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肾上腺素对内毒素血症大鼠早期炎症因子及急性肺损伤的影响 被引量:5

Effects of epinephrine on early inflammatory cytokines and acute lung injury in endotoxemic rats
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摘要 目的探讨肾E腺素对内毒素(lipopilysaccharide,LPS)所致大鼠肺损伤的保护作用及其作用机制。方法30只SD大鼠随机分为3组(每组10只):正常对照组大鼠静脉输注生理盐水2.4ml/(kg·h);LPS组大鼠静脉注射LPS6mg/kg后,静脉输注生理盐水2.4ml/(kg·h);肾上腺素组大鼠静脉注射LPS6mg/kg后,静脉输注肾上腺素0.6μg/(kg·min)。在LPS注射后2h和6h通过心导管抽血,ELISA法检测血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和IL-10水平,并在6h处死大鼠取肺脏组织,分别予肺组织含水量检测,HE染色观察肺组织病理学变化,以及ELISA法检测肺泡灌洗液(BALF)内TNF-α、IL-6和IL-10水平。结果(1)与正常对照组肺含水量(70.19%±5.87%)相比,LPS组肺含水量(85.24%±5.87%)明显升高(P〈0.05),与LPS组相比,肾上腺素组肺含水量(78.00%±6.41%)明显降低(P〈0.05)。(2)病理观察结果显示,LPS组大鼠肺泡隔内毛细血管充血、水肿及炎症细胞浸润,少部分肺组织可见肺不张及肺泡内水肿、出血。肾上腺素组大鼠肺病理损伤较LPS组明显减轻。(3)与LPS组相比,肾上腺素组各时点血清TNF—α及IL-6水平明显降低(P〈0.05),IL-10水平明显升高(P〈0.05)。(4)与LPS组相比,肾上腺素组大鼠BALF中TNF-α水平降低[(78±9)ng/Lvs.(102±16)ng/L],IL-6水平降低[(268±42)ng/Lvs.(347±50)ng/L],IL-10水平升高[(210±23)ng/Lvs.(146±34)ng/L](P〈0.05)。结论。肾上腺素可减轻LPS诱导的急性肺损伤,其保护作用可能与降低TNF—α、IL-6水平,升高IL-10水平有关。 Objective To investigate the effects of epinephrine in sepsis-associated lung injury in rats. Methods Thirty SD rats were randomly divided into three groups (n = 10 per group) :control group received intravenous 0. 9% saline 2.4 ml/( kg. h ) ; LPS group received intravenous LPS ( 6 mg/kg ) ; epinephrine treatment group received an infusion of epinephrine 0.6 p.g/( kg-min) after LPS intravenous injection. Blood samples were taken at 2 h and 6 h after LPS injection and the levels of serum tumor necrosis factor (TNF)-α,interleukin( IL)45 and IL-10 were detected. The rats were sacrificed at 6 h. The lung tissues and bronchoalveolar lavage fluid(BALF) were collected. Pathological changes of the lung tissues were observed under light microscope. Water content of lung,expression of TNF-α,IL-6 and IL-10 in BALF and in serum were detected. Results ( 1 ) The water content of lung in LPS group significantly increased compared with that in control group ( 85.24 % ± 5.87 % vs. 70. 19 % ± 5.87 % ) and epinephrine group ( 78.00 % ± 6.41% ) ( P 〈 0. 05 ). ( 2 ) Pathological examination showed that LPS could cause pulmonary capillary hyperemia, edema, inflammatory cells infiltration. Atelectasis and alveolar edema were found in small number of lung tissue. Compared with LPS group, epinephrine ameliorated the lung pathological injury. (3)Compared with LPS group,serum levels of TNF-α and IL-6 significantly decreased ( P 〈 0. 05 ), whereas IL-10 increased ( P 〈 0. 05) in epinephrine group. (4) Compared with LPS group,BALF levels of TNF-α (78 ±9)ng/L vs. ( 102± 16 ) ng/L ] and IL-6 E ( 268 ± 42 ) ng/L vs. ( 347 ± 50 ) ng/L ] significantly depressed ( P 〈 0. 05 ), whereas BALF levels of IL-10 [(210 ± 23 ) ng/L vs. ( 146 ±34 ) ng/L ] elevated ( P 〈 0.05 ) in epinephrine group. Conclusion Epinephrine could reduce the acute lung injury caused by LPS. Its protective effect may be related to decreasing the levels of TNF-α and IL-6 ,elevating IL-10 level.
出处 《中国小儿急救医学》 CAS 2016年第8期522-525,共4页 Chinese Pediatric Emergency Medicine
基金 广州市卫生和计划生育科技一般引导项目(20161A011026) 广州市科技计划项目(2014Y2-00181)
关键词 肾上腺素 脓毒症 炎症介质 急性肺损伤 大鼠 Epinephrine Sepsis Inflammatory mediators Acute lung injury Rats
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参考文献16

  • 1Suffredini AF, Munford RS. Novel therapies for septic shock o- ver the past 4 decades [ J ]. JAMA, 2011,306 ( 2 ) : 194-199. DOI: 10. 1001/jama. 2011. 909.
  • 2朱获绮,王莹.小儿严重脓毒症并发多器官功能障碍综合征的研究[J].中国小儿急救医学,2010,17(4):321-324. 被引量:7
  • 3Silverman AM. Septic shock: recognizing and managing this life-threatening condition in pediatric patients [ J ]. Pediatr Emerg Med Pract,2015,12 (4) : 1-25.
  • 4朱雪琦,刘清泉,姚咏明.脓毒症动物模型制备方法的研究进展[J].中国危重病急救医学,2006,18(2):114-116. 被引量:30
  • 5杨文敏,曾其毅.肾上腺素对内毒素血症大鼠细胞因子的影响[J].中国实用儿科杂志,2007,22(8):599-602. 被引量:2
  • 6Zhou X, Schmidtke P, Zepp F, et al. Boosting interleukin-10 production:therapeutic effects and mechanisms [ J ]. Curr Drug Targets Immune Endocr Metabol Disord ,2005,5 (4) :465-475.
  • 7Muthu K, Deng J, Gamelli R, et al. Adrenergic modulation of cytokine release in bone marrow progenitor-derived macrophage following polymicrobial sepsis [ J ]. J Neuroimmunol, 2005,158 ( 1-2 ) :50-57. DOI: 10. 1016/j. jneuroim. 2004.08. 003.
  • 8张力,叶笃筠,吴萍,万敬员,张代娟,吴涛,周小燕.肾上腺素对脂多糖诱导的小鼠巨噬细胞炎症介质表达的影响[J].华中科技大学学报(医学版),2004,33(5):538-540. 被引量:5
  • 9Singer M. Catecholamine treatment for shock-equally good or bad? [ J]. Lancet,2007,370(9588) :636-637.
  • 10Deng J, Muthu K, GameUi R, et al. Adrenergic modulation of splenic macrophage cytokine release in polymicrobial sepsis [ J ]. Am J Physiol Cell Physiol, 2004,287 ( 3 ) : C730-736. DOI: 10. 1152/ajpcell. 00562. 2003.

二级参考文献90

  • 1张力,叶笃筠,吴萍,万敬员,张代娟,吴涛,周小燕.肾上腺素对脂多糖诱导的小鼠巨噬细胞炎症介质表达的影响[J].华中科技大学学报(医学版),2004,33(5):538-540. 被引量:5
  • 2姚咏明,盛志勇.内毒素与革兰阳性菌致病因子的协同效应与意义[J].中国危重病急救医学,2005,17(4):193-196. 被引量:13
  • 3Watson RS,Carcillo JA,Linde-Zwirble WT,et al.The epidemiology of severe sepsis in children in the United States.Am J Respir Crit Care Med,2003,167 (5):695-701.
  • 4Watson RS,Carcillo JA.Scope and epidemiology of pediatric sepsis.Pediatr Crit Care Med,2005,6(3 Suppl):S3-S5.
  • 5Martin GS,Mannino DM,Eaton S,et al.The epidemiology of sepsis in the United States from 1979 through 2000.N Engl J Med,2003,348(16):1546-1554.
  • 6Dellinger RP,Carlet JM,Masur H,et al.Surviving sepsis campaign guidelines for management of severe sepsis and septic shock.Crit Care Med,2004,32(3):858-873.
  • 7Russell JA.Management of sepsis.N Engl J Med,2006,355(16):1699-1713.
  • 8Vanderschueren S,De Weerdt A,Malbrain M,et al.Thrombocytopenia and prognosis in intensive care.Crit Care Med,2000,28(6):1871-1876.
  • 9Baughman PR,Lower EE,Flessa HC,et al.Thrombocytopenia in the intensive care unit.Chest,1993,104(4):1243-1247.
  • 10Cawley MJ,Wittbrodt ET,Boyce EG,et al.Potential risk factors associated with thrombocytopenia in a surgical intensive care unit.Pharmacotherapy,1999,19(1):108-113.

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