腹内高压致肠黏膜屏障损伤的实验研究

目的观察不同程度腹内压（IAP）及其不同持续时间对兔肠黏膜屏障功能的影响。方法（1）取9只新西兰兔，制成腹内高压（IAH）模型（IAH模型组），将其IAP分别升至10、20、30mmHg（1mmHg=0．133kPa），维持1h后记录肠黏膜血流量。另检测正’常对照组兔（3只）的该项指标。（2）同前分组及设定IAP。维持IAP1．5h后，两组兔均以异硫氰酸荧光素-葡聚糖（FITC—D）及Ⅱ型辣根过氧化物酶（HRP-Ⅱ）灌胃。继续维持IAP0．5h后取两组兔门静脉血，检测FITC—D含量及HRP-Ⅱ活性。（3）取27只新西兰兔，分组及IAP设定同前，IAH模型组IAP为10、20mmHg时，均持、2、4h；IAP为30mmHg时，持续1、2h。抽取各组兔下腔静脉血，检测D-乳酸含量及二胺氧化酶（DAO）活性；取空肠肠段，常规制作切片，于光学显微镜及透射电镜下观察。结果（1）IAH模型组兔IAP为10mmHg时，其肠黏膜血流量接近正常对照组（P〉0．05）；IAP为20、30mmHg时，肠黏膜血流量分别比正常对照组减少了44％、80％（P〈0．01）。（2）IAH模型组兔IAP为10mmHg时，其门静脉血中FITC—D含量接近正常对照组（P〉0．05）；当IAP为20、30mmHg时，分别为正常对照组的4．8、7．0倍（P〈0．01）。HRP-Ⅱ的变化趋势与之一致。（3）IAH模型组兔IAP为10mmHg时，各时相点下血浆D-乳酸含量、DAO活性与正常对照组相近（P〉0．05）；IAP为20、30mmHg时，随着压力持续时间的延长，两指标均逐渐升高（P〈0．01）。（4）IAP为10mmHg持续2h，IAH模型组兔空肠黏膜轻度水肿；IAP20mmHg持续2h时，空肠黏膜明显水肿，中央乳糜管扩张，黏膜上皮下间隙扩大；肠上皮微绒毛变短，部分变性、坏死、脱落，线粒体高度肿胀、空泡化。IAP升至30mmHg，肠黏膜损伤进一步加重。结论IAH可导致肠黏膜屏障功能严重受损，这可能是继发全身性炎性反应综合征、脓毒症、腹腔间隙综合征及多器官功能衰竭重要原因。     

门静脉高压症时细菌移位与内毒素血症和一氧化氮之间关系的实验研究

目的 探讨门静脉高压症时细菌移位与内毒素血症和一氧化氮（NO）之间的关系。方法 采用门静脉部分缩窄（PVS）制成门静脉高压模型的30只大鼠均分为3组：模型组（B）、左旋精氨酸组（C）、单－甲基精氨酸组（D）。另10只大鼠接受假手术作为对照组（A）。术后2周取肠系膜淋巴结（MLN）、脾和血标本进行细菌培养;测定门静脉压力、内毒素和NO2^-水平;并用镧做示踪剂观察肠粘膜屏障通透性变化和粘膜 形态的改变。结果 PVS各组MLN细菌检出率高于A组,血浆内毒素水平均上升。PVS各组NO2^-和门静脉压力均较A组增高,在D组二者均较B组下降。细菌移位率、内毒素和NO2^-水平之间呈显著正相关。镧沉积到PVS各组的粘膜上皮细胞和其上下固有层细胞间,粘膜细胞的微绒毛有形态改变。结论 门静脉高压症可发生细菌移位的内毒素血症,可能与肠粘屏障通透性增强和破坏有关,提示细菌移位引起的内毒素血症并增加NO2^－水平。     

重症急性胰腺炎大鼠的早期细菌移位

目的:建立大鼠重症急性胰腺炎(SAP)模型,观察FITC标记的大肠杆菌突破肠屏障及其发生细菌移位的时间及途径。方法:健康雄性Wistar大鼠50只,随机分为SAP组(n=30)和假手术组(n=20);造模前3 h用FITC标记的大肠杆菌给大鼠灌胃,分别在造模后2、3、4、6、8 h处死动物,分别取胰腺、肠系膜淋巴结制备组织匀浆;另取门静脉血及腹水,离心取上清,荧光化学发光检测仪检测标本中FITC的荧光强度,确定细菌移位出现的途径及时间。结果:与假手术组相比,SAP组于造模后3 h在腹水,4 h在胰腺组织,6 h在肠系膜淋巴结中检测出较高强度的荧光(P<0.05),并以腹水中的荧光强度为最高;门静脉血至造模后8 h仍未检测到细菌移位。结论:腹水和淋巴液可能是SAP早期细菌移位的重要途径,细菌可通过上述途径早期发生移位。     

门静脉高压症病人肠道通透性、NO和内毒素的研究

目的　观察门静脉高压症病人的门静脉压力、肠道通透性、NO和内毒素水平 ;并分析它们之间的相互关系。方法　门静脉高压症病人 2 0例 ,分别检测肠道通透性、门静脉压力和外周血中NO和内毒素浓度。另有 2 0位健康志愿者作对照。结果　门静脉高压症病人较健康志愿者的肠道通透性 (0 132± 0 110vs 0 0 32± 0 0 18,P <0 0 1) ,外周血的NO浓度 (38 77± 13 71vs 2 1 77±3 0 1μmol/L ,P <0 0 0 1)和内毒素浓度 (0 5 7± 0 18vs 0 11± 0 0 5EU/ml,P <0 0 0 1)均非常明显的升高。研究还发现门静脉压力和这三者均有显著相关性 (r >0 45 ,P <0 0 5 ) ,另外肠道通透性与内毒素浓度 (r=0 5 2 9,P <0 0 5 )也存在相关性 ,而与NO浓度则无相关性 ;内毒素和NO之间没有发现相关性。结论　研究表明门静脉高压症病人肠道通透性、NO和内毒素水平显著升高。门静脉压力和这三者的显著相关说明门静脉压力升高是导致肠道通透性升高的直接因素 ,而内毒素和NO的升高维持了门静脉的高动力循环。     

重症急性胰腺炎伴肠屏障功能障碍患者的腹内压变化及意义

以42例重症急性胰腺炎(SAP)患者为研究对象,在确诊为SAP后进行腹内压(IAP)测量,同时化验肠屏障功能障碍标志物血清内毒素和尿L/M比值,如需手术则于术前、术后第3天再次测量上述指标。IAP平均值为(21.6±12.7)mm H2O(1 mm H2O=9.81×10-3kPa),23例(54.8%)诊断为腹内高压(IAH,IAH组),9例(21.4%)患者IAP<12 mm H2O(无IAH组),10例(23.8%)诊断为腹腔间隔室综合征(ACS,ACS组)。3组肠屏障功能障碍标志物血清内毒素和尿L/M比值水平差异有统计学意义(P<0.05),其中以ACS组最高,而无IAH组最低。相关分析发现,IAP与血清内毒素(r=0.214,P=0.026)和尿L/M比值(r=0.195,P=0.034)呈显著正相关。与术前相比,术后IAH、血清内毒素和尿L/M比值均显著降低。SAP并发肠屏障功能障碍可导致IAH和ACS,其可进一步增加肠屏障功能的损伤,手术仍是解决IAP升高和肠屏障功能障碍的有效手段。     

大鼠门静脉高压症及梗阻性黄疸时细菌移位与黄嘌呤脱氢酶和黄嘌呤氧化酶的关系

目的探讨大鼠门静脉高压症（porta; ju[ertemsopm,PH）及梗阻性黄疸（obstructive jaundioe,OJ）时,细菌移位（bacterial translocation,BT）与黄嘌呤氧化酶（xanthine oxidase,XO）、黄嘌呤脱氢酶（xanthine dehydrogenase,XD）之间的关系。方法将雄性SD大鼠60只随机分为对照组（A组）,胆总管结扎组（B组）和门静脉缩窄组（C组）,每组20只。术后第3周取肠系膜淋巴结、脾、肝组织及门静脉、腔静脉血细菌培养,测定门静脉压力（free portal pressure,FPP）,及肠XO,XD活性水平。结果B组及C组细菌移位率明显高于对照组（P〈0．01）,对照组为12％,B组和C组分别为28％和54％;B组和C组空肠XO水平活性明显高于对照组（P〈0．01）,B组和C组门静脉压力也较对照组升高。细菌移位率与XO活性成正相关（r=0．603）。XD活性水平无显著差异。结论门静脉高压症及梗阻性黄疸时可发生细菌移位,可能与肠黏膜屏障被破坏通透性增强有关,肠壁XO水平活性增强引起肠黏膜屏障通透性增高有助于细菌移位发生。     

火器多发伤时骨折早期固定减轻肠道屏障功能损害的研究

目的　探讨多发伤时骨折早期固定能否减轻肠道屏障功能的损害。　方法　 12只小型猪制作火器多发伤模型 ,即颅骨切线伤加双股骨干粉碎骨折 ,损伤严重度评分≥ 16后 ,随机分为对照组 (n =6 )和骨折内固定组 (n =6 )。伤前及伤后 6、12、2 4、4 8和 72h ,采用酶学分光光度法检测血浆D 乳酸水平 ,观察肠道通透性的变化 ;分光光度法检测血浆和小肠组织中二胺氧化酶 (DAO)含量 ;偶氮显色法鲎试验定量测定门静脉血浆内毒素浓度 ;常规方法做门静脉血细菌培养。　结果　对照组伤后血浆D 乳酸和DAO水平显著升高 ,并维持高水平到 72h ;小肠组织DAO含量明显降低 ,门静脉血浆内毒素水平明显升高 ,门静脉血细菌培养阳性率为 6 3 3%。骨折内固定组伤后 6和 12h血浆D 乳酸、DAO和内毒素水平也明显升高 ,但 2 4或 4 8h以后明显回落 ,72h与对照组相比差异有显著意义(P <0 0 5 ) ,细菌培养阳性率也低 (30 0 % ,P <0 0 5 )。　结论　多发伤后出现肠道通透性增高 ,肠黏膜完整性受损 ,有细菌、内毒素移位发生。骨折早期内固定可以减轻肠道屏障功能的损害 ,减少肠源性感染的机会。     

清热解毒方剂对腹腔感染大鼠肠黏膜屏障功能的影响

目的:观察腹腔感染状态下大鼠肠黏膜形态学和通透性的变化,观察肠源性内毒素体内移位途径,探讨清热解毒方剂肠屏障保护作用的机制.方法:采用人工胃液联合大肠杆菌腹腔内注射的方法建立大鼠腹腔感染模型.将Wistar大鼠分为3组:正常对照组(C组)、模型组(M组)、清热解毒方剂组(QRJD组),分别观察造模后6 h,24 h,72 h回肠的病理学改变以及尿液中乳果糖与甘露醇的比值(L/M)的变化.采用荧光化学发光法检测门静脉、乳糜管淋巴液、腹主动脉血以及肠系膜淋巴结、肝、肺、肠、脾组织FITC-LPS荧光强度.结果:模型组肠黏膜损伤,尿液L/M显著升高,脏器组织中FITC-LPS含量由高至低为:肠系膜淋巴结、肺、肝、肠、脾,体液中FITC-LPS含量以乳糜管淋巴液含量最高.清热解毒方剂组上述指标较模型组明显改善.结论:清热解毒方剂可以显著减轻大鼠腹腔感染所致肠黏膜损伤,改善肠黏膜通透性,减少肠源性内毒素移位,改善肠道屏障功能.     

CO_2气腹对急性腹膜炎大鼠细菌生长及移位的影响

目的研究不同气腹压力及作用时间对急性腹膜炎大鼠细菌生长繁殖和细菌移位的影响。方法于60只SD大鼠的腹腔内注射大肠杆菌标准混悬液,建立大鼠急性细菌性腹膜炎模型。本实验给予3类气腹压力:15 mm Hg(1 mm Hg=0.133 kPa)为高气腹压,5 mm Hg为低气腹压,空白对照大鼠未建立气腹;给予2类处理时间:1 h和3 h。将60只SD大鼠模型采用随机数字表法分为6组(每组10只),分别接受不同气腹压力和时间的组合处理。之后抽取腹水进行细菌定量培养和菌种分离鉴定,收集门静脉血进行血培养和内毒素含量测定。结果 (1)腹水细菌含量:析因设计的方差分析结果表明,不同气腹压力组的细菌含量不同(F=9.02,P=0.020),不同时间组的细菌含量也不同(F=8.47,P=0.003),且不同气腹压力组中时间的影响不同(F=8.07,P=0.020)。(2)血培养结果:6组大鼠都发生了细菌移位。3类气腹压力下1 h和3 h组之间的血培养阳性率类似(P0.05),2个时点下高气腹组的血培养阳性率均高于未建立气腹组(P0.05)。(3)门静脉血的内毒素含量:不同气腹压力组的内毒素含量不同(F=14.70,P0.01),高气腹组的内毒素含量高于低气腹组(P=0.018)和未建立气腹组(P0.01),且低气腹组的内毒素含量高于未建立气腹组(P=0.005);不同时间组的内毒素含量也不同(F=148.90,P0.01),3 h组的门静脉血内毒素含量高于1 h组;不同气腹压力组中时间的影响的差异不大(F=0.14,P=0.874)。结论 CO_2气腹促进了急性腹膜炎大鼠的肠道内毒素和细菌移位,并且随压力和时间的增加而严重。     

猪门静脉血流阻断后细菌及内毒素移位的研究

目的：研究猪门静脉血流阻断后细菌及内毒素移位，进一步了解门静脉系统淤血对肠粘膜屏障功能的影响。方法：将健康荣昌种猪随机分为假手术组（SO）、门静脉阻断45min(PVC-45')、60min(PVC-60')组，在阻断前、复流前、复流后1h时相点，取肠系膜淋巴结作细菌培养及取门静血作内毒素检测。结果：PCV-45'、60’组细菌培养及LPS均明显高于未阻断组（SO组）（P＜0.05)。结论：门静脉阻断后引起的肠粘膜缺血/缺氧，是肠粘膜屏粘膜障功能障碍的直接原因，细菌移位和内毒素变化是肠粘膜屏障功能受损的表现。     

选择性肠道去污染对肝硬化大鼠肝门阻断细菌移位、内毒素血症的影响

目的探讨选择性肠道去污染对肝硬化大鼠肝门阻断后肠道细菌移位、内毒素血症的效果。方法将制成肝硬化模型的60只雄性SD大鼠随机分为假手术组、肝门阻断30rain组（阻断组）及通过选择性肠道去污染预处理组（预处理组）,各20只。在实验术后30min及24h时分别取肠系膜淋巴结、肝、肺及门、腔静脉血作细菌培养,并取门、腔静脉血作内毒素检测。结果阻断组大鼠手术后30min即出现门、腔静脉血内毒素浓度升高（P〈0．01）,在手术24h后升高更明显。并在术后24h肠系膜淋巴结、肝组织及门、腔静脉血细菌培养出现阳性,主要为大肠杆菌。预处理组大鼠无论是手术30min还是24h后,门、腔静脉内毒素水平升高均不明显,较阻断组明显降低（P〈0．01）,肠道外组织及门、腔静脉血细菌培养阳性率也明显降低。结论肝硬化大鼠肝门阻断30min后早期即可出现内毒素血症,并于手术24h后出现明显肠道细菌移位。选择性肠道去污染能减少肝硬化大鼠肝门阻断后肠道细菌移位及内毒素血症的发生。     

Effects of prolonged increased intra-abdominal pressure on gastrointestinal blood flow in pigs

BACKGROUND: The aim of the study was to investigate the effects of prolonged intra-abdominal pressure on systemic hemodynamics and gastrointestinal blood circulation. METHODS: The intra-abdominal pressure in anesthetized pigs was elevated to 20 mmHg (7 animals), 30 mmHg (7 animals), and 40 mmHg (4 animals), respectively. These pressures were maintained for 3 h by intra-abdominal infusion of Ringer's solution. A control group of seven animals had normal intra-abdominal pressure (IAP). Transit time flowmetry and colored microspheres were used to measure blood flow. RESULTS: An IAP of 20 mmHg did not cause significant changes in systemic hemodynamics or tissue blood flow. An IAP of 30 mmHg caused reduced blood flow in the portal vein, gastric mucosa, small bowel mucosa, pancreas, spleen, and liver. Serum lactate increased in animals with an IAP of 30 mmHg, but microscopy did not disclose mucosal damage in the stomach or small bowel. An IAP of 40 mmHg was followed by severe circulatory changes. CONCLUSIONS: Prolonged IAP at 20 mmHg did not cause changes in general hemodynamics or gastrointestinal blood flow. Prolonged IAP at 30 mmHg caused reduced portal venous blood flow and reduced tissue flow in various abdominal organs, but no mucosal injury. A prolonged IAP of 40 mmHg represented a dangerous trauma to the animals.     

大鼠急性出血坏死性胰腺炎时细菌移位和茵陈蒿合承气汤的影响

目的 :研究大鼠急性出血坏死性胰腺炎 (牛磺胆酸钠胰胆管注射诱导 )细菌移位及其机制和茵陈蒿合承气汤的影响。 方法 :大鼠分成模型组、中药防治组、假手术组。术后观查外周血、门静脉血内毒素水平 ;肝、脾、胰、肠系膜淋巴结细菌移位率 ;盲肠内容物需氧菌总量和革兰阴性杆菌菌量 ;肠推进功能。 结果 :急性出血坏死性胰腺炎时外周血和门静脉血内毒素水平显著升高 ;肝、胰、肠系膜淋巴结组织细菌移位率显著升高 ;盲肠需氧菌总量和革兰阴性杆菌量显著升高 ;肠推进功能降低。应用茵陈蒿合承气汤能显著改善上述指标。 结论 :急性出血坏死性胰腺炎时存在细菌移位 ,茵陈蒿合承气汤能有效地减少急性出血坏死性胰腺炎时细菌移位的发生     

Adverse effects of increased intra-abdominal pressure on small bowel structure and bacterial translocation in the rat

BACKGROUND: The purpose of this study was to evaluate the effects of elevated intra-abdominal pressure (IAP) on intestinal structures and bacterial translocation in the rat. MATERIALS AND METHODS: Forty-two male Sprague-Dawley rats were randomly divided into three experimental groups of 14 rats each: the sham group underwent insertion of a balloon-tipped catheter; the IAP-15 group was subjected to a 15 mm Hg pneumoperitoneum for 60 minutes; and the IAP-25 group was subjected to a 25 mm Hg pneumoperitoneum for 60 minutes. Intestinal structural changes (bowel circumference, overall bowel and mucosal weight, mucosal DNA and protein, villus height, and crypt depth) and bacterial translocation to mesenteric lymph nodes, liver, spleen, portal blood, and peripheral blood were determined 24 hours following pneumoperitoneum. RESULTS: IAP-15 and IAP-25 rats demonstrated a significant decrease in: bowel and mucosal weight in the duodenum, jejunum, and ileum; mucosal DNA and protein in the jejunum and ileum; villus height in the jejunum: and crypt depth in the jejunum and ileum compared to the sham rats. Bacterial translocation was demonstrated in 60% of IAP-15 rats and in 80% of IAP-25 rats. CONCLUSION: Elevated IAP results in mucosal injury of the gut, causing mucosal hypoplasia, and increases bacterial translocation.     

Role of bacterial adherence and the mucus barrier on bacterial translocation: effects of protein malnutrition and endotoxin in rats.

OBJECTIVE: The purpose of the study was to investigate the potential relations between mucosal bacterial adherence, intestinal mucus and mucin content, and bacterial translocation. SUMMARY BACKGROUND DATA: The attachment of bacteria to mucosal surfaces is the initial event in the pathogenesis of most bacterial infections that originate at mucosal surfaces, such as the gut. The intestinal mucus layer appears to function as a defensive barrier limiting micro-organisms present in the intestinal lumen from colonizing enterocytes. Consequently, studies focusing on the biology of bacterial adherence to the intestinal mucosa likely are to be important in clarifying the pathogenesis of gut origin sepsis. METHODS: To explore the relations between intestinal bacterial adherence, mucus bacterial binding, and bacterial translocation, two models were used. One (protein malnutrition) in which profound alterations in intestinal morphology occurs in the absence of significant translocation and one (endotoxin challenge) in which bacterial translocation occurs and intestinal morphology is relatively normal. RESULTS: Protein malnutrition was not associated with bacterial translocation and measurement of enteroadherent, mucosally associated bacterial population levels documented that the total number of gram-negative enteric bacilli adherent to the ileum and cecum was less in the protein-malnourished rats than in the normally nourished animals (p < 0.01). Furthermore, there was an inverse relation between the duration of protein malnutrition and bacterial adherence to the intestinal mucosa (r = 0.62, p < 0.002). In contrast, after endotoxin challenge, the level of enteroadherent bacteria was increased and bacterial translocation was observed. The binding of Escherichia coli to immobilized ileal mucus in vitro was decreased significantly in protein-malnourished rats, whereas E. coli binding to insoluble ileal mucus was increased in the rats receiving endotoxin. CONCLUSIONS: This study indicates that the adherence of bacteria to the intestinal mucosal surface is an important factor in bacterial translocation, that intestinal mucus modulates bacterial adherence, and that increased levels of mucosally associated bacteria are associated with a loss intestinal barrier function to bacteria.     

肝移植术后腹腔间隙综合征的诊治体会

目的 总结肝移植术后腹腔间隙综合征(ACS)的诊治体会。方法 采用膀胱内压检测法间接测量腹内压(IAP),监测术后心、肺、肾功能。术后IAP大于20mmHg,同时有一项或多项器官功能受损诊断为ACS。合理补液,采用腹腔内重新置管引流、腹腔穿刺、肌松药等非开腹减压方法以治疗ACS。结果 9例ACS患者中,6例出现急性肾功能损害,其中4例表现为少尿或无尿;6例出现低氧血症,机械通气时间延长;4例心率明显增快,其中3例并发心衰。除2例死于多器官功能不全综合征外,7例患者经上述治疗后腹胀显著减轻,心肺肾功能恢复正常。结论 肝移植术后加强对ACS的重视、术后早期IAP的严密监测以及尽早的非开腹减压治疗具有较重要的临床意义。     

Intra-Abdominal Hypertension and Abdominal Compartment Syndrome Following Surgery for Ruptured Abdominal Aortic Aneurysm

OBJECTIVES: To investigate the importance of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS), based on the December 2004 consensus definition, on outcome after surgery for ruptured abdominal aortic aneurysm (rAAA). METHODS: Twenty-seven patients underwent open surgery for rAAA after the introduction of intra-abdominal pressure (IAP) measurements among patients at risk of IAH. Case-records were reviewed retrospectively. Seventeen patients underwent IAP-monitoring. RESULTS: Of eight patients with IAP <21 mmHg none developed colonic ischaemia or ACS. Of four patients with IAP 21-25 mmHg (IAH grade III), two underwent colonic resection. One patient treated with open abdomen died from cardiac arrhythmia. Five patients had IAP >25 mmHg (IAH grade IV). All developed ACS. Two were not decompressed and both developed pulmonary complications, one died. Two underwent colonic resection and one was treated with open abdomen, all three survived. Of 10 patients not monitored for IAP, one died of cardiac complications, but no patient developed signs of colonic ischaemia or ACS. Mortality at 30 days and 1 year was 3/27 (11%). CONCLUSION: IAH and ACS were common among patients undergoing surgery for rAAA. The ACS consensus definition seems appropriate in this clinical context. Monitoring IAP, and timely decompression of patients with IAH might improve outcome after surgery for rAAA.     

The Preventive Effect of Dopamine Infusion in Rats with Abdominal Compartment Syndrome

ABSTRACT

Background: The most significant perfusion disorder of the intra-abdominal viscera occurs in the abdominal compartment syndrome (ACS). Free oxygen radicals diffuse into the body during the reperfusion phase of ACS. Our aim was to determine the effects of dopamine infusion (3 μg/kg/min) on renal perfusion, cytokine levels, free oxygen radicals, and renal histopathological changes in the presence of ACS in a prospective randomized manner. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into four groups (n = 6). Group 1 was used as control. In group 2, air was inflated until the intra-abdominal pressure (IAP) reached 20 mmHg. In group 3, dopamine was infused for 60 min meanwhile IAP was kept at 20 mmHg. In group 4, dopamine was infused for 60 min before IAP rise. After this phase, renal artery (RA) perfusion was measured continuously. Myeloperoxidase activity (MPO), glutathione (GSH), and lipid peroxidation (MDA) levels were measured in tissue samples and histopathological scoring was performed. Results: Dopamine treatment before and during ACS significantly decreased MPO and MDA levels and also increased renal blood flow and GSH levels. However, histopathological damage was improved simultaneously. Conclusion: Dopamine infusion before and during ACS, increases renal perfusion and decreases free oxygen radicals. According to our findings, dopamine infusion may be proposed for the treatment of ACS and perfusion disorders in critically ill patients.     

Kinetics of endotoxin and tumor necrosis factor appearance in portal and systemic circulation after hemorrhagic shock in rats.

OBJECTIVE: This study was performed to investigate gut-derived bacterial translocation and the time course of endotoxin (lipopolysaccharide [LPS]) and tumor necrosis factor (TNF) appearance, both in portal and systemic circulation. SUMMARY BACKGROUND DATA: The significance of intestinal bacteria/endotoxin translocation or TNF formation in the development of systemic sepsis has been disputed. METHODS: A rat model of hemorrhagic shock (30-35 mm Hg for 90 min) and resuscitation was used. RESULTS: Bacterial translocation was histologically observed in the small intestinal wall 30 minutes after resuscitation. A significant increase in LPS concentrations was found in the portal vein (91.7 +/- 30.6 pg/mL) at 90 minutes, which remained steady until 150 minutes after shock. Lipopolysaccharide increased in the systemic circulation, the levels became significant at 120 minutes, and peaked (66.5 +/- 39.2 pg/mL) 150 minutes after shock. Tumor necrosis factor concentrations were found to be significantly elevated in both portal and systemic circulation (75.6 +/- 22.1 vs. 58.4 +/- 14.1 pg/mL) at 90 minutes post-shock. Although there was no further increase in TNF concentration in the portal blood. TNF peaked (83.5 +/- 17.7 pg/mL) in systemic circulation at 120 minutes and still was markedly increased at 150 minutes post-shock. In addition, higher LPS and TNF concentrations in systemic circulation were found in the nonsurvivors than in the surviving animals at the end of resuscitation. CONCLUSIONS: These results suggest that hemorrhagic shock may lead to early bacterial translocation in the intestinal wall and transient access of gut-derived LPS and LPS-induced mediators into the circulation predominantly via the portal circulation.     

Abdominelles Kompartmentsyndrom

Abdominal compartment syndrome (ACS) is characterized by a persistent pathologic increase in intra-abdominal pressure (IAP) exceeding 20 mmHg with consecutive dysfunction of multiple organ systems. The main causes of ACS are abdominal trauma, obstruction, infection, and sepsis, but it may also be initiated by extra-abdominal diseases. The gold standard for diagnosis is repeated assessment of the IAP measurements of bladder pressure. The incidence of ACS is up to 15% in operative ICUs and the therapy of choice for it is decompressive laparotomy. Nevertheless, mortality is high, up to 60%.