丙泊酚对大鼠肠缺血-再灌注后肺细胞间黏附分子-1蛋白表达的影响

Propofol reduces intercellular adhesion molecular - 1 expression in lung injury following intestinal ischemia/reperfusion in rats

目的 研究丙泊酚对大鼠肠缺血-再灌注(I／R)后肺细胞间黏附分子-1(ICAM-1)蛋白表达的 影响。方法 SD大鼠随机分为4组(n=8):①I／R组:暴露腹腔后夹闭肠系膜上动脉(SMA)1 h,开放再灌注 2 h;②丙泊酚预处理组(P1组):肠缺血前10 min给予丙泊酚;③丙泊酚治疗组(P2组):肠再灌注前10 min给 予丙泊酚;④假手术组:仅暴露SMA,不行肠I／R及丙泊酚输注。丙泊酚剂量为首剂10 mg／kg,然后以 10 mg·kg-1·h-1持续输注。所有动物于再灌注2 h处死,检测血浆和肺组织肿瘤坏死因子-α(TNF-α) 及肺组织MPO含量,免疫组化染色检测肺组织ICAM-1蛋白的表达。结果 肠I／R后动物血浆和肺组织 TNF-α含量及肺组织MPO含量、ICAM-1蛋白表达均增加。丙泊酚可以抑制上述改变,以P1组效果最明 显,其中血浆TNF-α及肺组织ICAM-1表达在I／R组和P1组间存在显著性差异(P均<0.05),而P2组上 述各指标显著高于假手术组。结论 ICAM-1在肠I／R后肺损伤的发生中发挥重要作用。肠I／R早期应用丙 泊酚可减少肺组织ICAM-1表达,在一定程度上减轻肺损伤。

Objective To investigate the effect of propofol on intercellular adhesion molecular - 1 (ICAM - 1) expression in the lung tissue following intestinal ischemia/reperfusion(I/R) in rats. Methods SD rats were randomly divided into 4 groups (n = 8 in each group). (1)Group I/R in which rats were subjected to 1 hour of occlusion of the superior mesenteric artery (SMA), followed by 2 hours of reperfusion. (2)Early treatment group (group P1), rats were subjected to the same procedure as group I/R with the additional administration of propofol beginning 10 minutes before ischemia with 10 mg/kg loading dose, followed by continuous infusion at 10 mg-1·kg-1 ·h-1.(2)Treatment group (group P2), rats were subjected identical insult as in group I/R with the administration of propofol started 10 minutes before reperfusion with 10 mg/kg loading dose, followed by continuous infusion at 10 mg·kg-1·h-1. (2)Sham -operation group, rats were subjected to laparotomy only, but received normal saline at 10 ml·kg-1·h-1. At the end of reperfusion, all animals were sacrificed. The activity of myeloperoxidase(MPO) and the content of tumor necrosis factor - a (TNF - a) were determined in the lung tissue, and plasma TNF - a content was also quantified. The ICAM - 1 expression in pulmonary endothelium was assessed by histochemical staining. Results All animals subjected to intestinal I/R demonstrated an increase in TNF - a in plasma and lung tissue, MPO activity and ICAM - 1 expression in lung tissue. It was much more pronounced in I/R group. Plasma TNF - a content was increased significantly in group I/R and P2. All the increase was less in quantity in the early treatment group of propofol than the other two groups, and there was significant difference in contents of plasma TNF - a and ICAM - 1 expression in lung between group I/R and group P1 ( both P<0. 05). Conclusion ICAM - 1 plays an important role in lung injury after intestinal I/R. The early treatment of propofol before intestinal I/R may be beneficial by reducing ICAM - 1 expression in lung injury.