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目的:比较3种不同浓度(3.6%,2.4%和1.2%)七氟醚预处理对内毒素性急性肺损伤大鼠肺组织的影响。方法:健康雄性SD大鼠36只,随机分为6组(n=6):对照组(A组)、单纯七氟醚吸入组(B组)、3.6%七氟醚预处理组(C组)、2.4%七氟醚预处理组(D组)、1.2%七氟醚预处理组(E组)、内毒素组(F组)。分别在给药后(LPS或生理盐水)6 h处死大鼠,观察肺组织病理学结果,测定肺组织湿干比(W/D)、髓过氧化物酶(MPO)活性及肺组织ICAM-1mRNA的表达。结果:与对照组比较,F组和不同浓度七氟醚预处理组肺组织病理损伤加重,肺W/D、MPO活性、ICAM-1mRNA表达升高(P<0.05)。与F组比较,C组肺组织病理损伤减轻,MPO活性和ICAM-1mRNA表达降低(P<0.05),但肺W/D无明显降低(P>0.05);D组肺组织病理损伤减轻,肺W/D、MPO活性、ICAM-1mRNA表达均降低(P<0.05),F组肺组织MPO活性降低(P<0.05),但肺W/D和ICAM-1mRNA表达无明显降低(P>0.05)。结论:2.4%七氟醚预处理可以减轻内毒素所致急性肺损伤,作用机制可能与其降低肺组织ICAM-1mRNA的表达上调,从而减少肺内中性粒细胞的浸润相关。
Objective: To compare the effects of three different concentrations (3.6%, 2.4% and 1.2%) of sevoflurane preconditioning on the lung tissue of LPS-induced acute lung injury in rats. Methods: Thirty - six healthy male Sprague - Dawley rats were randomly divided into 6 groups (n = 6): control group (group A), sevoflurane inhalation group (group B), 3.6% sevoflurane preconditioning group ), 2.4% sevoflurane pretreatment group (group D), 1.2% sevoflurane pretreatment group (group E) and endotoxin group (group F). The rats were sacrificed 6 h after administration (LPS or saline) respectively. The pathological results of lung were observed. The wet / dry ratio (W / D), the activity of myeloperoxidase (MPO) and the level of ICAM- 1 mRNA expression. Results: Compared with the control group, the pathological changes of pulmonary tissue in F group and sevoflurane preconditioning group were increased, and the activity of W / D, MPO and the expression of ICAM-1 mRNA in lung tissue were increased (P <0.05). Compared with group F, the pathological damage of lung tissue of group C was alleviated, the activity of MPO and the expression of ICAM-1 mRNA were decreased (P <0.05), but the lung W / D was not significantly reduced (P> 0.05) (P <0.05). The MPO activity in lung tissue in group F decreased (P <0.05), but the expression of W / D and ICAM-1 mRNA in lung tissue in group F was lower than that in group F . CONCLUSION: Preconditioning with 2.4% sevoflurane can attenuate acute lung injury induced by endotoxin, which may be related to the upregulation of ICAM-1 mRNA in lung tissue and the reduction of pulmonary neutrophil infiltration.