右美托咪定联合乌司他丁减轻脂多糖诱导的大鼠急性肺损伤

发布时间：2018-04-22 23:13

本文选题：右美托咪定 + 乌司他丁　；参考：《中国病理生理杂志》2014年01期

【摘要】：目的:研究右美托咪定(DEX)联合乌司他丁(UTI)对脂多糖(LPS)诱导的大鼠急性肺损伤(ALI)的影响。方法:健康雄性Wistar大鼠40只,随机分为5组:生理盐水对照组(NS组)、LPS模型组(L组)、右美托咪定治疗组(L+D组)、乌司他丁治疗组(L+U组)和右美托咪定+乌司他丁治疗组(L+D+U组)。对照组股静脉给予5 mL/kg生理盐水(NS);模型组股静脉给予LPS(10 mg/kg);右美托咪定治疗组股静脉给予LPS(10 mg/kg),即刻持续输注右美托咪定(1μg·kg-1·h-1);乌司他丁治疗组股静脉给予LPS(10 mg/kg),即刻腹腔注射乌司他丁(50 000 U/kg);右美托咪定联合乌司他丁治疗组股静脉给予LPS后立即持续输注右美托咪定(1μg·kg-1·h-1)及腹腔注射乌司他丁(50 000 U/kg)。在注射LPS或NS后6 h处死动物。血气分析检测动脉血氧分压(PaO2)、pH和碱剩余(BE);HE染色光镜下观察肺组织病理学变化并进行肺损伤评分;检测肺组织湿干重比(W/D)、髓过氧化物酶(MPO)活性、丙二醛(MDA)、肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、巨噬细胞炎症蛋白2(MIP-2)、一氧化氮(NO)及前列腺素E2(PGE2)的含量;检测支气管肺泡灌洗液(BALF)中白蛋白浓度;提取肺组织核蛋白,检测NF-κB p65的表达。结果:与NS组比较,L组动脉血PaO2、pH和BE降低,肺组织水肿、出血、炎症细胞浸润程度及肺损伤评分上升,肺组织TNF-α、IL-1β、MIP-2、MDA、NO、PGE2含量及W/D升高,MPO活性升高,肺组织NF-κB表达明显升高。与L组相比,联合治疗组动脉血PaO2、pH和BE上升,肺组织水肿、出血、炎症细胞浸润程度及肺损伤评分降低,TNF-α、IL-1β、MIP-2、MDA、NO、PGE2含量及W/D降低,MPO活性降低,肺组织NF-κB表达降低;与L组相比,右美托咪定和乌司他丁单独治疗组上述指标没有明显变化。结论:右美托咪定联合乌司他丁能够减轻脂多糖诱导的大鼠急性肺损伤。
[Abstract]:Aim: to study the effects of dexmetomidine (DEX) combined with ulinastatin (UTI) on acute lung injury induced by lipopolysaccharide (LPS) in rats. Methods: 40 healthy male Wistar rats were used. They were randomly divided into 5 groups: normal saline control group (NS group), LPS model group (L group), dexmetomidine treatment group (L D group), ulinastatin treatment group (L U group) and dexmetomidine ulinastatin treatment group (L D group). The control group was given 5 mL/kg normal saline for 5 mL/kg; the model group was given LPS(10 mg / kg; the right metoimidine treated group was given LPS(10 mg / kg; the right metoimidine 1 渭 g kg-1 h-1 was continuously infused immediately; the ulinastatin treatment group was given LPS(10 mg / kg by femoral vein and immediately intraperitoneally. Ulinastatin (50 000 U / kg) was injected, dexmetoimidine combined with ulinastatin (50 000 U / kg) was continuously infused immediately after LPS was given to the femoral vein in the treatment group, and Ulinastatin 50 000 U / kg / kg was intraperitoneally injected with dexmetomidine 1 渭 g kg-1 h-1. The animals were killed 6 hours after injection of LPS or NS. The arterial partial pressure of oxygen (Pao _ 2) and the pH of Pao _ 2 and the activity of myeloperoxidase (MPO) were detected by blood gas analysis, the pathological changes of lung tissue were observed and lung injury score was scored under light microscope with HE staining. The wet / dry weight ratio of lung tissue and the activity of myeloperoxidase (MPO) were measured. The contents of malondialdehyde (MDAA), tumor necrosis factor 伪 (TNF- 伪), interleukin-1 尾 (IL-1 尾), macrophage inflammatory protein (2) MIP-2P, nitric oxide (no) and prostaglandin E 2 (PGE2), albumin concentration in bronchoalveolar lavage fluid (BALF), and the expression of NF- 魏 B p65 in lung tissue were detected. Results: compared with NS group, Pao _ 2 pH and be were decreased, lung tissue edema, hemorrhage, inflammatory cell infiltration and lung injury score were increased. The contents of TNF- 伪 -IL-1 尾 -MIP-2MDA-PGE2 and the activity of MDA-PGE2 and the expression of NF- 魏 B in lung tissue were increased. Compared with group L, Pao _ 2 pH and be were increased, lung tissue edema, hemorrhage, degree of inflammatory cell infiltration and lung injury score were decreased in the combined treatment group. The contents of TNF- 伪 IL-1 尾 MIP-2MDAN PGE2 and W/ D decreased the activity of MPO, and the expression of NF- 魏 B in lung tissue was decreased, compared with that in the L group. There were no significant changes in dexmetomidine and ulinastatin alone. Conclusion: dexmetomidine combined with ulinastatin can attenuate acute lung injury induced by lipopolysaccharide in rats.
【作者单位】：南方医科大学附属珠江医院麻醉科;深圳市人民医院麻醉科;
【分类号】：R563

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