论文部分内容阅读
目的建立腹腔注射穿孔性腹膜炎腹水(PPAF)诱导大鼠急性肺损伤(ALI)模型,探讨ALI的发生机理和L-精氨酸(L-Arg)的作用。方法 60只SD大鼠建立消化道穿孔性腹膜炎(PP)模型,收集PPAF;48只大鼠按随机数字表法分为NS组(n=16),PPAF组(n=16)和L-Arg组(n=16)。各组大鼠再按随机数字表法分为7 h和12 h 2个亚组。检测外周血WBC计数、血清NO及脂质过氧化物丙二醛(MDA)水平、肺组织病理损害评分、肺组织湿/干质量比、肺组织髓过氧化物酶(MPO)水平和肺细胞凋亡情况。结果 PPAF组各时间点血WBC计数、血清NO及MDA水平、肺组织MPO水平、肺组织病理损害评分、湿/干质量比和细胞凋亡率均高于NS组(P<0.01)。L-Arg组血清NO水平显著高于PPAF组(P<0.01),血清MDA水平、肺组织MPO水平、肺组织病理损害评分和湿/干质量比以及细胞凋亡率均显著低于PPAF组(P<0.05)。PPAF组和L-Arg组12 h血清NO水平、肺湿/干质量比和细胞凋亡率均显著高于7 h(P=0.000)。PPAF组和L-Arg组血清NO水平与血清MDA水平(r=-0.257,P=0.021)、肺组织MPO水平(r=-0.444,P=0.011)和肺细胞凋亡率(r=-0.351,P=0.010)呈负相关。各组血清MDA与肺细胞凋亡率呈正相关(r=0.969,P<0.001)。结论腹腔注射PPAF可诱导大鼠ALI,肺内氧化反应增强和细胞凋亡参与了ALI的发生,而L-Arg对ALI具有保护作用。
Objective To establish a rat model of acute lung injury induced by peritoneal peritonitis (PPAF) and investigate the mechanism of ALI and the effect of L-arginine (L-arginine). Methods Sixty Sprague-Dawley rats were randomly divided into NS group (n = 16), PPAF group (n = 16) and L-Arg Group (n = 16). The rats in each group were divided into two subgroups: 7 h and 12 h by random number table. Peripheral blood WBC count, serum NO and malondialdehyde (MDA) levels, lung tissue pathological damage score, lung wet / dry mass ratio, lung tissue myeloperoxidase (MPO) levels and lung cells Apoptosis. Results The levels of blood WBC, serum NO and MDA levels, lung tissue MPO level, lung tissue pathological damage score, wet / dry mass ratio and apoptosis rate in PPAF group were higher than those in NS group at each time point (P <0.01). Serum NO level in L-Arg group was significantly higher than that in PPAF group (P <0.01), serum MDA level, lung tissue MPO level, lung tissue pathological damage score and wet / dry weight ratio and apoptosis rate were significantly lower than those in PPAF group P <0.05). NO level, lung wet / dry mass ratio and apoptosis rate in 12 h after PPAF and L-Arg treatment were significantly higher than those of 7 h (P = 0.000). The level of serum NO and the level of serum MDA (r = -0.257, P = 0.021), the level of MPO in lung tissue (r = -0.444, P = 0.011) and the rate of lung cell apoptosis in PPAF and L-Arg groups (r = -0.351 , P = 0.010) was negatively correlated. Serum MDA in each group was positively correlated with the rate of lung cell apoptosis (r = 0.969, P <0.001). Conclusion Intraperitoneal injection of PPAF can induce ALI in rats, and the enhancement of lung oxidative response and apoptosis are involved in the pathogenesis of ALI. L-Arg has a protective effect on ALI.