胰岛素抵抗大鼠主动脉内皮功能的机制探讨

目的 探讨胰岛素抵抗(insulin resistant，IR)大鼠主动脉内皮功能的变化及其机制。方法 SD大鼠高果糖(high fructose，HF)饲养8周制备IR模型，采用血管环灌流实验观察血管收缩和舒张功能的变化，同时测定主动脉一氧化氮合成酶(nitric oxide synthase，NOS)的活性和血清一氧化氮(nitric oxide，NO)的含量。结果 (1)高果糖组离体主动脉对乙酰胆碱(acetylcholine，Ach)的舒张反应明显减弱，对新福林(L-Phenylephrine，PE)的收缩反应明显增强。(2)两组大鼠离体主动脉对硝普钠(sodium nitropmsside，SNP)的舒张反应差异无显著性。(3)高果糖组主动脉：NOS活性明显降低，尤以组织型一氧化氮合酶(constitutive nitric oxide synthase，cNOS)下降明显，同时血清NO显著降低。结论 胰岛素抵抗大鼠主动脉内皮功能异常，其可能机制一方面与cNOs的活性降低、NO释放减少有关，另一方面与高胰岛素血症有关。

Study of Mechanism of Aortic Endothelial Function in Rats With Insulin Resistance

Objectives To investigate endothelial function of the aortia in rats with insulin resistance(IR) and the underlying mechanism. Methods Male Sprague - Dawley(SD) rats were fed with high fructose (HF) to induce IR model for 8 weeks. The thoracic aortic rings of SD rats were mounted on a bath system, contraction and relaxation of aortic rings were measured. Aortic nitric oxide synthase (NOS ) activity and nitric oxide (NO) levels were tested. Results (1)The relaxative response of thoracic aortic rings to acetylcholine(Ach) was depressed and the contractive response to L- Phenylephrine(PE) were enhanced significantly in the HF group. (2)Sodium nitro prusside (SNP) induced vasodilator responses did not differ significantly in two groups. (3) Aortic cNOS activity and NO levels were significantly lowered in the HF group. Conclusion The deficiency of cNOS activity and NO production may contribute to the vascular endothelial dysfunction in rats with insulin resistance. Besides, it could be caused by hyperinsulinemia.