硫化氢后处理对大鼠肺缺血再灌注损伤的影响

目的用外源性硫化氢后处理大鼠肺缺血再灌注损伤模型，检测其对肺缺血再灌注损伤的影响。方法将24只健康SD大鼠，随机分成3组，每组8只，分别为：假手术（Sham）组、肺缺血再灌注（I／R）组及I／R＋硫氢化钠（NailS）干预组。在每组实验结束后取大鼠肺组织，观察肺组织病理学的变化，检测大鼠肺湿／于重（W／D）比值，肺组织丙二醛（MDA）含量及超氧化物岐化酶（SOD）活性的测定，提取支气管肺泡灌洗液（BALF）检测BALF中白细胞计数、中性粒细胞百分比及肺通透性指数。结果I／R组肺组织W／D值、MDA水平与Sham组比较显著升高（P〈0．05），而I／R＋硫氢化钠（NariS）干预组明显低于I／R组（P〈0．05）；I／R组肺组织SOD活性与Sham组比较显著降低（P〈0．05），I／R＋硫氢化钠（NariS）干预组明显高于I／R组（P〈0．05）。肺组织病理结果表明，I／R＋硫氢化钠（NaHS）干预组与I／R组比较损伤减轻，肺泡腔内炎性细胞减少。结论硫化氢后处理通过减轻肺水肿、降低氧自由基水平有关，对肺缺血再灌注损伤具有保护作用。

Impact of hydrogen sulfide postconditioning on ischemia-reperfusion injury in lung of rats

Objective To research the impact of hydrogen sulfide （H2S） on oxidative damage in lung of rats after is- chemia-reperfusion. Methods Twenty-four SD rats were randomly divided into sham group （n=8）, lung ischemia-reper- fusion group （I/R group, n=8） and I/R＋NaHS group （n=8）. At the end of the experiment, examined the lung pathologic change, ratio of lung wetweight to dryweight （W/D）, malondialdehyde （MDA） and myeloperoxidase （MPO） content and activities of superoxide dismutase（SOD） in lung tissues and protein concentrations, WBC count, and PMN percentage in broncho-alveolar lavage fluid were determined. Results The W/D ratio of lung tissue and contents of MDA in lung tis- sue in the I/R group and I/R＋NaHS groups were significantly higher than those in the sham group （P〈0.05）, while the indices above in I/R＋NaHS group were significantly lower than those in the I/R group （P〈0.005）; The activities of SOD in lung tissue in the I/R group and I/R＋NaHS group were significantly lower than those in the sham group （P〈0.05）, while the indices above in I/R＋NaHS group were significantly higher than those in the I/R group （P〈0.05）. The lung pathologic change also showed that pre-administration of NariS could relieve lung ischemia-reperfusion injury. Con- clusion These findings suggest that hydrogen sulfide postcondition has better protective effects on ischemia-reperfusion injury of lung in rats, its mechanism involves attenuate pulmonary edema and oxyradical elimination.