[Objective] Ischemia reperfusion (I/R) injury is still inevitable for lung transplantation and ischemic postconditioning (I-postC) may benefit the function of a grafted lung. We investigated the influence of I-postC on expression of the apoptosis gene of canine donor lungs and observed the histomorphological changes under optical microscope. [Methods] Single left-lung orthotopic transplantation (LTx) was performed on 12 pairs of donor-and-recipient matched Beagle dogs. They were randomly subjected into an ischemic postconditioning (I-postC) group (n= 6) or a control group (n= 6). The transplantation procedure in control group was performed routinely, while I-postC protocol was added in the early stage of reperfusion for the experimental group: 10 seconds of reperfusion followed by 10 seconds of blockade, repeated three times. Expression of apoptosis gene Bcl-2 and Bax were measured by reverse transcription polymerase chain reaction (RT-PCR). Pathological changes of the donor lung were observed under an optical microscope. [Results] Compared with the experimental group, expression of Bcl-2 protein was up-regulated while expression of Bax protein was down-regulated. Observed under optical microscope, pulmonary inflammatory reaction was more moderate in I-postC group. [Conclusions] I-postC can attenuate the damage of ischemia-reperfusion injury. I-postC may affect the endogenous pathway of apoptosis by inhibiting expression of Bax and enhancing expression of Bcl-2.%[目的]观察供体犬肺再灌注后早期供体肺组织脂质过氧化反应的变化,了解缺血后处理对供体犬肺植入后细胞凋亡基因表达的变化情况.[方法]随机选取12对比咯犬,组成供受体,进行异体左侧单肺移植术.随机分成两组,对照组:6对犬,进行供受体左侧异体单肺移植,不予缺血后处理的干预,按常规方式进行.缺血后处理组:6对犬,进行供受体左侧异体单肺移植,常规方式获取的供体犬肺植入后,再灌注早期实施3个周期的10 s再灌～10s再阻断,总时程1 min的缺血后处理.于供体犬肺再灌注后1、2h时间点采集供肺标本检测超氧化物歧化酶(SOD)的活性、丙二醛(MDA)的含量；采用RT-PCR技术检测供体肺脏再灌注后1、2h时间点细胞凋亡基因Bcl-2、Bax的表达；光镜下观察供体犬肺植入后1、2h时间点肺组织的病理变化,应用SPSS 13.0统计软件处理,以P＜0.05为统计学上有显著差别.[结果]供体肺脏植入时间平均(35.9±1.7)min.缺血后处理组在1、2h时间点的供体肺组织SOD活性水平较对照组升高、MDA含量较对照组减低,有统计学差异(P＜0.05)；对照组与实验组相比较,肺组织再灌注后1、2h时间点,Bc12蛋白表达上调(P＜0.05),而Bax蛋白表达下调(P＜0.05)；缺血后处理组肺组织光镜下观察在各时间点的炎症反应均较对照组的变化轻微.[结论]缺血后处理可以抑制再灌注时氧化自由基的堆积,从而减少供体肺的缺血再灌注损伤；缺血后处理能够通过抑制促凋亡Bax蛋白的表达,及促进抗凋亡Bc12蛋白表达,从而影响内源性细胞凋亡途径.
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