目的:探讨豚鼠耳蜗微血管内皮细胞通透性的分子调控机制。方法:使用体外培养的豚鼠耳蜗血管纹微血管内皮细胞,建立耳蜗微血管内皮细胞通透性调控的体外模型;用霍乱毒素(CT)和速尿作为处理因素,检测其对豚鼠耳蜗微血管内皮细胞环磷酸腺苷(cAMP)和F-肌动蛋白(F-actin)含量的影响,以及对牛血清白蛋白和伊文氏兰通透率的影响。结果:CT能使豚鼠耳蜗微血管内皮细胞cAMP的含量显著增加(P<0.01),F-actin的含量显著减少(P<0.05),且核周F-actin减少尤为明显,使牛血清白蛋白和伊文氏兰的通透率显著降低(均P<0.01);相反,速尿能使耳蜗微血管内皮细胞cAMP的含量显著减少(P<0.01),F-actin的含量显著增加(P<0.01),且核周F-actin增多尤为明显,使牛血清白蛋白和伊文氏兰的通透率显著增高(P<0.01和P<0.05)。结论:cAMP是体外耳蜗血管纹微血管内皮通透性调控的主要分子机制之一。耳蜗血管纹微血管内皮细胞通透性的改变与内皮细胞形状的改变及肌动蛋白丝在内皮细胞中的分布和含量的变化有关。 Objective: To investigate the molecular mechanism of the permeability of cochlear microvascular endothelial cells in guinea pigs. Methods: The in vitro model of cochlear microvascular endothelial cell permeability was established by in vitro culture of guinea pig cochlear microvascular endothelial cells. Cholera toxin (CT) and furosemide were used as the treatment factors to detect the effects of cyclophosphamide on cochlear microvascular endothelial cells Adenosine (cAMP) and F-actin (F-actin) content, and the impact of bovine serum albumin and Evans blue permeability. Results: The cAMP content in cochlear microvascular endothelial cells of guinea pigs was significantly increased (P <0.01), the content of F-actin was significantly decreased (P <0.05), and the decrease of F-actin in nucleus was more obvious, (P <0.01). On the contrary, furosemide induced a significant decrease of cAMP content in cochlear microvascular endothelial cells (P <0.01) and a significant increase of F-actin content (P <0.01) Moreover, the increase of F-actin in the nucleus was more obvious, which made the permeability of bovine serum albumin and Evans blue significantly increased (P <0.01 and P <0.05). Conclusion: cAMP is one of the major molecular mechanisms regulating the permeability of microvascular endothelial cells in cochlear stria vascularis. Changes in the permeability of cochlear vascular microvascular endothelial cells and endothelial cell shape changes and actin filaments in endothelial cells in the distribution and content changes.