肝脏缺血再灌注后急性肺损伤的机制及丙泊酚对其的保护作用

Propofol attenuates acute lung injury after hepatic ischemia/ reperfusiou

目的 观察肝脏缺血再灌注后急性肺损伤的发病机制及丙泊酚的保护作用。方法成年封闭群SD雄性大鼠48只，采用随机数字表法随机分为：假手术组（Sham）：假手术2h（Sham2）组；假手术6h（Sham6）组；缺血再灌注组（IR）：缺血再灌注2h（IR2）组；缺血再灌注6h（IR6）组及丙泊酚组（P）：丙泊酚2h（P2）组；丙泊酚6h（P6）组。P组自缺血前30min静脉输注丙泊酚1mg·kg^-1·min^-1。Sham组及IR组按0．1mL·kg^-1·min^-1速率输注乳酸钠林格氏液，时间30min。在再灌注后2h、6h测定肺灌洗液肿瘤坏死因子-α（TNF-α），超氧化物歧化酶（SOD），丙二醛（MDA），肺组织髓过氧化物（MPO）浓度及肺组织湿／干重（W／D）比值并计算肺组织学评分。结果IR组及P组大鼠缺血再灌注后肺泡灌洗液TNF—α的水平较Sham组明显升高，但P组再灌注2h、6h时均明显低于IR组。Sham组SOD水平与P组相比差异无统计学意义。IR各组SOD值均显著降低，P组SOD值与IR组相比明显升高。在大鼠肝脏缺血／再灌注后，IR各组MDA值均显著升高，在再灌注后6h达到高峰。P组MDA轻度升高，但明显低于IR组，与Sham组相比差异无统计学意义。IR组大鼠的肺W／D值、MPO及组织学评分均明显高于Sham组及P组。结论丙泊酚通过抑制炎性因子的分泌，减轻氧化应激损伤等机制，对肝脏缺血再灌注损伤后肺部的继发性损伤有明显的保护作用。

Objective To investigate the mechanism of acute lung injury after hepatic ischemia / reperfusion and the protective effect of propofol. Methods Forty-eight male SD rats were randomly divided into Sham2 group, Sham6 group; IR2 group （ IR2 ）, IR6 group （ IR6 ） ; P2 group （ P2 ）, P6 group （P6）. The 1 mg·kg^- 1· min^- 1 propofol was infused from 30 min before ischemia in P groups, and the same volume sodium lactate Ringer’s solution was infused in Sham and IR groups. The concentration of TNF-α, superoxidedimutase （ SOD）, malondialdehyde （ MDA）, myeloperosidase （ MPO ）, lung wet/dry weight ratio and lung histological scores were measured at the points of 2 and 6 hour after reperfusion. Results TNF-α levels were higher in IR and P groups than those in sham groups but the values in P groups were lower than those in IR groups. SOD levels decreased greatly in IR groups, there were great difference between P and IR groups. MDA levels increased greatly in IR groups and reached the peak value at 6 hour after reperfusion. MDA levels in P groups were lower than those in IR groups and there were no difference between P and sham groups. The ratio of Wet/dry levels, MPO and lung histological scores were increased greatly after reperfusion in IR and P groups. But the value in P groups was lower than those in IR groups. Conclusions Acute lung injury after hepatic ischemia / reperfusion is mainly induced by the oxidant stress and neutrophil infiltration in lung tissues. Propofol may have effects of antioxidation and decrease neutrophil infiltration which attenuate lung injury induced by hepatic ischemia / reperfusion.