大鼠脊髓损伤致截瘫后肠道细菌移位的实验研究

目的：探讨大鼠脊髓损伤致截瘫后是否发生肠道细菌移位。方法：建立大鼠脊髓损伤性截瘫模型，以脊髓损伤性截瘫后12h、24h、48h大白鼠为实验组，未损伤脊髓的正常大白鼠为对照组。在无菌条件下，采集动物下腔静脉血进行内毒素定量测定和细菌培养，采集肝、脾、肠系膜淋巴结、肠腔内容物作细菌培养并进行菌种鉴定。取实验组和对照组各动物的肝、脾、肠系膜淋巴结、空肠、回肠进行病理切片HE染色检查，取空、回肠进行电镜检查。结果：大鼠脊髓损伤致截瘫后24h开始出现内毒素血症，截瘫后48h出现细菌移位。结论：大鼠脊髓损伤致截瘫后将发生肠道细菌移位，提示脊髓损伤截瘫的病人应尽早给予抗生素治疗。     

肝门阻断对肝硬化大鼠肠黏膜屏障的影响

目的 探讨肝硬化大鼠肝门阻断后肠道黏膜屏障结构和功能的改变.方法 40 只肝硬化模型雄性SD 大鼠被随机分为假手术组、肝门阻断10 min、肝门阻断20 min、肝门阻断30min 组,每组各10 只.在行肝门阻断术后18 h 乳果糖、甘露醇混合液灌胃,6 h 后收集尿液,检测乳果糖和甘露醇排出率及比值（L/M）,并于术后24 h 取未段回肠行病理组织学和电镜检查.结果 肝硬化大鼠肝门阻断10 min 时即出现明显小肠病理损伤,电镜下可见小肠微绒毛肿胀、缩短,紧密连结变宽.阻断20 min 时,小肠微绒毛缺失、脱落,细胞器肿胀.阻断30 min 时,可见部分肠黏膜细胞坏死,微绒毛脱落以及紧密连结破坏.肝门阻断10 min 组大鼠的尿中L/M 比值（0.069 ±0.022）明显高于假手术组（0.047 ± 0.016）,并随肝门阻断时间延长增高越明显.结论 肝硬化大鼠肝门阻断后可导制肠道黏膜通透性增加,肠黏膜屏障功能受损.     

喹吖因对肠道缺血再灌注损伤后肠道细菌/内毒素移位的影响

目的 探讨磷脂酶A2（PLA2）抑制剂喹吖因对大鼠肠道缺血再灌注（gut ischemia reperfusion,GIR)损伤后肠源性细菌／内毒素移位的影响。方法 42只wistar大鼠随机分为正常组（6只）和GIR损伤组（36只）。GIR损伤组又分为GIR损伤对照组、再灌注后3h喹吖用药组和12h喹吖用药组,每组12只。取正常对照组、GIR损伤对照组及用药组48、72h门、腔静脉血测定内毒素含量、腔静脉血浆TNFα含量和肠系膜淋巴结、肝、肺、肾等肠道外器官组织进行细菌培养。结果 早期应用喹吖因,无论是GIR损伤后3h用药组还是12h用药组,均可明显降低GIR损伤后血浆内毒素和TNFα水平（P＜0．01）;显降低GIR损伤后肠系膜淋巴结和肺、肝、肾组织器官中的细菌移位发生率（P＜0．05－0．01）。结论 GIR损伤后早期应用喹吖因可显地降低肠源性细菌／内毒素移位,减轻促炎性介质和细菌因子的释放,减轻肠道外脏器损伤。     

肝门阻断后细菌移位和门静脉血中内毒素变化的研究

目的　研究肝门部血流阻断后肠粘膜损害所致细菌移位及门静脉血中内毒素的变化。方法　采用兔动物模型,在无菌条件下机械性阻断肝十二指肠韧带,观察阻断后15,20,30min和60min时门静脉血中内毒素值和肠系膜淋巴结细菌培养阳性数。结果　实验组肝门阻断后门静脉血内毒素值和细菌培养阳性数明显高于对照组(P<0.01),且随阻断时间延长加重。结论　缺血、缺氧是肠粘膜屏障损害的直接原因,深入对肠粘膜屏障功能保护的研究将有利于指导临床工作。     

高原鼠L-精氨酸预处理与第一肝门阻断时肠道细菌易位

目的探讨高原鼠L-精氨酸预处理对第一肝门阻断时肝缺血再灌注损伤和肠道细菌易位有无保护作用。方法SD大鼠在高原环境饲养14天后分为假手术组(5只)及实验组(持续阻断30分钟及60分钟组,L-精氨酸预处理加持续阻断30分钟及60分钟,每组5只)。无菌条件下用无损伤血管夹阻断大鼠第一肝门建立肝脏缺血再灌注(I/R)模型,再灌注24小时后在无菌条件下分别取门静脉血、回肠系膜淋巴结进行肠道细菌培养。观察外源性L-精氨酸预处理对第一肝门阻断时肝缺血再灌注损伤与肠道细菌易位有无保护作用。结果假手术组未培养出细菌;持续阻断30分钟组2例、持续阻断60分钟组5例、外源性断60分钟组5例血液及淋巴结均培养出大肠埃希氏菌。与假手术组比较,差异非常显著;持续阻断60分钟组亦明显高于持续阻断30分钟组,便各预处理组与相同阻断时间组之间无差异。结论高原第一肝门阻断的时间及肝缺血再灌注损伤对肠道细菌易位有显著的影响,但外源性L-精氨酸预处理对高原第一肝门阻断时肝缺血再灌注损伤和肠道细菌易位无明显的保护作用。     

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。     

静脉注射内毒素法制作大鼠肠道细菌易位模型

目的探讨静脉注射内毒素制作大鼠肠道细菌易位模型的方法。方法60只雄性SD大鼠(体重200～250g)随机分为4组(15只/组)。其中3组为实验组,按组别不同分别给予尾静脉注射内毒素2、4、6mg/kg;对照组给予尾静脉注射生理盐水0.5ml。观察各组大鼠的体温、呼吸频率、外周血白细胞计数及死亡率,7d后将各组大鼠分别开腹取门静脉血、下腔静脉血、肠系膜淋巴结、肝、脾和胰腺组织作细菌培养。结果注射内毒素后各组大鼠的体温、呼吸频率及外周血白细胞均有不同程度的升高。2mg/kg组大鼠无死亡,组织细菌培养阳性率为24.4%。4mg/kg组的死亡率为20.0%,细菌培养阳性率为47.2%,其中肠系膜淋巴结阳性率为83.3%。6mg/kg组的死亡率为46.7%,细菌培养阳性率为64.6%,其中肠系膜淋巴结阳性率为100.0%。结论4mg/kg剂量的内毒素静脉注射是制作大鼠肠道细菌易位模型的较为理想可行的方法。     

阻断淋巴通道对梗阻性黄疸大鼠肠道细菌易位的影响

目的　从阻断淋巴通道角度探讨实验性梗阻性黄疸肠道细菌易位作用的机理。方法结扎Wistar大鼠胆管,制作梗阻性黄疸模型,6 0只大鼠分为假手术组(A组)、梗阻性黄疸组(B组)和梗阻性黄疸 乳糜管结扎组(C组) ,每组各2 0只,于术后15d剖腹分别抽取下腔静脉血、门静脉血,检测其内毒素、肿瘤坏死因子 α(TNF α)、白细胞介素6 (IL 6 )的含量,并对肠系膜淋巴结、肺组织行细菌培养,对末端小肠及肺组织行病理学检查。结果　大鼠梗阻性黄疸模型建立后15d ,外周静脉和门静脉血浆中内毒素含量均明显升高(P <0 0 1) ,同时外周静脉血浆TNF α、IL 6含量、肠系膜淋巴结及肺组织细菌培养阳性率亦明显升高(P <0 0 1) ,并伴有肺泡腔出血水肿及大量炎性细胞浸润;乳糜管结扎显著降低外周血内毒素、TNF α、IL 6含量(P <0 0 1) ,明显减轻肺细菌易位率及肺病理损伤程度(P<0 0 1)。结论　阻断淋巴通道可减轻梗阻性黄疸时肠道细菌易位所致的高内毒素血症及炎症因子的过表达,改善肺损伤程度     

选择性肠道去污和盲肠造口/结肠灌洗对猪急性重症胰腺炎后肠源性细菌/内毒素移位的影响

目的:观察选择性肠道去污(SDD)和盲肠造口、结肠灌洗对猪急性重症胰腺炎(ASP)后肠源性细菌/内毒素移位的影响。方法:选健康长白种猪23头,体重16 ks~22 kg,雌雄不限,随机分为4组:组Ⅰ:假手术对照组(n=5);组Ⅱ:ASP对照组(n=6);组Ⅲ:ASP+SDD预防组(n=6);组Ⅳ:ASP+盲肠造口、结肠灌洗组(n=6)。在麻醉状态下,进腹向胰总管注入1 ml／kg·BW 5％牛磺胆酸钠混合液(内含8 000~10 000 BAEE单位胰蛋白酶/ml,pH7.6)诱导ASP。假手术对照组以0.9％NaCl磷酸盐缓冲液取代5％牛磺胆酸钠混合液。分别于ASP诱导前30 min、诱导后6 h、24 h、48 h、72 h采集腔静脉血作内毒素(LPS)测定(鲎试剂法)。ASP后72 h,采集门、腔静脉血及大小肠系膜淋巴结、肺组织、肺门淋巴结、胰腺组织作系列细菌定量培养和细菌鉴定。结果:预防性SDD不仅可非常显著地降低粪便培养中肠杆菌数(P<0.01),而且使血浆LPS水平明显下降,血和组织器官中移位细菌数量明显降低。盲肠造口、结肠灌洗亦可有效地降低血浆内毒素水平及组织器官中移位细菌数量。结论:预防性SDD或盲肠造口／结肠灌洗均可有效地减少胰腺炎性肠道细菌/内毒素移位,尤其后者可能具有重要的临床指导意义。     

大鼠肝缺血及再灌注所致肠黏膜损伤及丹参的保护作用

目的 研究大鼠肝缺血再灌注小肠黏膜损伤及丹参预处理的保护作用.方法 在肝缺血45 min条件下,动物随机分为四组,正常对照组(CO组)、假手术组(SO组)、缺血再灌注组(IR组)、丹参预处理组(SM组),按再灌注后不同时间(0、3、12、24、72 h)分为5个亚组,每组5只.SM组在阻断第一肝门30 min前经尾静脉推注丹参注射液6 g/kg加生理盐水40 ml/kg,其余各组按40 ml/kg给予生理盐水尾静脉注入,SO组开腹后仅解剖肝门,不钳夹肝蒂.分别在再灌注0、3、12、24、72 h取上段空肠行病理学检查、二胺氧化酶(DAO)活性测定、肠系膜淋巴结菌群易位检查.结果 在肝缺血45 min再灌注不同时限点SM组空肠黏膜损伤较IR组明显减轻,且肠组织DAO活性、肠系膜淋巴结细菌培养阳性率均低于IR组(P<0.05).结论 在肝缺血再灌注损伤中小肠有明显淤血性损伤,DAO活性明显下降,肠系膜淋巴结细菌培养率明显上升,丹参预处理对肝缺血再灌注所致小肠黏膜损伤具有保护作用.     

Bacterial translocation, endotoxaemia and apoptosis following Pringle manoeuvre in rats

BACKGROUND: Intraoperative occlusion of the hepatoduodenal ligament (Pringle manoeuvre (Pm)) is often employed for the reduction of blood loss during liver surgery. No data exist to date on the effects of Pm on mucosal barrier dysfunction, systemic bacterial translocation (BT), endotoxaemia and apoptosis. MATERIALS AND METHODS: Sixty-five male Wistar rats in three groups: I (n=25) controls, II (n=20) sham operation, III (n=20) occlusion of the hepatoduodenal ligament (Pm). Tissue samples from mesenteric lymph nodes (MLNs), liver, lungs and spleen were analysed after 30 min and at 24 h. Endotoxin was measured in portal and aortic blood and routine haematological and biochemical parameters were measured before and after Pm. RESULTS: No differences were found in the blood parameters before and after Pm, but a significant increase in contaminated MLNs and liver was noted. All cultured bacteria were enteric in origin. Portal and aortic endotoxin were significantly increased. Overall the ileal architecture remained intact in all specimens studied and no significant pathology was observed. The ABC increased after Pm significantly (P<0.01). CONCLUSION: Normothermic Pm of 30 min duration results in immediate and delayed gut barrier failure by significantly increasing BT and endotoxaemia which might be attributed to portal stasis leading to intestinal congestion as well as temporary liver ischaemia. Apoptosis increased significantly 30 min after performing the Pm.     

烫伤大鼠肠内毒素移位对淋巴细胞凋亡的影响

目的 探讨烫伤大鼠脾脏和肠系膜淋巴结（mesenteric lymph nodes,MLNs)淋巴细胞凋亡与肠道LPS移位的关系。方法 30％TBSAⅢ度烫伤Wistar大鼠及对照组,取门、腔静脉血用鲎基质显色法定量LPS;脾脏和MLNs切片以TUNEL－POD法染色,应用Cooldccd成象系统、Spot和IPP（Imagine proplus)4.10a软件进行凋亡细胞计数和透射光光密度分析。结果 烫伤后大鼠门、腔静脉血LPS水平显增加（P＜0．01）,伤后6h达峰值;门静脉LPS 3－48h显高于腔静脉（P＜0．01）。TUNEL－POD染色结果,MLNs伤前几乎未见凋亡淋巴细胞,但伤后显增多（P＜0．01）,以3h为明显;脾脏伤前凋亡淋巴细胞多集中在皮质,伤后显减少（P＜0．01）,24h后略有恢复。透射光光密度值分析表明,伤后24h内脾脏凋亡淋巴细胞的光密度值较伤前明显降低（P＜0．01）;伤后48h内MLNs凋亡淋巴细胞光密度值较伤前显增高（P＜0．01）。结论 大鼠严重烫伤早期即发生肠源性LPS血症;肠道移位LPS可诱导MLNs淋巴细胞大量凋亡,脾脏中凋亡淋巴细胞数量显减少,提示大鼠严重烫伤后可能存在脾脏免疫功能异常。     

脾肾分流术对肝炎后肝硬变门静脉高压症肠道功能的保护作用

目的探讨脾肾分流术对肝炎后肝硬变门静脉高压症肠道功能的保护作用。方法69例肝炎后肝硬变门静脉高压症并有食道胃底静脉曲张破裂出血病史的病人按入院先后分为脾肾分流组和断流组。术中、术后动态测量自由门静脉压（free portal pressure,FPP）,术后1、3、5、7、9d检测门静脉血内毒素、D-乳酸水平,术前及术后7d尿乳果糖／甘露醇（lactulose／manicol,LAC／MAN）比值。结果近期观测FPP,发现稳定期分流组明显低于断流组（P〈0．05）。分流组脾窝引流液明显少于断流组,体温恢复正常时间、肛门恢复排气及开始进食所需时间明显短于断流组（P〈0．05）。分流组术后1d内毒素、D．乳酸显著低于断流组;且下降较快,术后3d又显著低于术后1d;术后5d进入稳定期（P〈0．05）。而断流组内毒素、D．乳酸下降较慢,术后5d才显著低于术后1d,术后7d进入稳定期（P〈0．05）。分流组术后LAC／MAN比值显著低于断流组（P〈0．05）。结论脾肾分流术既能维持有效的向肝门静脉血流灌注;又能适当降低门静脉压,减轻胃肠血流瘀滞,对肝炎后肝硬变门静脉高压症肠道有明显的保护作用。     

布-加综合征大鼠动物模型的建立

目的探索采用下腔静脉缩窄术建立布-加综合征大鼠动物模型的可行性。方法将50只SD大鼠采用完全随机法随机分为实验组和假手术组,全麻开腹,分离肝上下腔静脉。实验组借鉴缩窄门静脉主干法,丝线环绕结扎肝后下腔静脉,使下腔静脉横截面积缩窄约80%。2组分别于术后不同时间点（第1、4、8、12周）行腹部彩超、肝功能、血常规及肝脏病理学检查。结果实验组在第4周时均出现肝后下腔静脉及主肝静脉梗阻,淤血性肝硬变,腹水,肝脾肿大,门静脉扩张,肝实质内交通支开放,而假手术组正常。模型建立后第4周时,实验组大鼠肝功能中ALB及血常规中WBC、PLT、RBC、HGB较假手术组明显降低（P〈0.05）,ALT、AST、AKP、TBIL、DBIL、TBA较假手术组明显升高（P〈0.05）。结论下腔静脉缩窄术可成功建立布-加综合征大鼠动物模型。     

猪到猴异位辅助性肝移植模型的建立

目的建立长白小家猪到恒河猴异位辅助性肝移植模型,总结手术操作要点。方法以健康雄性长白小家猪和健康恒河猴各5只建立猪到猴异位辅助性肝移植模型。以长白小家猪作为肝移植供体,以恒河猴作为受体。保留长白小家猪的右后叶和部分右前叶作为供肝,移植到受体的左肾窝和左结肠旁沟处。短暂阻断受体的腹主动脉和下腔静脉血流后,将移植肝的门静脉和肝下下腔静脉分别与受体的腹主动脉和下腔静脉行端侧吻合。结扎移植肝的肝动脉,不予重建。术后观察受体的一般情况和生存时间。结果成功建立4对肝移植模型,供肝切取时间24～35min、（30±5）min,供肝修整时间31～51min、（40±10）min,受体下腔静脉阻断时间23～36min、（30±6）min,受体腹主动脉阻断时间22～38min、（30±8）min,肝移植手术时间130～310min、（220±80）min,术中失血35～48mL、（42±6）mL。术后均无吻合口血栓形成及胆漏发生。4只受体分别于术后48、54、88及96h死亡,死亡原因均为排斥反应及术中失血过多。结论猪到猴异位辅助性肝移植模型的可重复性强、手术易操作、移植器官灌注良好,可用于猪到非人类灵长类动物肝移植的进一步研究。     

The gut as a portal of entry for bacteremia. Role of protein malnutrition.

The current studies were performed to determine the influence of malnutrition alone or in combination with endotoxemia in promoting bacterial translocation from the gastrointestinal tract. Bacterial translocation did not occur in control, starved (up to 72 hours), or protein-malnourished (up to 21 days) mice not receiving endotoxin. Bacterial translocation to the mesenteric lymph nodes (MLNs) occurred in 80% of control mice 24 hours after receiving endotoxin (p less than 0.01). However, the combination of malnutrition plus endotoxin was associated with a higher incidence of translocation to the systemic organs (p less than 0.01), and higher numbers of bacteria per organ (p less than 0.01), than was seen in normally nourished mice receiving endotoxin. Additionally, mice that were protein malnourished were more susceptible to the lethal effects of endotoxin than were control animals, and the mortality rate was directly related to the degree of malnutrition (R2 = 0.93) (p less than 0.05). Histologically, endotoxin in combination with protein malnutrition resulted in mechanical damage to the gut mucosal barrier to bacteria. Thus, in the mice that were protein malnourished the spread of bacteria from the gut could not be controlled nor could translocated bacteria be cleared as well as normally nourished mice receiving endotoxin. These results support the concept that under certain circumstances the gut may serve as a clinically important portal of entry for bacteria.     

Does steroid pretreatment increase endotoxin release during clinical cardiopulmonary bypass?

OBJECTIVE: The mechanism involved in the endotoxemia frequently recognized during cardiopulmonary bypass remains unclear. It has also been suggested that endotoxin levels were higher in steroid-pretreated patients undergoing cardiopulmonary bypass. METHODS: Twenty patients undergoing cardiopulmonary bypass were randomly pretreated with steroids (methylprednisolone, 30 mg/kg) or placebo. Blood samples for endotoxin measurement were drawn simultaneously from the superior and inferior venae cavae before heparin administration, 5 and 50 minutes after the onset of bypass, 5 minutes after aortic declamping, at the end of bypass, and 1, 2, and 20 hours after the end of cardiopulmonary bypass. RESULTS: The perioperative variables in the two groups were similar. Blood endotoxin levels were higher in the inferior vena cava than in the superior vena cava immediately after the onset of bypass. Endotoxin levels in inferior vena cava blood were significantly lower in steroid-pretreated patients than those in patients not receiving steroids. CONCLUSIONS: Endotoxin is released during cardiopulmonary bypass from the region drained by the inferior vena cava. Steroid pretreatment may actually reduce endotoxin release during bypass.     

入肝门静脉动脉化对大鼠肝脏损害的初步研究

目的：初步研究入肝门静脉完全动脉化加门腔分流术对大鼠肝脏的损害程度。方法100只肝硬化造模大鼠随机分为A组（n=40）,入肝门静脉完全动脉化（PVA）＋门腔分流（PCS）;B组（n=40）,仅行门腔完全分流;C组（n=20）,门静脉阻断30 min＋右肾切除。分别将各组大鼠术前和术后1、2、4、8周的肝组织切片行肝细胞诱导型一氧化氮合成酶（iNOS）免疫组织化学染色,然后进行图像分析。各取8只正常大鼠,分别于PVA术前及术后4、8周行肝组织切片,马松染色后分析正常大鼠PVA手术前后肝脏纤维增生情况。结果（1）A组2只（5%）大鼠肝脏切片中常规HE染色可见汇管区明显扩张,小叶间静脉内径显著扩张,静脉壁增厚明显,壁内可见红染的纤维增生。（2）大鼠刚完成肝硬化造模时,肝细胞胞质的iNOS表达至峰值,3组平均IOD达600583±32828;3组大鼠术后均较术前有明显下降,差异有统计学意义（P＜0.01）;术后4周内, A组仍明显高于B、C两组,差异有统计学意义（P＜0.01）;至术后8周时,3组iNOS表达差异无统计学意义。（3）正常大鼠肝间质胶原纤维染色在术前及术后4、8周的总累积光密度值差异无统计学意义。结论术后8周内,PVA不会导致正常大鼠肝间质纤维化增加,可使部分肝硬化大鼠汇管区及小叶间静脉壁纤维化;PVA对肝细胞的损害主要集中在术后4周内,待肝脏对新的血流动力学改变及其相应的影响达到稳态后,PVA对肝脏的损害则不明显。     

庆大霉素肠管去污染对大鼠实验性胰腺炎时细菌易位的影响

目的探讨庆大霉素对实验鼠肠管去污染预防重症胰腺炎并发胰腺感染性坏死的效果。方法经胰胆管插管注射无菌的５％牛磺胆酸钠制成大鼠重症胰腺炎模型。大鼠分成重症胰腺炎组（１组）;轻型胰腺炎组（２组）;重症胰腺炎加盲肠给予庆大霉素组（３组）;重症胰腺炎加庆大霉素肌肉注射组（４组）和实验对照组。术后观察各组大鼠回肠系膜淋巴结、胰腺、肝脏和血液的肠源性细菌培养阳性率。结果实验后７２小时,１组大鼠（１１只）肠系膜淋巴结培养阳性率为１００％（１１／１１）,胰腺和肝脏分别为８２％（９／１１）和２７％（３／１１）,但血液培养阴性。２组（１０只）大鼠肠系膜淋巴结培养阳性仅３０％（３／１０）,余器官培养结果均为阳性;３组（１２只）肠淋巴结和胰腺组织培养阳性率分别为４２％（５／１２）和３４％（４／１２）;而４组大鼠肠淋巴结、胰腺、肝脏和血液培养阳性率依次为１００％（１１／１１）、９１％（１０／１１）、９％（１／１１）、９％（１／１１）。结论经肠管直接给予庆大霉素去污可降低重症胰腺炎感染并发症,经肌肉注射则否。     

Bacterial translocation to the thoracic duct in a setting of ischemia, partial resection and reperfusion of the porcine liver.

BACKGROUND/AIMS: Bacterial translocation is postulated as a risk factor in the development of a systemic inflammatory response syndrome (SIRS). Research on this topic has focused on the detection of bacteria and endotoxin in blood or mesenteric lymph nodes (MLNs). We investigated whether bacterial translocation occurs beyond the MLNs into the thoracic duct in a setting of ischemia, partial resection and reperfusion of the porcine liver. METHODS: A porcine model of severe, extra-intestinal tissue injury, consisting of prolonged hepatic ischemia and reperfusion, in combination with hemihepatectomy, was used (experimental group, n = 5 pigs). To prevent venous congestion of the gut during ischemia, a temporary portal-caval shunt was created. In 5 animals (sham group) a sham portal-caval shunt was constructed while liver ischemia, partial resection and reperfusion were not induced. Thoracic duct lymph, portal blood and systemic blood were collected, and analyzed for the presence of bacteria and endotoxin. RESULTS: In the experimental group, the incidence of bacterial translocation to the thoracic duct was significantly higher during early reperfusion compared to the sham group (5/5 animals versus 1/5 animals, p < 0.05). CONCLUSION: This study demonstrates bacterial translocation into the thoracic duct. Translocation at this level leads to direct discharge of bacteria and endotoxin into the systemic circulation and therefore, may potentially enhance the development of SIRS.