The experimental research of lung protection mechanism in deep hypothermic circulatory arrest cardiopulmonary bypass

Abstract:

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.