Department of Cardiovascular Surgery, Shanghai Jiaotong University, Shanghai, China.
Eur Rev Med Pharmacol Sci. 2013 Jul;17(13):1789-99.
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.
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.
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.
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.
缺血预处理(IP)已被用于减少几种模型中的缺血再灌注损伤。目前尚不清楚 IP 是否足以防止深低温停循环(DHCA)心肺转流(CPB)引起的肺损伤。
24 头小猪随机分为四组:常规 CPB(CPB)、CPB+DHCA(DHCA)、CPB+IP+DHCA(IP-1)和 CPB+缺氧缺血预处理+DHCA(IP-2)。CPB 期间三个时间点测量肺静态顺应性(Cstat)和肺血管阻力(PVR)作为肺功能指标。放射免疫法检测 TNF-α、IL-8 和 IL-10 的表达。流式细胞仪测定 CD18 表达。切除部分肺组织测量湿/干重比(W/D),部分固定观察病理变化。
DHCA 组 Cstat 明显下降,PVR 升高。IP 可预防 DHCA 引起的肺功能障碍,尤其是 IP-2 治疗。CPB 后所有组均产生更多细胞因子,但水平不同。DHCA 组仅左心房/肺动脉 CD18 表达的单核细胞比例下降,CPB 后 1h 的 IP-1 组和 IP-2 组的多形核白细胞比例下降。虽然 IP-2 组的肺 W/D 与 CPB 前相比增加,但明显低于 DHCA 组。组织学发现 IP 组的肺损伤较 DHCA 组轻。
DHCA 加重肺炎症性损伤,IP 可能逆转这种损伤。在 CPB 期间的肺 IP 过程中用肺动脉灌注维持通气似乎比单一肺动脉灌注更优越。