头孢噻甲羧肟对烧伤后肠源性感染的预防作用

采用30%TBSA Ⅲ度烫伤大鼠模型,分不同时相(伤后3、6和12h)腹腔注射头孢噻甲羧肟,并通过血液、内脏和肠系膜淋巴结中细菌的定性和定量分析,评价头孢噻甲羧肟对预防烫伤大鼠绿脓杆菌肠源性感染的效果。结果表明,伤后3h 和6h 开始用药组,肠源性感染的发生率明显下降(分别为 P<0.001和 P<0.05),而伤后12h 开始用药组则无明显降低(P>0.05),但其肝、肾组织中的菌量也明显减少(P<0.01)。同时我们还动态观察了烫伤大鼠血液和内脏组织中药物的浓度,结果表明,用药后血、肝和小肠粘膜中能迅速达到有效药浓度,并维持4h 以上,但肠系膜淋巴结中未检测到药物。提示:大面积烧伤病人早期,短程使用有针对性的抗生素,对预防肠源性感染可能是有益的。     

头孢噻甲羧肟对烧伤后肠源性感染的预防作用

采用３０％ＴＢＳＡⅢ度烫伤大鼠模型，分不同时相（伤后３，６和１２ｈ）腹腔注射头孢噻甲羧肟，并通过血液，内脏和肠系膜淋巴结中细菌的定性和定量分析，评价头孢噻甲羧肟对预防烫伤大鼠绿脓杆菌肠源性感染的效果。结果表明，伤后３ｈ和６ｈ开如用药组，肠源性感染的发生率明显下降（分别为Ｐ＜０．００１和Ｐ＜０．０５），而伤后１２ｈ开始用药组则无明显降低（Ｐ＞０．０５），但其肝，肾组织中的菌量也明显减少（Ｐ＞０．０１     

应用头孢噻甲羧肟后烧伤病人体内的药代动力学改变

将１０名烧伤面积３０％～６０％含Ⅲ度伤的患者分为休克期组（ｎ＝５）和休克期后组（ｎ＝５），并设正常对照组（ｎ＝６），进行药代动力学比较研究。并通过高效液相法动态分析了应用头孢噻甲羧肟后，血浆、尿液和烧伤水疱液中的浓度。结果显示：休克期组与正常对照组比较差异有非常显著意义，表观分布容积（０．４５±０．０６Ｌ／ｋｇ对０．２３±０．０５Ｌ／ｋｇ）、非肾清除率（３０．５４±２１．９７ｍｌ·ｍｉｎ（－１）对１１．０８±４．９１ｍｌ·ｍｉｎ（－１））等虽增加，但药物的消除相半衰期却延长（３．２０±１．１２ｈ对１．８９±０．１５ｈ）。提示在大面积烧伤的早期，用药剂量不需增加。烧伤病人水疱液中可测出有效的抑菌浓度，为１．００４～２１．６２ｍｇ／Ｌ。证明早期全身性用药，可穿透Ⅱ度烧伤组织。     

应用头孢噻甲羧肟后烧伤病人体内的药代动力学改变

将10名烧伤面积30％～60％含Ⅲ度伤的患者分为休克期组(n=5)和休克期后组(n=5),并设正常对照组(n=6),进行药代动力学比较研究。并通过高效液相法动态分析了应用头孢噻甲羧肟后,血浆、尿液和烧伤水疱液中的浓度。结果显示:休克期组与正常对照组比较差异有非常显著意义,表观分布容积(0.45±0.06L/kg 对0.23±0.05L/kg)、非肾清除率(30.54±21.97ml·min~(-1)对11.08±4.91ml·min~(-1))等虽增加,但药物的消除相半衰期却延长(3.20±1.12h 对1.89±0.15h)。提示在大面积烧伤的早期,用药剂量不需增加。烧伤病人水疱液中可测出有效的抑菌浓度,为1.004～21.62mg/L。证明早期全身性用药,可穿透Ⅱ度烧伤组织。     

抗肿瘤坏死因子抗体和头孢噻甲羧肟对急性胆道感染肝损害的保护作用

在急性胆道感染大鼠模型上检测血浆肿瘤坏死因子（ＴＮＦ）、内毒素（ＥＴ）水平及血清谷丙转氨酶（ＡＬＴ）活性；观察肝组织结构和超微结构，抗ＴＮＦ单克隆抗体（ＴＮＦ－ＭＡｂ）和头孢噻甲羧肟的保护作用，结果显示：急性胆道感染组血浆ＴＮＦ、ＥＴ水平显著升高，血清ＡＬＴ活性也显著升高，肝组织病理变化明显；ＴＮＦ－ＭＡｂ与头孢噻甲羧肟保护组血浆ＴＮＦ，ＥＴ水平及血清ＡＬＴ活性显著下降，肝组织病理变化较轻，结果提示ＴＮＦ是急性胆道感染肝损害的重要介质；ＴＮＦ－ＭＡｂ和头孢噻甲羧肟对胆道感染肝损害有保护作用。     

严重烧伤后的肠源性感染

1962年 ,肖光夏等[1] 提出了肠源性感染的概念 ,1965年 ,Ｍａｒｋｌｅｙ等在实验中观察到 ,无菌烧伤动物的生存率高于普通烧伤动物。无菌动物在烧伤前服用大肠杆菌组的生存率明显低于未服菌组。说明在严重烧伤后 ,肠道内细菌可能参与整个病程的发展。 1983年 ,马利等[2 ] 以异硫氰荧光素标记肠道菌 ,进行烧伤动物的体内示踪 ,证明了严重烧伤后的肠道菌能移位到血液与肝、脾、肺、肾。随后 ,彭毅志等[3] 以直接荧光标菌法 ,在荧光显微镜下 ,直接观察到组织匀浆中存在游动的示踪活菌。府伟灵等[4 ] 用丫啶橙荧光素标菌 ,发现少量肠道菌还可布…     

严重烧伤后肠粘液成分变化与肠源性感染的关系

为探讨烧伤后回肠粘膜的病理变化，肠粘液及其中ＩｇＡ成分的变化及这些变化与肠源性感染关系，我们利用小鼠制作ＴＢｓＡ２５％Ⅱ度烧伤模型，分别于伤后０．１，１，６，１２，２４小时观察；（１）小肠末端的病理病变；（２）测定小肠粘液层厚度及粘液中蛋白，己糖，唾液酸的含量；（３）检测粘液ＩｇＡ血清ＩｇＡ及粘膜囿有层中分泌ＩｇＡ浆细胞数；（４）各时相小肠系膜淋巴结的细菌培养。     

单剂量头孢呋肟与多剂量头孢唑林预防胆囊切除术后感染比较

７９例选择性胆囊切除术后具有高度感染危险性的患者被随机分为三组。第一组：术前静脉推注头孢呋肟１．５克，术后再静脉推注生理盐水３次；第二组：术前静脉推注头孢唑林１．５克，术后再推注３次。以上二组均于术前３０分钟给药，术后每隔６小时给药１次。第三组：于术前第一天开始静脉滴注头孢唑林５．０克，术后当天及第一、二天各静脉滴注头孢唑林５．０克。结果显示这三种方法预防选择性胆囊切除术后感染的效果之间差异无显著性。说明单剂量头孢呋肟与多剂量头孢唑林对预防胆囊切除术后感染具相同的能力，而且方法更为简单。     

肠道双歧杆菌与烫伤大鼠肠源性细菌/内毒素移位

目的　观察肠道双歧杆菌在肠源性细菌 /内毒素移位中的变化和作用。　方法　制作严重烫伤大鼠模型 ,同时设假伤组。检测细菌和内毒素 (LPS)移位及盲肠膜菌群变化 ,ELISA法检测血浆白细胞介素 6(IL 6)浓度。　结果　大鼠严重烫伤后脏器细菌移位明显增多 (P <0 .0 1) ;血LPS水平在致伤 1、3、5d后分别为 (0 .2 3 6± 0 148)Eu/ml、(0 .197± 0 .15 6)Eu/ml、(0 10 4± 0 .0 90 )Eu/ml,显著高于假伤组的 (0 .0 72± 0 .0 49)Eu/ml(P <0 .0 5 ) ;盲肠膜菌群中双歧杆菌数剧减 2 0～2 5 0倍、真菌数剧增至 5～ 60倍、大肠杆菌数增加 0 .5～ 3 0倍 ,双歧杆菌与大肠杆菌比值由假伤组的2 5 0 0 0∶1降为伤后的 4～ 80 0∶1;血浆IL 6水平显著增高。经分层统计 ,与未发生肠道细菌移位大鼠相比 ,盲肠膜菌群移位大鼠的双歧杆菌量减少约 12 0倍 ,真菌数增加约 5 0倍 ,大肠杆菌数增加约 3 0倍。盲肠膜菌群中双歧杆菌数量与血浆中IL 6、LPS浓度呈负相关 (r1=- 0 .4817,r2 =- 0 .4912 ,P <0 .0 1) ,血IL 6和LPS浓度间存在显著正相关 (r =0 .82 5 8,P =0 .0 0 0 1)。　结论　严重烫伤可导致大鼠盲肠膜菌群紊乱 ,细菌和LPS移位增加 ;盲肠膜菌群中双歧杆菌的比例和数量的减少 ,可能促使了严重烫伤后肠源性细菌 /内毒素移位     

天然蒙脱石防治烧伤后肠道细菌移位的实验研究

目的　探讨天然蒙脱石对烧伤大鼠肠道细菌移位的防治作用。　方法　SD大鼠54只,分为正常对照组6只、烧伤对照组与烧伤治疗组各24只。后两组大鼠预先喂服转染了质粒pUC19的示踪菌JM109,证实质粒已定植于其肠道后,制成30%TBSAⅢ度烫伤(以下称烧伤)模型。烧伤治疗组大鼠伤后立即喂服天然蒙脱石0. 6g d-1 kg-1,烧伤对照组大鼠不喂服药物。观察正常对照组大鼠以及烧伤对照组、烧伤治疗组大鼠伤后12h和1、3、5d血液、肠系膜淋巴结细菌移位情况,并行酶切鉴定;检测大鼠肠组织丙二醛(MDA)及超氧化物歧化酶(SOD)的含量;用病理学方法观察整段小肠的损伤情况,测量空肠黏膜绒毛高度并计算基底膜细胞核分裂相。　结果　血液细菌培养:伤后1、5d,烧伤对照组阳性鼠数多于正常对照组,烧伤治疗组阳性鼠数少于烧伤对照组(P<0 05).肠系膜淋巴结细菌定量:烧伤治疗组伤后1、5d为(38±16)、(68±20)集落形成单位(CFU) /g;烧伤对照组伤后1、5d为( 228±67 )、( 183±29 )CFU/g,明显高于前者(P<0. 01 ).MDA、SOD含量:烧伤治疗组与烧伤对照组伤后各时相点比较,差异有统计学意义(P<0. 05).烧伤治疗组大鼠伤后各时相点空肠绒毛高度及基底膜细胞核分裂相明显高于或多于烧伤对照组(P<0. 05或0. 01)。　结论　天然蒙脱石对严重烧伤大鼠肠     

氯化镧对烫伤鼠肠道细菌移位的防治研究

目的　探讨氯化镧对烫伤鼠肠道细菌移位的作用及其机制。　方法　SD大鼠分为正常对照组 (A)、烧伤对照组 (B)及烧伤治疗组 (C) ,每组 30只。采用PUC19质粒转染大肠杆菌示踪加限制性内切酶指纹图谱分析法 ,对肠道菌向肠系膜淋巴结 (MLN)及血液中的播散进行示踪及定量研究。　结果　阳性菌落经酶切图谱分析后 ,证实B、C组MLN匀浆及血液培养生长细菌与灌胃的细菌具有完全相同的酶切图谱 ;C组MLN菌量在伤后 3、5d低于B组 (P <0 .0 5 )。C组血细菌阳性率在伤后 3d低于B组 (P <0 .0 5 )。C组血ET、NO及NOS量在伤后 1、3、5d均低于B组 (P <0 0 1)。C组肠组织MDA量在伤后 1、3、5d低于B组 (P <0 .0 1) ,C组肠组织SOD量在伤后 1、3d高于B组 (P<0 .0 5 )。　结论　血和MLN培养出的细菌由肠道细菌移位而来 ;氯化镧能有效防治肠道细菌移位 ;氯化镧通过抗菌、降低血中的ET、抑制NOS的活性减少NO的生成、提高SOD的活性并使MDA的产生下降等途径减少肠道细菌移位。     

The role of thermal injury on intestinal bacterial translocation and the mitigating role of probiotics: A review of animal and human studies

IntroductionBurn patients represent a combination of nutritionally deplete and calorically demanding individuals who are susceptible to morbidity and mortality. A source of sepsis in thermal injury patients is the gastrointestinal tract with its interaction of normal and potentially pathogenic bacteria. The normal flora of the intestines maintains the equilibrium of the gut and prevents bacterial translocation (BT) through numerous mechanisms, all of which are disrupted as a consequence of thermal injury. Probiotic supplements with varying strains of bacteria have the potential to stabilize the integrity of the gut lining and decrease the incidence of BT after thermal injury.MethodsA literature review was conducted for animal and human studies in English addressing probiotic therapy in thermal injury. Keywords, “probiotics,” “thermal injury” and “burn” were utilized. Reference lists for each analyzed article were also examined to ensure completeness of literature search. Each article was reviewed for methodology, results and conclusions.ResultsEleven and six unique articles were identified addressing probiotics in thermal injury in animal and human studies, respectively. Heterogeneity between studies and limited demographic and outcome reporting prevented meta-analysis and comprehensive recommendations to be formalized.ConclusionWhile heterogeneity did not allow for meta-analysis, the results overall suggest a preventative, if not therapeutic, potential for probiotics in patients after thermal injury. Despite initial concern that probiotic therapy could lead to systemic infection in immune compromised individuals, this was not observed in the analyzed studies. Numerous unanswered questions exist in regards to optimizing probiotic therapy in patients after thermal injury.     

四君子汤加味防治烫伤后大鼠肠道损伤和细菌移位实验研究

目的　研究中药四君子汤加味对减轻烫伤后肠道损伤的影响。　方法　Wistar大鼠随机分为 3组 :烫伤治疗组 (简称治疗组 )管饲党参、茯苓、白术、甘草、大黄中药煎剂 2ml,2次 d ,烫伤对照组 (简称对照组 )和正常组管饲同量蒸馏水。根据指标设定于伤后不同时相点 ,分别处死大鼠检测肠粘膜和血浆中肿瘤坏死因子 (TNF)、一氧化氮 (NO)、丙二醛 (MDA)、ATP酶活性及肠粘液中S IgA含量 ,观察肠粘膜病理变化 ,行脏器组织细菌培养、血培养。　结果　中药四君子汤加味可明显降低烫伤大鼠血浆和肠粘膜TNF、NO和MDA含量 ,维持肠粘膜细胞分泌S IgA的功能 ,恢复T细胞数量 ,减轻肠粘膜屏障损害 ,减少脏器细菌检出率。　结论　中药四君子汤加味能够减轻肠粘膜损伤 ,防止肠道细菌移位     

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.     

The effect of N-acetylcysteine on oxidative stress in intestine and bacterial translocation after thermal injury

Ischemia due to transient splanchnic vasoconstriction following major burns causes oxidative and/or nitrosative damage in intestinal tissue followed by reperfusion injury. Thus, burn injury leads to breakdown in the intestinal mucosal barrier which can induce bacterial translocation (BT). As an antioxidant and anti-inflammatory agent the protective effects of N-acetylcysteine (NAC) are documented in several studies. This study was designed to determine the effect of NAC treatment on the oxidative stress in the intestine and BT after burn injury. To evaluate this, 32 Wistar rats were randomly divided into four groups as sham (n = 8), burn (n = 8), pre-burn, NAC injection (150 mg kg⁻¹, intraperitoneally) 15 min before thermal injury (n = 8), post-burn, NAC injection (150 mg kg⁻¹, intraperitoneally) 2 h after thermal injury. Under anesthesia, the shaved dorsal skin of rats was exposed to boiling water for 12 s to induce burn injury in a standardized manner. Twenty-four hours later, tissue samples from mesenteric lymph nodes (MLN), spleen, and liver were obtained under sterile conditions for microbiological analysis and ileum samples were harvested for biochemical analysis. In the burn group, the incidence of isolating bacteria in MLN, spleen, and liver specimens was significantly higher than other groups. NAC treatment prevented burn-induced BT in both pre- and post-burn groups. Thermal injury caused a significant decrease in glutathione (GSH) level, significant increases in malondialdehyde (MDA) and myeloperoxidase (MPO) activity at post-burn 24th hour. Treatment of rats with NAC significantly elevated the reduced GSH levels while decreasing MDA levels and MPO activity. These data suggested that NAC has a crucial cytoprotective role in intestinal mucosal barrier and preventive effects against burn injury-induced BT.     

严重烫伤小鼠肠黏膜相关淋巴细胞变化与肠道细菌移位

目的探讨小鼠烫伤后肠黏膜相关淋巴细胞变化与肠道细菌移位的关系。方法将40只BALB/c小鼠随机分为正常对照组及烫伤后12、24、72 h组,每组10只。正常对照组不致伤, 其余各组小鼠背部造成20％TBSAⅢ度烫伤后,按时相点处死并留取标本。计数全段小肠集合淋巴结 (PP结)个数及淋巴细胞总数。应用流式细胞仪检测小鼠PP结CD3+、CD4+、CD19+淋巴细胞比例和绝对数,并检测主要脏器肠道细菌移位率。结果烫伤后12、24、72 h组PP结淋巴细胞总数分别为 (4．05±0．28)×106、(2．64±0．39)×106、(2．83±0．46)×106个,均少于正常对照组的(4．54±0．58)× 106个(P<0．05或0．01)。与正常对照组比较,烫伤后72 h组PP结淋巴细胞悬液中CD3+、CD4+百分比明显降低(P<0．05)。伤后各组小鼠CD3+、CD4+、CD19+淋巴细胞绝对数明显减少。各烫伤组肠道细菌移位率分别为16％、52％、30％,均高于正常对照组(4％),其中烫伤后24、72 h组与正常对照组比较,差异有统计学意义(P<0．05)。结论烫伤后肠黏膜相关淋巴细胞减少是肠源性感染的重要因素。     

急性坏死性胰腺炎大鼠肠道黏膜屏障功能的损害及肠道细菌移位

目的观察急性坏死性胰腺炎（ANP）时肠道黏膜屏障的变化和肠道细菌移位。方法选择SD大鼠，逆行胰胆管穿刺法诱导制备大鼠ANP模型并分为两组，分别为假手术组（SO）和坏死组（ANP）。术后24h，观察大鼠ANP模型的回肠黏膜通透性、回肠绒毛高度和黏膜厚度的变化，测定血浆D-乳酸浓度和血浆内毒素水平，并行脏器细菌培养。结果ANP组血浆内毒素水平较SO组升高（P〈0．01），细菌培养SO组均无阳性，ANP组细菌培养总阳性率为55．6％，其中以腹水细菌培养阳性率最高，为75．0％，菌种鉴定主要为肠球菌和变形杆菌。ANP组24h后血浆D-乳酸浓度高于SO组，差异有统计学意义（P〈0.01）。ANP组24h回肠黏膜发生病理形态学的改变，从绒毛高度和黏膜厚度测量值上观察发现ANP组肠壁明显变薄。结论本组实验中，大鼠ANP时的回肠黏膜病理形态学的变化提示ANP大鼠肠道的机械屏障明显受损；血浆D-乳酸浓度的显著上升，证明它可从功能上反映ANP大鼠肠道屏障功能的损害。大鼠ANP时的内毒素水平和脏器细菌培养阳性率的升高，证明内毒素血症和肠道细菌移位是由于早期肠道通透性升高和肠道屏障受损所致。