卡巴胆碱对犬烧伤休克早期口服补液效果的影响

目的 观察卡巴胆碱对50%总体表面积(TBSA)Ⅲ度烧伤早期口服补液效果的影响.方法 Beagle犬17条,先期行颈动、静脉、胃及膀胱置管,24 h后用凝固汽油燃烧造成50%TBSAⅢ度烧伤.随机分为不补液组、胃内补液组和胃内补液+卡巴胆碱组.伤后第1个24 h不补液组无治疗,其余2组于伤后30 min开始经胃内输注葡萄糖-电解质液或葡萄糖-电解质液复合卡巴胆碱(20 μg/kg).第1个24 h补液量为4 ml·kg~(-1)·%TBSA~(-1);伤后24 h起各组动物均实施静脉补液,至72 h处死动物.测定两胃内补液组伤后8 h内胃排空率,各组72 h内平均动脉压(MAP)、心输出量(CO)、尿量、血浆肿瘤坏死因子(TNF)-α含量以及伤后72 h脏器组织一氧化氮合酶(NOS)活性变化.结果 伤后3组MAP、CO、尿量及胃排空率均显著降低,血浆TNF-α含量显著增高.两胃内补液组MAP和CO高于不补液组;胃内补液+CAR组CO和胃排空率伤后4 h起显著高于胃内补液组(P<0.01),伤后24 h尿量也显著多于胃内补液组,伤后2、4和8 h血浆TNF-α含量以及伤后72h心、肝和空肠组织NOS活性显著低于胃内补液组(P<0.01或P<0.05).结论 卡巴胆碱能提高50%TBSA烧伤早期口服补液的复苏效果,其作用机制可能与促进胃排空和减轻炎症反应有关.     

卡巴胆碱对多器官功能障碍综合征小鼠脏器功能和结构的保护作用

目的:观察卡巴胆碱(carbachol,Car)对酵母多糖致多器官功能障碍综合征(MODS)小鼠多脏器功能和结构损伤的防护作用。方法:采用腹腔注射酵母多糖的方法复制小鼠MODS模型。雄性C57BL/6小鼠随机分为正常对照组(n=10),MODS 6、24、48 h组(n=30)和MODS Car 6、24、48 h防治组(n=30)。MODS组在致伤后腹腔注入生理盐水;MODS Car防治组在致伤前24 h内分3次灌胃注入卡巴胆碱。观察酵母多糖致伤后早期(48h内)动物死亡率,检测各组血丙氨酸转氨酶活性、尿素氮和肌酐水平,镜下观察致伤后48 h动物肝、肺、肾、心等脏器的组织病理学改变。结果:在酵母多糖致伤后48h内,MODS组小鼠死亡率达26.6%,MODS Car防治组的小鼠死亡率为10.0%。MODS组小鼠血浆ALT、BUN和Cr在伤后6h升高,而同时间点经卡巴胆碱预处理的小鼠血浆ALT、BUN和Cr仅略有升高,明显低于MODS组。光镜下观察发现,MODS组小鼠肝脏、肺脏、肾脏和心脏发生明显的病理改变,主要表现为脏器实质细胞浊肿、变性,间质充血、水肿和炎性细胞浸润,而卡巴胆碱防治组小鼠上述病变明显减轻。结论:预防性给予卡巴胆碱可以降低MODS急性期动物的死亡率,减轻脏器功能和结构的损伤,对急性炎症期的脏器损伤具有保护作用。     

卡巴胆碱对烧伤休克犬口服补液时胃肠功能和循环指标的影响

目的：研究拟胆碱药卡巴胆碱对烧伤休克口服补液犬血循环指标和胃肠功能的影响。方法：健康雄性杂种犬24只,采用凝固汽油燃烧法制成30%TBSAⅢ度烧伤模型。随机分为不补液（NR）组、口服葡萄糖-电解质溶液（ORS液）组和口服葡萄糖电解质液＋卡巴胆碱（ORS/CAR）组,分别于伤前和伤后3、6、9、24、48h测定平均动脉压（MAP）、胃黏膜内pH值（pHi）、肠腔内压力（IP）、血浆D-乳酸含量、血浆二胺氧化酶（DAO）活性及24、48 h尿量等指标,同时记录伤后呕吐量。结果：烧伤后ORS组和ORS/CAR组犬MAP及48 h尿量在各时间点差异均无显著性（P均〉0.05）,但均高于NR组（P均〈0.05）;烧伤后NR组胃pHi低于两补液组（P〈0.05）,并且ORS组胃phi低于ORS/CAR组（P〈0.05）;烧伤后各组IP、DAO和D-乳酸均升高,其中ORS组IP和DAO始终高于ORS/CAR组（P〈0.05）;ORS组D-乳酸仅在伤后48h与ORS/CAR组有差异（P〈0.05）。结论：卡巴胆碱能显著改善烧伤休克口服补液时的胃肠功能和循环指标,提高烧伤休克口服液体复苏的疗效。     

卡巴胆碱对烫伤休克大鼠肺血管通透性影响的初步研究

目的:研究烫伤休克大鼠液体复苏时给予卡巴胆碱对肺血管通透性和含水量的影响.方法:78只Wistar大鼠随机分为3组:烫伤组(n=36),卡巴胆碱治疗组(n=36)和正常组(n=6).采用30%TBSA Ⅲ度烫伤模型,应用改良伊文思蓝渗出法测定伤前及伤后4、8和12 h(n=6)肺组织血管通透性及肺含水量的变化.结果:伤后4 h卡巴胆碱治疗组伊文思蓝含量为(45.11±4.19)μg/g,较烫伤组(75.18±3.80)μg/g明显降低(P＜0.01),而与正常组(42.51±5.07)μg/g比较无统计学差异;伤后4 h、8 h卡巴胆碱治疗组的肺含水量显著低于烫伤组[(76.03±1.70)%比(78.46±1.42)%,(76.57±1.27)%比(80.15±1.84)%,P＜0.05和P＜0.01];伤后12 h肺组织血管通透性及含水量与烫伤组比较均无统计学差异.结论:卡巴胆碱能降低烧伤早期肺血管通透性及含水量增加,有助于烧伤休克早期的治疗.     

卡巴胆碱改善重度烫伤大鼠胃血流量和胃排空功能的初步研究

目的:探讨不同剂量卡巴胆碱对烫伤大鼠胃血流量和胃排空功能的影响.方法:40只Wistar雄性大鼠,随机分为假烫组(n=5)、单烫组(n=5)和口服卡巴胆碱组(n=30),后者又根据卡巴胆碱剂量不同分为20、40、60、80、100、120 μg/kg组(每组5只).假烫组大鼠均给予0.1%酚红溶液1.5 ml灌胃.单烫组和口服卡巴胆碱组大鼠均经30%TBSAⅢ度烫伤后立即给予0.1%酚红溶液1.5 ml灌胃,口服卡巴胆碱组于伤后0.5 h给予相应剂量卡巴胆碱 1 ml生理盐水灌胃.大鼠均于伤后2 h处死,观察不同剂量卡巴胆碱对大鼠胃血流量及胃排空率的影响.结果:烫伤后大鼠胃排空率为(29.50±13.42)%,明显低于假烫组(92.19±5.24)%,P＜0.01.伤后2 h胃血流量从伤前的(476.00±71.24)U降低到(103.60±51.28)U,P＜0.01.烫伤后给予不同剂量卡巴胆碱均能增加胃排空率和胃血流量,但以60 μg/kg最为显著(P＜0.01).结论:卡巴胆碱对烧伤休克大鼠胃血流量和胃排空有显著促进作用,最佳剂量为60μg/kg.     

卡巴胆碱抗炎作用受体机制的初步研究

目的:研究拟胆碱药卡巴胆碱抗炎作用的受体机制.方法:采集大鼠腹腔巨噬细胞,分4组进行实验:①阴性对照组:无荧光标记的N型胆碱能受体α7 亚基(α7nAChR)的特异性拮抗剂α-银环蛇毒素(α-Bgt)处理巨噬细胞;②阳性对照组:异硫氰酸荧光素标记的α-银环蛇毒素(FITC-α-Bgt)标记巨噬细胞;③烟碱对照组:高浓度烟碱(500 μmol/L)饱和处理后,再以FITC-α-Bgt标记巨噬细胞;④卡巴胆碱组:高浓度卡巴胆碱(500 μmol/L)饱和处理后,再以FITC-α-Bgt标记巨噬细胞.处理完成后在荧光显微镜下观察各组细胞的荧光强度并摄片.结果:荧光显微镜下阴性对照组无明显荧光,阳性对照组可见明显荧光;而卡巴胆碱组荧光强度较阳性对照组明显减弱,与烟碱对照组荧光强度类似.结论:卡巴胆碱能与α-Bgt竞争性地结合α7nAChR,其抗炎作用通过胆碱能抗炎通路作用于α7nAChR实现.     

卡巴胆碱对大鼠脓毒症所致肝功能损害的保护作用

目的：研究卡巴胆碱对脓毒症大鼠促炎症因子所致肝损伤的保护作用。方法：雄性SD大鼠32只,采用盲肠结扎穿孔术（CLP）制备大鼠脓毒症模型。随机分为CLP组和卡巴胆碱干预组（CAR组）,每组16只,CLP后立即静脉注射CAR10μg／kg（CAR组）或等量生理盐水（CLP组）。于CLP后6h和12h取血检测血浆丙氨酸转氨酶（ALT）活性,然后处死取肝组织,检测肿瘤坏死因子-α（TNF-α）和一氧化氮（NO）含量、髓过氧化物酶（MPO）活性以及肝组织含水率。结果：CAR组肝组织TNF-α含量显著低于CLP组,CLP后6h[（358．15±82．55）pg／g比（536．12±104．25）pg／g]和12h[（500．85±122．53）pg／g比（740．50±133．47）pg／g]差异非常显著（P〈0．05）;NO和MPO水平也显著低于CLP组（P〈0．05）。CLP后6hCAR组与CLP组血浆ALT活性[（48．6±3．0）U／Lvs．（55．3±4．0）U／L]和组织含水率[（70．9±2．9）％vs．（75．2±2．2）％]比较,差异均有统计学意义（P〈0．05）。结论：卡巴胆碱对大鼠腹腔脓毒症引起的肝功能损害有明显保护作用,其机制可能与其抑制肝脏TNF-α和N0水平、降低MPO活性,减轻肝组织炎症和水肿有关。     

卡巴胆碱对LPS刺激外周血白细胞释放TNFα的影响

目的：观察拟胆碱药物卡巴胆碱对LPS刺激正常人和大鼠外周血白细胞释放TNFα的影响。方法：在LPS刺激的稀释全血或单个核细胞中加入卡巴胆碱孵育,用ELISA方法测定培养细胞上清液中TNFa的浓度,用免疫组化方法显示单个核细胞TNF表达量。结果：LPS刺激外周血白细胞释放TNFα,并呈时间依赖关系。LPS诱导单个核细胞TNFα表达增加,而卡巴胆碱抑制LPS的这些效应。结论：卡巴胆碱具有潜在的抗炎效应。     

卡巴胆碱预防术后腹腔粘连的实验研究

目的 观察拟胆碱药卡巴胆碱预防腹腔粘连的作用。方法 44只雄性Wistar大鼠按完全随机法分为假手术组（n=12）、手术对照组（n=16）及卡巴胆碱组（n=16，卡巴胆碱50ug／kg），后2组采用开腹后无菌干纱布摩擦大鼠盲肠蚓突部，钳夹和刮伤腹壁法制作大鼠腹腔粘连动物模型。各组于术后第7d和第14d各处死一半动物，参考Phillips 5级分类法并结合本模型特点进行大体粘连程度分级评分；取粘连组织切片行HE染色观察粘连组织病理变化，免疫组化法观察粘连组织Ⅰ型胶原含量变化，并进行图像分析。结果 卡巴胆碱组第7d与第14d大体粘连程度评分均明显低于手术对照组，差异有统计学意义（P〈0．01）；HE染色显示卡巴胆碱组比之手术对照组炎症反应轻，偶见增生纤维结缔组织；Ⅰ型胶原含量卡巴胆碱组第7d与第14d均明显低于手术对照组（P〈0．01）；各组内第7d与第14d比较，腹腔大体粘连程度评分和I型胶原含量差异无统计学意义（P〉0．05）。结论 拟胆碱药卡巴胆碱能显著预防大鼠腹腔粘连形成，降低粘连程度。     

卡巴胆碱对脓毒症大鼠促炎症细胞因子所致心肌损伤的保护作用

目的：研究卡巴胆碱对脓毒症大鼠促炎症因子所致心肌损伤的保护作用。方法：雄性SD大鼠32只,采用盲肠结扎穿孔术（CLP）制备大鼠脓毒症模型,随机分为CLP组、卡巴胆碱干预组（CAR组）,每组16只。CLP术后立即静脉注射CAR10μg／kg（CAR组）或等量生理盐水（CLP组）。各组大鼠于CLP术后6h和12h取血检测血浆肌酸激酶同工酶（CK—MB）活性;然后处死动物,取心肌组织,测定肿瘤坏死因子-α（TNF-α）水平、一氧化氮（NO）含量、髓过氧化物酶（MPO）活性以及组织含水率。结果：CLP术后6h和12h,CAR组血浆CK—MB水平显著低于CLP组（P〈0．05）,CAR组心肌组织TNF-α水平、N0含量和MPO活性显著低于CLP组（P〈0．05）。CAR组心肌组织含水率均低于CLP组[6h：（69．5±2．3）％vs．（74．3±2．6）％,P〈0．05;12h：（71．4±2．4）％vs．（76．7±2．1）％,P〈0．05]。结论：卡巴胆碱能显著抑制脓毒症大鼠心肌促炎症因子水平,减轻心肌组织水肿和功能损害。卡巴胆碱的抗炎和心肌保护作用机制可能与兴奋胆碱能抗炎通路有关。     

重视烧伤后肠道紧密连接屏障功能障碍的研究

Severe burn injury is often accompanied by intestinal epithelial tight junction barrier dysfunction, which is believed to be closely associated with postburn shock, inflammation, hypermetabolism, infection, organ dysfunction etc. Recent studies have documented the critical role of tight junction-associated protein regulation in intestinal epithelial barrier dysfunction induced by severe burn injury. Myosin light chain (MLC) phosphorylation regulated by both myosin light chain kinase, which can phosphorylate MLC directly, and Rho-associated kinase,which can inhibit MLC phosphatase and then induce MLC phosphorylation indirectly, play a critical role in intestinal epithelial tight junction barrier dysfunction which occurs in severe burn injury. Recent advances have provided new insights into the mechanisms and the therapeutic strategies of intestinal epithelial tight junction barrier dysfunction following severe burn injury.     

烧伤后肠上皮通透性变化机制和对策

After a series of studies, we found that the intestinal permeability was increased, tight junction protein (zonula occluden-1 ) obviously decreased and redistributed, accompanied by an increase in expression of myosin light chain (MLC) phosphorylation in severely burned rats. After using inhibitor of MLC kinase ( ML-9 2mg/kg) or of Rho-associated kinase (Y-27632 2mg/kg), above-mentioned changes could be alleviated. Therefore, to regulate the MLC phosphorylation of tight junction protein and perijunctional actin-myosin ring may be one of the key links to lessen the intestinal epithelium permeability after burn injury.     

Low HLA-DR expression on CD14+ monocytes of burn victims with sepsis, and the effect of carbachol in vitro

This study aimed to investigate changes in the expression of human leukocyte antigen-DR (HLA-DR) on CD14⁺ monocytes in the peripheral blood of burn victims with delayed resuscitation in relation to the development of sepsis, and the effect of carbachol in vitro. The study population comprised 25 people with burns of at least 30% of total body surface area and delayed resuscitation, and 20 healthy volunteers as controls. Peripheral blood was collected on post-burn days 1, 3, 7, 14 and 28. When 7 participants developed sepsis, their peripheral blood was drawn on 2 consecutive days. Expression of HLA-DR on CD14⁺ monocytes in peripheral blood of burned participants was lower than that of controls, and fell further with the development of sepsis, when the rate and concentration of tumour necrosis factor-α (TNF-α) rose above those of controls and burned participants without sepsis. Expression of HLA-DR on CD14⁺ monocytes was negatively correlated with interleukin-10 (IL-10) levels on post-burn days 1, 7 and 28. In vitro, HLA-DR expression on monocytes also decreased with lipopolysaccharide (LPS) stimulation, but after treatment with carbachol, rose in a concentration-dependent manner. Thus expression of HLA-DR on CD14⁺ monocytes may be a useful parameter for monitoring the immune function of burn victims with and without sepsis. Carbachol significantly inhibited LPS-induced immunosuppression in human monocytes in vitro.     

不同营养支持途径对烧伤大鼠肠三叶因子表达的影响

目的探讨不同营养支持途径对烧伤大鼠肠三叶因子（ITF）及其mRNA表达的影响及可能的机制。方法采用30%体表面积Ⅲ度烧伤大鼠模型,随机分成伤前对照（C）组,静脉营养（PN）及肠道营养（EN）组。EN和PN组除营养支持途径不同外,其它条件均相同。在此基础上采用原位杂交、免疫组化和高效液相色谱等手段观察了烧伤后两组大鼠ITF及ITFmRNA的变化。结果正常大鼠小肠中ITF及ITFmRNA均有一定表达,它们主要分布于肠绒毛杯状细胞中。烧伤后PN组大鼠肠道组织结构严重受损,ITFmRNA表达明显降低,肠杯状细胞分泌ITF的能力大幅下降,特别是ITF二聚体的含量远远低于伤前（P＜0.01）。两组比较,EN组大鼠肠组织中ITF及ITFmRNA水平明显高于PN组,同时EN组肠粘膜受损程度也明显低于PN组。结论严重烧伤后肠粘膜结构受损是ITF合成下降的主要原因,肠道营养与静脉营养相比可降低伤后ITF特别是ITF二聚体下降的幅度。     

Septicaemia after burn injury: a comparative study

Seventy-nine (8.4%) patients during June 1992–May 1996 (Group-1) and 68 (7.2%) patients from June 1996 to May 2000 (Group-2) who developed septicaemia at the burns unit of Al-Babtain Centre for Plastic Surgery and Burns, Kuwait, were retrospectively studied and compared. The mean age of 26 years, male predominance, flame burns as main aetiology and mean burn percentage of ≥40% was observed in both the groups. Both groups revealed extensive flame burn, inhalation injury, intubation and difficult resuscitation as the risk factors. The proportion of satisfactory resuscitation increased significantly (P<0.001) in Group-2. The septicaemia commonly occurred within 2 weeks postburn but the number of episodes during 5 days postburn was less in Group-2. The surface wound was found to be the likely source of entry of the organisms into the blood stream in both the groups. The gram positive organisms were dominant aetiologic factor in both groups but an increase frequency of Acnetobacter was found in Group-2. The proportion of MRSE and Pseudomonas septicaemia was significantly higher (P<0.01) in the Group-1. The rate of survivors, in both the groups was higher among operated patients but it was significantly higher (P<0.001) in the Group-1. A mortality rate 20.6% in Group-2 decreased against Group-1, which can be attributed to better resuscitation, nutritional care, early detection of septicaemia, appropriate antibiotics and early wound excision and skin grafting. MOF was the cause of death of 60.9% in Group-1 and 85.7% in Group-2. There was no role of prophylactic antibiotic in burn patients in the incidence of septicaemia and mortality.     

严重烫伤大鼠淋巴循环中三种重要炎症介质的变化

目的 了解淋巴途径在烫伤大鼠肠道细菌移位中的作用.方法 制备羰花青荧光染料CM-DIL标记的大肠埃希菌菌液(数量级109CFU/L).将60只成年雄性Wistar大鼠按照信封法随机分为烫伤组、假伤组,每组30只.2组大鼠经胃灌注已制备的标记菌液0.5 mL后,烫伤组致30%TBSA深Ⅱ度烫伤,伤后立即行液体复苏;假伤组大鼠皮肤经25℃水浴10 s模拟烫伤并同法复苏.采集2组大鼠伤后2、24、72 h(每时相点10只)的肠系膜淋巴结(MLN)、肝脏、肠系膜淋巴液(MLF)、肝静脉血标本.分别采用荧光示踪法和细菌培养法检测细菌移位情况;用鲎试剂显色基质法定量测定上述4种标本中内毒素含量,并计算MLF和肝静脉血的内毒素携带量.对实验数据行t检验或单因素方差分析.结果 (1)荧光示踪法检测显示活菌呈短棒状,液体标本中可见单体或两三个联体的可移动活菌;死菌呈不规则碎片状.假伤组伤后2 h有少量标记菌,24 h数量达高峰;烫伤组伤后2 h标记菌较多,24、72 h仍处于较高水平.烫伤组各种标本比较,MLN内标记菌最多,伤后24 h达高峰[(5872±1976)×103 CFU/g],明显多于假伤组[(216±110)×103 CFU/g,t=30.129,P=0.000],72 h有所减少但仍多于假伤组(t=4.323,P=0.000);血液内标记菌最少.(2)细菌培养法检测:假伤组120份标本中,29份细菌培养呈阳性占24.2%;烫伤组120份标本中,72份培养阳性占60.0%.2组大鼠除血液标本在各时相点均未检出活菌外,其余3种标本伤后2 h或24 h可培养出活菌.烫伤组MLN和肝脏较其余2种组织检出更多活菌;伤后24 h,该组MLN、肝脏以及MLF标本中细菌数量均明显多于假伤组(t值分别为4.353、4.354、4.965,P值均等于0.000).(3)内毒素含量:烫伤组大鼠伤后各时相点4种标本的内毒素含量均高于假伤组,其中肝脏、MLF内毒素含量伤后2 h即达高峰.此时相点烫伤组4种组织间内毒素含量比较,差异有统计学意义(F=258.47,P=0.000),其中肝脏、MLN、MLF内毒素含量较高,且明显高于假伤组(t值分别为43.378、43.123、22.423,P值均等于0.000);MLF内毒素含量约为血液中含量的9倍.(4)烫伤组伤后各时相点MLF、血液内毒素携带量均高于假伤组.结论 用CM-DIL标记细菌能够较全面反映细菌移位情况,淋巴途径在细菌移位中发挥重要作用.

Abstract：

Objective To investigate the role of lymphatics in bacterial translocation from intestine of rats with burn. Methods Escherichia coli (E. coli) labeled with chloromethylbenzamidodialkylcarbocyanine (CM-DIL) were prepared. Sixty adult male Wistar rats were randomly divided into scald group and sham injury group according to the envelope method, with 30 rats in each group. Rats in both groups were gavaged with 0. 5 mL fluid containing CM-DIL-labeled E. coli. Rats in scald group were inflicted with 30% TBSA deep partial-thickness scald (verified by pathological section) and resuscitated with fluid. Rats in sham injury group were sham injured by bathing in 25 ℃ water for 10 s(verified by pathological section)and also received with fluid infusion. Mesenteric lymph node (MLN), liver, mesenteric lymph fluid (MLF), and liver vein blood (LVB) were harvested at post injury hour (PIH) 2, 24, and 72. Bacteria translocation was detected with fluorescent tracing technique and bacteria culture. The endotoxin content in above-mentioned four kinds of specimens was quantitatively determined with chromogenic substrate limulus amebocyte lysate. The carrying capacity of endotoxin in MLF and LVB was calculated. Data were processed with t test or one-way analysis of variance. Results (1) Living bacteria were in short-stick form, and they were seen moving in single or in doubles or triples in sample fluid. Dead bacteria were in irregular aggregates. Labeled bacteria in small amount were detected in sham injury group, their number peaked at PIH 24. A large amount of labeled bacteria were detected in scald group at PIH 2, which peaked at PIH 24 and decreased at PIH 72. The largest amount of labeled bacteria were found in MLN in scald group as compared to those in the other samples, and the number peaked at PIH 24 [(5872 ± 1976) × 103 CFU/g], which was obviously higher than that [(216 ± 110) × 103 CFU/g, t =30. 129, P =0.000] in sham injury group. The number of bacteria decreased at PIH 72, but it was still significantly different from that in sham injury group ( t =4. 323, P =0.000). The number of bacteria in LVB was the smallest. (2) 29 (24.2%) samples out of the 120 samples in sham injury group were positive for bacteria. 72 (60.0%) samples out of the 120 samples in scald group were positive for bacteria. No alive bacterium was detected at any time point in LVB sample in both group; the other three samples were detected with alive bacteria since PIH 2. There were more alive bacteria detected in MLN and liver as compared with the other two kinds of samples in scald group. The amount of bacteria in MLN, liver, and MLF in scald group were higher than those in sham injury group(with t value respectively 4. 353, 4. 354, 4. 965, P values all equal to 0. 000). (3) The endotoxin level in each kind of sample at each time point was obviously higher in scald group than that in sham injury group, and it peaked at PIH 2 in liver and MLF. The difference of endotoxin level among 4 kinds of samples in scald group at PIH 2 was statistically significant(F = 258.47, P = 0. 000) , and the endotoxin level was higher in liver, MLN, and MLF. They were obviously higher than those in sham injury group(with t value respectively 43. 378, 43. 123, 22. 423, P values all equal to 0. 000). The endotoxin level in MLF was 9 times of that in LVB. (4) The carrying capacity of endotoxin in LVB and MLF at each time point in scald group was higher than that in sham injury group. Conclusions CM-DIL marked bacteria can reflect the microbial translocation condition. The lymphatic route is an important pathway for bacteria translocation.