绿脓杆菌烧伤创面脓毒症急性肺损伤大鼠肺组织细胞凋亡的研究
摘要
目的观察绿脓杆菌所导致的烧伤创面脓毒症急性肺损伤(ALI)大鼠肺组织的细胞凋亡及肺损伤情况。
方法以SPF级SD大鼠为试验动物,完全随机地分为两组,试验组采用烫伤后痂下注射绿脓杆菌复制创面脓毒症模型,对照组烫伤后痂下注射生理盐水作为对照。分别于烫伤后创面痂下注射细菌或生理盐水0h、2h、12h、24h和48h以1%的戊巴比妥钠25mg/kg腹腔注射麻醉后处死大鼠。切取痂组织,进行组织细菌定量检测。取出肺组织,行肺组织HE染色,观察病理变化,肺组织损伤评分。TUNEL法检测细胞凋亡,计量凋亡指数(AI),分析细菌含量与凋亡指数之间的关系。
结果试验组创面组织细菌定量明显超过同时间对照组细菌含量,随时间变化逐渐增多,且于2h即达到10~5CFU/g。肺组织病理检查显示肺组织HE染色可见肺泡间隔增宽,间质充血水肿,肺泡腔变窄,炎症细胞渗出,小气道损伤等病理改变,试验组损伤改变明显重于同时间对照组,且随时间变化,损伤逐渐加重。肺组织损伤评分以量化的形式反映肺组织损伤变化,通过肺损伤评分反映试验组损伤改变明显重于同时间对照组,且证实两组之间的改变存在统计学差异。TUNEL法检测发现肺组织内细胞发生凋亡,细胞包括支气管上皮细胞、肺泡上皮细胞、血管内皮细胞以及炎症细胞。试验组AI明显高于同时间对照组AI,且在24hAI最高,随着时间延长AI呈现先增长后下降趋势。组织细菌量与AI相关性分析显示,组织细菌量在0h-24h与AI呈正线性相关。
结论绿脓杆菌导致脓毒症时肺组织内大量细胞发生凋亡,在急性肺损伤早期,随着创面组织细菌量增加,脓毒症的加重,肺组织的凋亡亦增加。随着脓毒症的逐渐加重,肺损伤也逐渐加重。
Objective To investigate the pulmonary apoptosis and observe the changes of lung of acute lung injury(ALI) in burn wound sepsis caused by Pseudomonas aeruginosa.
Methods SPF SD rats were used as experimental animal ,and they were classified into 2 groups randomly. The test group were inoculated with Pseudomonas aeruginosa at the burn site immediately after the thermal injury to induce sepsis,while the control group were inoculated with saline at the burn site immediately after the thermal injury. At the time of 0,2,12 , 24 and 48 hours after inoculation , the rats were killed after injection of 1% Pentobarbital by 25mg/kg in abdominal cavity. Eschars were cutted off, and the amount of bacteria was counted. Lungs were fixed for haematoxylin and eosin(HE) stain. morphometrical tests were applied to assess lung histopathology changes in acute lung injury. Apoptosis was determined by TUNEL test ( Terminal deoxynucleotidyl transferase - mediated dUTP nick end labeling) and optical microscope, Apoptosis Index(AI) was calculated, and the correlation between the bacteria amount of the eschars and AI was analyzed.
Results The bacteria amount of the eschars in test group exceeded the bacteria amount of the eschars in congtrol group at the same time,and the amount of bacteria increased over time. Interstitial edema occurred with massive infiltration of the inflammatory cells , alveolar spaces got more narrow,and the pulmonary architecture was damaged. The damage of lungs in test group was more serous than that in control group,and the damage of lungs aggravated over time. Morphometrical tests also showed that the damage of lungs in test group was more serous than that in control group. TUNEL test showed more positive cells compared with control group. AI reached the peak at 24hour.AI has linear correlation with the bacteria amount of eschars during 0-24hours.
Conclusion In the early phase of ALI,AI increases with the aggravation of sepsis, and the damage of the lungs exacerbate with theaggravation of sepsis.
方法以SPF级SD大鼠为试验动物,完全随机地分为两组,试验组采用烫伤后痂下注射绿脓杆菌复制创面脓毒症模型,对照组烫伤后痂下注射生理盐水作为对照。分别于烫伤后创面痂下注射细菌或生理盐水0h、2h、12h、24h和48h以1%的戊巴比妥钠25mg/kg腹腔注射麻醉后处死大鼠。切取痂组织,进行组织细菌定量检测。取出肺组织,行肺组织HE染色,观察病理变化,肺组织损伤评分。TUNEL法检测细胞凋亡,计量凋亡指数(AI),分析细菌含量与凋亡指数之间的关系。
结果试验组创面组织细菌定量明显超过同时间对照组细菌含量,随时间变化逐渐增多,且于2h即达到10~5CFU/g。肺组织病理检查显示肺组织HE染色可见肺泡间隔增宽,间质充血水肿,肺泡腔变窄,炎症细胞渗出,小气道损伤等病理改变,试验组损伤改变明显重于同时间对照组,且随时间变化,损伤逐渐加重。肺组织损伤评分以量化的形式反映肺组织损伤变化,通过肺损伤评分反映试验组损伤改变明显重于同时间对照组,且证实两组之间的改变存在统计学差异。TUNEL法检测发现肺组织内细胞发生凋亡,细胞包括支气管上皮细胞、肺泡上皮细胞、血管内皮细胞以及炎症细胞。试验组AI明显高于同时间对照组AI,且在24hAI最高,随着时间延长AI呈现先增长后下降趋势。组织细菌量与AI相关性分析显示,组织细菌量在0h-24h与AI呈正线性相关。
结论绿脓杆菌导致脓毒症时肺组织内大量细胞发生凋亡,在急性肺损伤早期,随着创面组织细菌量增加,脓毒症的加重,肺组织的凋亡亦增加。随着脓毒症的逐渐加重,肺损伤也逐渐加重。
Objective To investigate the pulmonary apoptosis and observe the changes of lung of acute lung injury(ALI) in burn wound sepsis caused by Pseudomonas aeruginosa.
Methods SPF SD rats were used as experimental animal ,and they were classified into 2 groups randomly. The test group were inoculated with Pseudomonas aeruginosa at the burn site immediately after the thermal injury to induce sepsis,while the control group were inoculated with saline at the burn site immediately after the thermal injury. At the time of 0,2,12 , 24 and 48 hours after inoculation , the rats were killed after injection of 1% Pentobarbital by 25mg/kg in abdominal cavity. Eschars were cutted off, and the amount of bacteria was counted. Lungs were fixed for haematoxylin and eosin(HE) stain. morphometrical tests were applied to assess lung histopathology changes in acute lung injury. Apoptosis was determined by TUNEL test ( Terminal deoxynucleotidyl transferase - mediated dUTP nick end labeling) and optical microscope, Apoptosis Index(AI) was calculated, and the correlation between the bacteria amount of the eschars and AI was analyzed.
Results The bacteria amount of the eschars in test group exceeded the bacteria amount of the eschars in congtrol group at the same time,and the amount of bacteria increased over time. Interstitial edema occurred with massive infiltration of the inflammatory cells , alveolar spaces got more narrow,and the pulmonary architecture was damaged. The damage of lungs in test group was more serous than that in control group,and the damage of lungs aggravated over time. Morphometrical tests also showed that the damage of lungs in test group was more serous than that in control group. TUNEL test showed more positive cells compared with control group. AI reached the peak at 24hour.AI has linear correlation with the bacteria amount of eschars during 0-24hours.
Conclusion In the early phase of ALI,AI increases with the aggravation of sepsis, and the damage of the lungs exacerbate with theaggravation of sepsis.
引文
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[4]KrizekTJ.Robson.M.C.:Evolution of quantitative baetorlology In wound management.J.Am.Surg 130:579-584;1975.
[5]Zhou ZH,Sun B,Lin K,et al.Prevention of rabbit acute lung injury by surfactant,inhaled nitric oxide,and pressure support ventilation.A m J Respi r Crit Care Med,2000,161:581
[6]Taddonio etal:Rapid Quantification of Bactcrlal and Fungal Growth In Bufll Wounds Biopsy Homogenate Cram Stain Versus Microbial Culture Results.Burns Vol.14(3)P180-4.1988.
[7]许伟石等:焦痂了细菌定量的意义。上海第二医学院学报。第3期,P17-22,1982。
[8]杨扬,陈胜喜,张卫星,等.缺血预处理对人在体肺组织细胞凋亡及调控基因蛋白bcl-2表达的影响[J].湖南医科大学学报,2002,27(1):43-45.
[9]Fein AM,Calalang2Colucci MG,Calalang2Colucci MG.Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock.Crit Care Clin,2000,16(3):289 - 317
[10]Sehultz M J,van der Poll T.Animal and human models for sepsis(J).Ann Med,2002,34:573 -581.
[11]Mathiak G,Szewezyk D,A bduah F,et al.An improved clinically relevant sepsis model in the conscious rat(J).Crit Care M ed,2000,28:1947- 1952.
[12]Sewnath M E,Olszyna D P,Birjmohun R,et al.IL 10 deficient mice demonstrate multipe organ failure and increased mortality during Escherichia coliperitonitis despite an accelerated bacterial clearance(J).J Immuno l,2001,166:6323- 6331.
[13]胡森.MODS动物模型(M)//盛志勇,胡森.多器官功能障碍综合征.北京:科学出版社,1999:185-199.
[14]Lekkou A,Karakantza M,Mouzaki A,et al.Cytokine production and monocyte HLA- DR expression as predictors of outcome for patients with community acquired severe infections(J).Clin Diagn Lab Immunol,2004,11:161-167.
[15]Deitch E A.Animal models of sep sis and shock:a review and lessons learned (J).Shock,1998,9:1 -11.
[16]宋林萍,张星火,李莉,等.脓毒症患者血流动力学数值与动脉压力波形关系的探讨(J).中国危重病急救医学,2002,14:457-460.
[17]Remick D G,Newcomb D E,Bolgos G,et al.Comparison of the mortality and inflammatory response of two models of sepsis:lipopolysaccharide vs cecal ligation and puncture[J].Shock,2000,13:110-116
[18]Remick D G,Manohar P,Bolgos G,et al.Block of tumor necrosis factor reduces lipopolysaccharide lethality,but no t the lethality of cecal ligation and puncture(J).Shock,1995,4:89 -95.
[19]Gurfinkel R,Czeiger D,Douvdevani A,et al.Ketamine improves survival in bum injury followed by sepsis in rats.Anesth Analg.2006 Aug;103(2):396-402,table of contents.
[20]乔亮,杨惠忠,袁克俭,等.抑制应激反应措对严重烧伤大鼠早期创面侵袭性感染的影响.中华烧伤杂志.2005,02:85-88
[21]Busch NA,Zanzot EM,Loiselle PM,et al.A model of infected bum wounds using Escherichia coli O18:K1:H7 for the study of gram-negative bacteremia and sepsis.Infect Immun.2000 Jun;68(6):3349-51.
[22]Weibel ER.Fractal geomatry:a design principle for living organisms.A m J Physiol,1991,261:L361
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