前列腺素E_1减轻大鼠移植肺缺血/再灌注损伤作用及机制的探讨

Effect and mechanism for prostaglandin E_1 to ameliorate ischemia-reperfusion injury after rat lung transplantation

目的探讨受鼠在肺移植后注射前列腺素E1(PGE1)对移植肺缺血/再灌注损伤的影响及机制。方法取36只SD大鼠,随机配对建立左肺移植模型,实验分为两组,PGE1组:受鼠在移植肺再灌注后开始静脉滴注PGE1至术后1h。对照组:供鼠、受鼠肺移植前后未行任何特殊处理,只进行肺移植。受鼠再灌注1 h后,夹闭右肺门5 min,进行动脉血气分析检测。取移植肺组织测髓过氧化物酶(MPO)活性、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、肺湿/干重比(W/D)以及观察移植肺的病理学形态。结果 PGE1组动脉血氧分压/吸氧浓度(PaO2/FiO2)值较对照组升高,W/D显著低于对照组,差异有统计学意义(P<0.05)。PGE1组与对照组相比,MPO活性明显降低,SOD活性明显增高,MDA含量明显增高,W/D明显下降。PGE1组炎症细胞浸润明显较对照组轻。结论受鼠在肺移植后静脉注射PGE1能改善移植肺的氧合,减轻缺血/再灌注损伤,其机制可能与其抗氧化自由基损伤、抑制中性白细胞激活及抑制炎症细胞浸润有关。

Objective To investigate the effects of prostaglandin E1（PGE1）on lung ischemia-reperfusion injury after reperfusion.Methods Thirty-six health adult male Sprague-Dawley rats were randomly allocated to the control and the PGE1 group.Lung transplantation was performed in a＂cuff-like＂vessel anastomosis technique.After 1-h reperfusion,the right hilus was clipped for 5 min,then blood sample was collected from carotid artery for arterial blood gas analysis.The lung graft was harvested for measuring wet/dry weight ratio（W/D）,the activity of myeloperoxidase（MPO）and hemocuprein（SOD）,and the content of malondialdehyde（MDA）,and observing pathology morphous.Results After 1-h reperfusion,compared to the control group,PaO2/FiO2 was improved significantly in the PGE1 group（279.46±90.48 VS.155.23±48.42,P0.05）.The wet/dry ratio of lung（W/D）was lower than that in control group（17.3±3.9 VS.25.8±4.8,P0.05）.The activities of MPO were significantly reduced in PGE1 group（1.78±0.44 VS.3.23±0.68,P0.01）.The activities of SOD were significantly increased（0.83±0.08 VS.0.50±0.07,P0.01）.The content of MDA in the lung tissue of PGE1 group was significantly higher than that of the control group（0.38±0.09 VS.0.55±0.07,P0.01）.Inflammatory cell infiltration was also significantly reduced.Conclusion Vein shot PGE1 might improve pulmonary oxygenation,mitigate ischemic-reperfusion injury.The mechanism is related to its anti-oxi-dative effect and the inhibition of neutrophils activation and infiltration.