中文摘要：

目的：以ATP敏感性钾通道（K_（ATP））SUR2B/Kir6.1亚型开放剂埃他卡林（Ipt）为工具药,研究激活SUR2B/Kir6.1通道扩张肺微动脉作用特征,并探讨其可能的分子机制。方法：利用离体微血管压力-直径监测灌流技术,检测Ipt对大鼠四级肺微动脉的舒张效应（n=6~8）,观察内皮损伤后或用K_（ATP）通道拮抗剂格列苯脲（Gli）、环氧合酶（COX）抑制剂吲哚美辛（Indo）、一氧化氮合酶（NOS）抑制剂L-Nω-硝基精氨酸甲酯（L-NAME）预孵后肺微动脉舒张率的变化。结果：Ipt能够扩张肺微动脉,最大舒张率为（60.53±2.08）%。内皮细胞损伤后,Ipt扩张肺微动脉作用明显减弱,最大舒张率为（9.47±1.56）%,与对照组相比存在显著性差异（P〈0.01）。预孵Gli、Indo、L-NAME后,最大舒张率分别下降为（17.49±1.47）%、（37.00±3.88）%、（24.91±2.30）%,与对照组相比均存在显著性差异（P〈0.01）。结论：其选择性开放K_（ATP）通道SUR2B/Kir6.1扩张肺微动脉作用具有内皮细胞依赖性,与其促进内皮细胞释放一氧化氮（NO）和前列环素（PGI_2）相关。

英文摘要：

Objective： To study the dilatation characteristics of ATP-sensitive potassium channel（K_（ATP）） SUR2B/Kir6. 1 subtype opener iptakalim（ Ipt） in pulmonary arterioles,and to explore its possible mechanism. Methods： Vessels pressure- diameter monitoring perfusion technique was used to observe the dilatation effects of Ipt in rats fourth pulmonary arterioles（ n = 6 ~ 8）. After the pulmonary arterioles were pre-treated with removing endothelium or pre-incubated with K_（ATP）channel blocker glibenclamide（ Gli）,cyclo-oxygenase（COX） inhibitor indomethacin（Indo） and nitric oxide synthase（NOS） inhibitor L-Nω-Nitro-arginine methyl ester（L-NAME）,the dilatation effects of Ipt were observed. Results： Pulmonary arterioles could be relaxed by Ipt,the maximal relaxation rate was（60. 53 ± 2.08） %. Compaired with control group,the effects of Ipt in endothelium denuded arterioles were significantly decreased,the maximal relaxation rate was（9. 47 ± 1. 56） %（ P 0. 01）. The maximal relaxation rate were decreased to（17. 49 ± 1. 47） %,（37. 00 ± 3. 88） %and（24. 91 ± 2. 30） % respectively after Gli,Indo,L-NAME were pre-incubated（ P 0. 01）. Conclusion： Pulmonary arterioles can be relaxed by Ipt. The selective activation of K_（ATP）SUR2 B / Kir6. 1 subtype by Ipt was involved in its mechanisms. The endothelium-dependently dilatation of Ipt was related to nitric oxide（ NO） and prostacyclin（ PGI_2） released by endothelial cells.