells by high-speed bullet pressure wave may activate the inositol phospholipid metabolism via some direct pathway instead of G protein, thus generating IP3 and diacylglycerol. IP3 may be involved in the release of early ET-1, and the activation of PKC by diacylglycerol is involved in the regulation of ET-1 gene expression.