Evaluation of early macrophage activation and NF-kappaB activity in pulmonary injury caused by deep hypothermia circulatory arrest: an experimental study.

This study aimed to analyze changes in nuclear factor-kappa B (NF-kappaB), inflammation factors, and macrophages in pulmonary tissue under deep hypothermia circulatory arrest (DHCA) at different time points, which can be used to infer the role of early macrophage activation and NF-kappaB activity in pulmonary injury. The possible pathogenic mechanisms of DHCA-induced pulmonary injury were investigated in this study to provide an experimental basis for clinical lung protective strategies. Piglets (n = 12) were randomly divided into 2 groups, with 6 piglets in each group. The control group had ambient temperature cardiopulmonary bypass (CPB), and the experimental group had DHCA. Both groups had conventional CPB with 30 min of parallel circulation. Changes in NF-kappaB and inflammatory factors were examined in each group at 6 different time points. At 0.5 h after ischemia-reperfusion, NF-kappaB expression in the nucleus of pulmonary tissue reached its peak, and brown-stained nuclei were mainly polymorphonuclear antibodies. At 1 h after ischemia-reperfusion, plasma tumor-necrosis factor (TNF)-alpha in the experimental group was significantly increased compared with that before reperfusion (P < 0.05). The plasma levels of interleukin (IL)-8 and IL-6 in the experimental group were significantly increased at 1.5 h after ischemia-reperfusion compared with the levels before reperfusion (P < 0.05). Early activation of NF-kappaB under DHCA might play an important role in DHCA-induced pulmonary injury.