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1. 1. 第一人民医院心血管外科,上海,200080
2. 2. 上海交通大学医学院上海儿童医学中心心胸外科,上海,200127
纸质出版日期:2012,
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董莉亚, 郑景浩, 施 盛, 等. 肺缺血预处理对深低温停循环肺损伤保护的实验研究[J]. 重庆医科大学学报, 2012,37(2):110-113.
DONG Liya, ZHENG Jinghao, SHI Sheng, et al. The experimental research of lung protection mechanism in deep hypothermic circulatory arrest cardiopulmonary bypass[J]. Journal of Chongqing Medical University, 2012,37(2):110-113.
董莉亚, 郑景浩, 施 盛, 等. 肺缺血预处理对深低温停循环肺损伤保护的实验研究[J]. 重庆医科大学学报, 2012,37(2):110-113. DOI:
DONG Liya, ZHENG Jinghao, SHI Sheng, et al. The experimental research of lung protection mechanism in deep hypothermic circulatory arrest cardiopulmonary bypass[J]. Journal of Chongqing Medical University, 2012,37(2):110-113. DOI:
目的:评估肺缺血预处理(Ischemic preconditioning,IP)对心脏手术深低温停循环(Deep hypothermic circulatory arrest,DHCA)中肺损伤的保护效果。方法:24只幼猪随机分4组:常规体外循环(Cardiopulmonary bypass,CPB)再灌注组(基线组,n=6)、无肺IP的DHCA组(对照组,n=6)、单纯肺IP的DHCA组(IP-1组,n=6)和合并肺缺血缺氧预处理的DHCA组(IP-2组,n=6)。在CPB前、结束即刻和结束后1 h分别检测左心房(Left atrium,LA)和肺动脉(Pulmonary artery,PA)血中TNF-α、IL-8、IL-10水平以及中性粒细胞、单核细胞上CD18的表达值,计算LA/PA值衡量肺区释放炎症介质量和激活白细胞量;取小块肺组织测肺湿干重比。结果:(1)4组CPB后TNF-α、IL-8和IL-10的LA/PA值均增加;相对基线组,TNF-α对照组和IP-1组CPB后1 h显著增加,IL-8对照组CPB后两时点和IP-1组CPB结束即刻显著增加,IL-10都显著升高;相对对照组,TNF-α仅IP-2组CPB后1 h显著降低,IL-8、IL-10两IP组都显著降低;(2)CPB后单核细胞上CD18表达值比值仅对照组显著降低,而中性粒细胞上CD18表达值比值,IP-1组CPB后1 h和对照组、IP-2组CPB后两时点均显著降低;相对基线组单核细胞上比值仅对照组CPB后两时点和IP-1组CPB后1 h显著降低,中性粒细胞上比值,对照组、IP-1组显著降低,IP-2组仅CPB结束即刻显著降低;相对对照组单核细胞上比值IP-2组CPB后1 h显著增加,中性粒细胞上比值,IP-1组和IP-2组也均在CPB后1 h显著增加;(3)肺湿干重比值,对照组、IP-2组在CPB后显著增加,IP-1组仅在CPB后1 h显著增加;与基线组比较,对照组CPB后两时点和IP-1组CPB后1 h显著增加;与对照组比较,仅IP-2组比值显著减少。结论:研究示DHCA加剧了体外循环肺组织炎症反应,证实了肺IP可以减轻DHCA缺血再灌注炎症反应性肺损伤;合并肺缺血缺氧预处理的DHCA组相对于单纯肺IP的DHCA组,对肺功能具有更好的保护趋势。
Objective:To investigate whether lung IP for a short period prior to surgery is sufficient to prevent symptoms of lung ischemia reperfusion injury(LIRI),especially the inflammatory response. Methods:24 piglets were divided randomly into four groups:regular CPB reperfusion group(baseline group,n=6),DHCA group without lung IP(control group,n=6),DHCA group with single pulmonary artery(PA) perfusion twice in the lung IP process(IP-1,n=6),and DHCA group with lung ventilation together with PA perfusion twice in the lung IP process(IP-2,n=6). Blood was simultaneously drawn from the left atrium(LA) and thepulmonary artery(PA);The levels of TNF-α,IL-8 and IL-10,as well as the adhesion molecules CD18 on leukocytes,were determined. As a measure of the pulmonary release,ratios of LA/PA levels were calculated.A piece of lung tissue was taken to measure the wet to dry lung weight ratio(W/D) at three time points. Results:(1)The lung itself significantly produced more TNF-α,IL-8 and IL-10 after CPB in each group;Compared with baseline group,LA/PA ratios for TNF-α at 1 h post-CPB in both control group and IP-1 group were signifi-cantly increased,the ratios for IL-8 in control group after CPB and in IP-1 group at the end of CPB were significantly increased,the ratios for IL-10 in other three groups were all increased;Compared with control group,LA/PA ratios for TNF-α in IP-2 group at 1 h Post-CPB were significantly decreased,the ratios for IL-8 and IL-10 were all significantly decreased in IP groups.(3)Compared with Pre-CPB,LA/PA ratios of CD18 on monocytes only in control group significantly decreased after CPB,whereas ratios of CD18 on PolymorPhonuclear leukocytes(PMNs)in IP-1 group at 1 h Post-CPB and in both control group and IP-2 group after CPB were significantly decreased;Compared with baseline group,LA/PA ratios of CD18 on monocytes in control group after CPB and in IP-1 group at 1 h Post-CPB were significantly increased,the ratios of CD18 on PMNs in both control group and IP-1 group after CPB and in IP-2 group at the end of CPB were significantly increased;Compared with control group,LA/PA ratios of CD18 on monocytes in IP-2 group and ratios of CD18 on PMNs in both IP-1 and IP-2 groups at 1 h Post-CPB were significantly increase.(4)Compared with Pre-CPB,lung W/D ratios in both control and IP-2 group after CPB and in IP-1 group at 1 h Post-CPB were significantly increased;Compared with baseline group,ratios in control group after CPB and in IP-1 group at 1 h Post-CPB were significantly increased;Compared with control group,only in IP-2 group the ratios signifi-cantly decreased. Conclusion:Our data indicate that DHCA aggravates lung inflammatory response during CPB;lung IP has a pro-tective effect in LIRI during DHCA;moreover,maintaining ventilation together with PA perfusion in the lung IP process during CPB trends to excel single PA perfusion.
深低温停循环缺血预处理缺血再灌注损伤
deep hypothermic circulatory arrestischemic preconditioningischemia reperfusion injury(IRI)
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