目的 观察持续气道正压（continuous positive airway pressure，CPAP）对高龄肺癌患者单肺通气（one-lung ventilation，OLV）中非通气侧肺泡灌洗细胞IL-1β和IL-8 mRNA的表达，在分子水平上探讨CPAP对肺炎性反应的影响。方法 选择单肺通气下年龄>65岁的肺癌开胸手术患者28例，ASA Ⅰ~Ⅱ级，随机分为对照组（n=14）和CPAP组（n=14）。对照组在麻醉期间非通气侧肺的支气管导管直接开口于大气中，CPAP组麻醉期间非通气侧肺持续给予CPAP（压力3~5 cmH₂O，1 cmH₂O=1.02 Pa）。在单肺通气开始和通气2 h后分别对两组患者非通气侧肺用纤维支气管镜行支气管肺泡灌洗（bronchoalveolar lavage，BAL），从灌洗液中收获细胞提取RNA，逆转录合成cDNA，以β-actin为内标准作PCR后电泳扫描求积，检测肺泡灌洗细胞IL-1β和IL-8 mRNA的表达。结果 单肺通气2 h后，对照组比CPAP组非通气侧肺肺泡灌洗液中IL-8和IL-1β mRNA的表达显著增加（P<0.01）。结论 单肺通气中非通气侧肺给予适度的CPAP可以有效减少高龄肺癌患者肺泡灌洗细胞促炎性细胞因子mRNA的表达水平，抑制肺局部炎症反应，对非通气侧肺可能有一定的保护作用。

Objective To investigate the effects of continuous positive airway pressure (CPAP) on the expression of IL-1β and IL-8 mRNA in alveolar lavage cells of old patients with lung tumor during one-lung ventilation (OLV). Methods Twenty-eight patients with lung tumor, ASA Ⅰ-Ⅱ, aged above 65 years old who underwent lobectomy were randomly divided into CPAP group (n=14) and control group (n=14). There was no ventilation on the non-ventilated lung which was opened to the air in control group. Oxygen was administered via CPAP (Pressure 3-5 cmH₂O, 1 cmH₂O=1.02 Pa) system to the non-ventilated lung during OLV in CPAP group. Alveolar lavage cells were harvested by bronchoalveolar lavage at the beginning of OLV and 2 hours after OLV. RNA was extracted from the harvested cells and cDNA was synthesized by reverse transcription. The expression of IL-8 and IL-1β mRNA was measured by semi-quantitative PCR with β-actin as an internal standard. Results The expressions of IL-1β and IL-8 mRNA was significantly higher 2 hours after OLV than that at the beginning of OLV in control group. The increase was slight in CPAP group. There were statistical differences in IL-8 and IL-1β mRNA expressions between CPAP group and control group was significant (P<0.01). Conclusions CPAP used during OLV in old patients with lung tumor may reduce the expressions of IL-1β and IL-8 mRNA in alveolar lavage cells, which can inhibit inflammatory responses in the lungs. CPAP may provide a protective effect on non-ventilated lung.