中文摘要：

目的探讨持续输注不同剂量瑞芬太尼对大鼠肺缺血一再灌注损伤血管内皮生长因子（VEGF）的影响及其可能的肺保护机制。方法清洁级健康成年雄性SD大鼠40只（300—350g），按随机数字表法分为5组（n,=8）：假手术（S）组、肺缺血一再灌注（IR）组和瑞芬太尼持续输注（R）组，R组再分为3个亚组（R1、R2、R3）：阻断左肺门前，先予以每组1μg／kg负荷剂量的瑞芬太尼，随即对R1、112、R3各亚组在肺门阻断前15min分别以0．2、0．6、1．2μg／（kg·min）的速率输注瑞芬太尼至再灌注结束。s组和IR组输入与R组等容量的0．9％生理盐水。实验结束后，处死动物，留取肺组织光镜下观察其形态学变化，测定肺组织湿干质量比重（W／D），ELISA测定血清和肺组织VEGF浓度。结果与S组比较，其余4组肺组织均出现了不同程度的损伤，IR组肺W／D和血清VEGF浓度均显著增高（P〈0．001或0．05）；与IR组相比，R1、R2和R3组肺组织损伤相对减轻，肺W／D、肺组织和血清VEGF浓度均降低，除R1组肺组织VEGF浓度外，其余差异均有统计学意义；R1、R2和R3组随着输注速率的提高，肺W／D、肺组织和血清VEGF浓度逐渐降低。结论瑞芬太尼对肺缺血一再灌注损伤具有确切的保护作用，与剂量有关，对VEGF的抑制可能是其机制之一。

英文摘要：

Objective To explore the effects of different doses of remifentanil continuous infusion on VEGF expression of lung ischemia - reperfusion injury in rats and possible mechanism of lung ischemia- reperfusion injury. Methods Forty SPF adult male SD rats weighing 300 ~ 350 g were randomly devided into five groups（ n = 8 each）, shamp operating group （group S） ：not occluded the left hilus pulmonis but explosed it; isehemia reperfusion group （group IR）： 45 rain ischemia ＋ 2 h reperfusion ;three subgroups of remifentanil （ group R1, R2, R3 ） ： 45 vain isehemia ＋ 2 h reperfusion, before the left hilus pulmonis occlusion, remifentanil 1μg/kg bolus followed immediately by an continuous infusion 0. 2,0.6 and 1.2 μg/（ kg-min）, respectively, the group S and IR were given the same volume saline. The continuous fusion was stopped and the rats were sacrified by exsanguinations at the end of reperfusion, the lung tissue was removed for measuring lung wet/dry ration and microscope examination , the concentration of VEGF in lung tissue and serum was tested by enzyme- linked immunosorbent assay. Results Compared with group S, the lung tissue appeared different degrees of injury, W/D and the concentration of VEGF in serum of group IR was all signaficanfly increased （P 〈 0. 001 or 0.05） ; Compared to group IR, W/D and the concentration of VEGF in lung tissue and serum mas all reduced, but not the concentration of VEGF in lung tissue in group RI （ P 〉 0. 05 ） ; WID andthe concentration of VEGF in lung tissue and serum seemed to be on decrease due to the rise of dose of remifentanil, compared with group R1, the reduction of VEGF of lung tissue in group R2 was not statistically significant（P 〉 0.05 ） ; compared to group R2, the decrease of concentration of VEGF in lung tissue and serum in group R3 was all not statistically significant （ P 〉 0. 05 ）. Conclusion Remifentanil definitely protected against LIRI, and correlated with dose, downgraded impression of VEGF in lung tissue and se