PURPOSE: Ischemic preconditioning (IP) has been used to reduce ischemia-reperfusion injury in several models. It remains unknown whether IP is sufficient to prevent deep hypothermic circulatory arrest (DHCA) cardiopulmonary bypass (CPB) induced lung injury. MATERIALS AND METHODS: Twenty-four piglets were randomly divided into four groups: routine CPB (CPB), CPB + DHCA (DHCA), CPB + IP + DHCA (IP-1) and CPB + hypoxia-ischemia preconditioning + DHCA (IP-2). Lung static compliance (Cstat) and pulmonary vascular resistance (PVR) were measured as indicators of lung function at three points during CPB. TNF-α, IL-8 and IL-10 expressions were detected by radioimmunoassay. CD18 expression was determined by flow cytometer. Some lung tissues were excised to measure the wet/dry weight ratio (W/D) and some were fixed to observe pathological changes. RESULTS: Cstat significantly decreased whereas PVR increased in DHCA group. IP prevented DHCA-induced lung functional impairment, especially IP-2 treatment. More cytokines were produced after CPB in all groups, but with varying level. Left atrium/pulmonary artery ratio of CD18 expression on monocytes decreased only in DHCA group, whereas which on polymorphonuclear neutrophils decreased in DHCA group, IP-1 group at 1h post-CPB and IP-2 group. Although lung W/D was increased in IP-2 group compared with pre-CPB, but significantly lower than that in DHCA group. Histological findings showed less lung injuries in IP groups than DHCA group. CONCLUSIONS: DHCA aggravates lung inflammatory injury and IP may reverse this injury. Maintaining ventilation with pulmonary artery perfusion in the lung IP process during CPB seems to be more superior to single pulmonary artery perfusion.
PURPOSE: Ischemic preconditioning (IP) has been used to reduce ischemia-reperfusion injury in several models. It remains unknown whether IP is sufficient to prevent deep hypothermic circulatory arrest (DHCA) cardiopulmonary bypass (CPB) induced lung injury. MATERIALS AND METHODS: Twenty-four piglets were randomly divided into four groups: routine CPB (CPB), CPB + DHCA (DHCA), CPB + IP + DHCA (IP-1) and CPB + hypoxia-ischemia preconditioning + DHCA (IP-2). Lung static compliance (Cstat) and pulmonary vascular resistance (PVR) were measured as indicators of lung function at three points during CPB. TNF-α, IL-8 and IL-10 expressions were detected by radioimmunoassay. CD18 expression was determined by flow cytometer. Some lung tissues were excised to measure the wet/dry weight ratio (W/D) and some were fixed to observe pathological changes. RESULTS: Cstat significantly decreased whereas PVR increased in DHCA group. IP prevented DHCA-induced lung functional impairment, especially IP-2 treatment. More cytokines were produced after CPB in all groups, but with varying level. Left atrium/pulmonary artery ratio of CD18 expression on monocytes decreased only in DHCA group, whereas which on polymorphonuclear neutrophils decreased in DHCA group, IP-1 group at 1h post-CPB and IP-2 group. Although lung W/D was increased in IP-2 group compared with pre-CPB, but significantly lower than that in DHCA group. Histological findings showed less lung injuries in IP groups than DHCA group. CONCLUSIONS: DHCA aggravates lung inflammatory injury and IP may reverse this injury. Maintaining ventilation with pulmonary artery perfusion in the lung IP process during CPB seems to be more superior to single pulmonary artery perfusion.