七氟烷预处理对脂多糖致大鼠急性肺损伤的保护作用

目的 评价七氟烷预处理对脂多糖(lipopolysaccharide,LPS)所致大鼠急性肺损伤(acute lung injury,ALI)的影响.方法 72只SD大鼠随机分成6组:NS组、LPS组和七氟烷预处理(S-1 h组、S-6 h组、S-12 h组、S-24 h组).通过气管内滴注LPS建立大鼠ALI模型.大鼠在气道内给予LPS或NS后6 h处死,检测不同时间点七氟烷预处理(2.4%,30 min)对支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中白细胞计数、细胞因子TNF-α和IL-1β水平,肺组织髓过氧化物酶(myeloperoxidase,MPO)活性,肺血管通透性及肺组织病理学等的影响.结果 与NS组相比,LPS组肺组织损伤程度,BALF白细胞计数以及TNF-α和IL-1β水平,血管通透性和肺组织MPO活性均显著增高(P<0.01).给予LPS前1 h和24 h七氟烷预处理能降低肺组织MPO活性,BALF中IL-1β水平及白细胞计数(P<0.01),而S-6h组和S-12 h组与IPS组相比无明显差别.七氟烷预处理均能够降低肺血管通透性和BALF中TNF-α水平(P<0.01),且以S-1 h和S-24h组为显著(P<0.01).提示七氟烷预处理对LPS所致肺损伤具有早期和延时的保护作用.结论 气道内给予LPS1 h和24 h前七氟烷预处理对LPS致大鼠ALI具有保护作用.

Protective effects of sevoflurane pretreatment on LPS-induced acute lung injury in rats

Objective To investigate the effects of sevoflurane pretreatment on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Methods Seventy -two Sprague -Dawley rats were randomly divided into 6 groups: NS group, LPS group and sevoflurane pretreatment (S-l h group, S-6 h group, S-12 h group and S-24 h group). The rat model of ALI was established by intratracheal instillation of LPS. Animals were sacrificed at 6 h after LPS or NS administration. Leukocyte count, concentration of TNF-α and IL-β in bronchoalveolar lavage fluid (BALF); pulmonary capillary permeability, myeloperoxidase (MPO) activity of lung tissue; lung histological changes were compared in rats with or without sevoflurane pretreatment (2.4% inspired for 30 min) at different times before LPS instillation. Results Compared with the NS group,severe injury of lung tissues and increase in leukocyte count in BALF, Production of TNF-α and IL-1β in BALF, pulmonary capillary permeability and MPO activity in the lung were significantly increased in rats treated with LPS (P<0.01). MPO activity, leukocyte count and production of IL-1βin BALF were reduced when sevoflurane was given 1 or 24 h before but not at 6 or 12 h before LPS instillation(P<0.01). Sevoflurane pretreatment also attenuated pulmonary capillary permeability and production of TNF-α in BALF (P<0.01). Pulmonary capillary permeability and concentration of TNF-α in S-l h and S-24 h group was lower than S-6 h and S-12 h group (P<0.01). Sevoflurane pretreatment was effective at 1 h and 24 h suggesting sevoflurane has early and late protection against LPS-induced lung injury. Conclusion Sevoflurane pretreatment has protective effects against acute lung injury when given 1 or 12 h before LPS instillation.