Neutrophil depletion in rats reduces burn-injury induced intestinal bacterial translocation

OBJECTIVE: To determine whether neutrophil depletion could eradicate intestinal bacterial translocation in bum-injured rats. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: The rats were intravenously administered a rabbit anti-rat neutrophil antibody causing profound neutropenia and subjected to a 30% total body surface area scald burn. MEASUREMENTS AND MAIN RESULTS: The depletion of neutrophils from the intestine was assessed via measurements of myeloperoxidase (MPO) activity in the intestinal homogenates. In addition, the presence of activated/extravasated neutrophils in intact intestines was determined via immunohistochemical localization of neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase component protein p47phox. Bacterial translocation was measured using agar cultures and by determining Escherichia coli beta-galactosidase gene via polymerase chain reaction/Southern blot analyses of mesenteric lymph node and spleen, liver, lung, and blood. MPO measurements demonstrated a six-fold increase above the control value in the intestinal tissue in rats on day 1 postburn. The presence of activated neutrophils (expression of p47phox protein) was also markedly increased in the intestines of these rats. The increased MPO activity and p47phox expression accompanied a translocation of indigenous E. coli into the mesenteric lymph node without a spread to other organs. The administration of anti-neutrophil antibody to burn animals prevented an increase in MPO activity and bacterial translocation. CONCLUSION: These studies indicate that enhanced intestinal bacterial translocation caused by burn injury could be related to the increased infiltration of activated neutrophils into the intestinal tissue after bum. The release of neutrophil products such as superoxide anion may effect intestinal tissue damage leading to bacterial translocation of indigenous E. coli.     

Inhibition of poly(adp-ribose) polymerase reduces cardiomyocytic apoptosis after global cardiac arrest under cardiopulmonary bypass

Cardiomyocytic apoptosis occurs after cardiopulmonary bypass (CPB) despite the use of perfusion techniques and cardioplegic solutions. Reactive oxygen species (ROS) cause single-strand DNA breaks and activate nuclear poly(ADP-ribose) polymerase (PARP), which leads to cellular damage. Therefore, the inhibition of PARP might protect cardiomyocytes from oxidative injuries. In this study, experiments were designed to determine whether a PARP inhibitor could decrease the myocardial ischemia/reperfusion injury after cardioplegia-induced global cardiac arrest under CPB, attenuate the appearance of cardiomyocytic apoptosis, and decrease damage from ROS. New Zealand white rabbits (10 in each group) were subjected to total CPB. Rabbits were weaned from CPB and reperfused for 4 h before the hearts were harvested. 3-Aminobenzamide and/or 3-aminobenzoic acid was added to the cardioplegic solution. The ascending aorta was cross-clamped for 60 min while intermittent cold crystalloid cardioplegic solution was infused into the aortic root every 20 min. The reperfused hearts were harvested and studied for evidence of apoptosis using the TUNEL method and Western blot analyses. The oxidative insults were checked using ELISA to detect plasma isoprostane and cytokines levels. The occurrence of cardiomyocytic apoptosis was significantly less in PARP inhibitor recipients than in PARP-inhibitor-naive controls. Plasma isoprostane and various cytokines were significantly elevated in PARP-inhibitor-naive controls but significantly reduced in PARP inhibitor recipients. Western blot analysis revealed similar patterns. PARP inhibitor-supplemented crystalloid cardioplegic solution diminished postischemic cardiomyocytic apoptosis and ROS-mediated injuries after global cardiac arrest under CPB, possibly via inhibiting both caspase-dependent and -independent apoptotic pathways, which also preserved postischemic myocardial contractility.     

失血性休克对大鼠肠道细菌易位和血浆内毒素水平的影响及其意义

目的 探讨失血性休克对肠道细菌易位和血浆内毒素水平的影响。方法 采用甲基－^3胸腺嘧啶核苷（[^3H]-TdR）标记致病人肠杆菌，大失血性休克前注入大鼠的胃肠道，然后于失血性休克的不同阶段，通过检测^3H的放射活性和应用放射自显影的方法进行示踪，同时检测血浆内毒素的含量。结果 失血性休克早期即可发生肠源性内毒素血症；当休克发展到一定严重程度时，肠道细菌可进入血液循环，并侵及多个脏器。结论 失血性休克可致肠源性内毒素血症和肠道细菌易位性感染。     

Supplementation and inhibition of nitric oxide synthesis influences bacterial transit time during bacterial translocation in rats

In the obstructed gut, nitric oxide (NO) may influence intestinal barrier function and translocation of bacteria. By using a novel experimental approach, we investigated the effect of supplementation and inhibition of NO synthesis on the time interval necessary for translocation of green fluorescent protein-transfected Escherichia coli (GFP-uv E. coli) in a rat model of small bowel obstruction. In anesthetized Wistar rats, 4 x 10(8) GFP-uv E. coli were administered into a reservoir of terminal ileum formed by ligature. Animals were randomized to receive either i.v. arginine (10 mg/kg), aminoguanidine (300 mg/kg), L-NAME (25 mg/kg), or saline (control). Translocation of GFP-uv E. coli was assessed using intravital video microscopy. Minimal transit time of translocation was measured as time from injection of GFP-uv E. coli into the gut lumen until bacteria were observed in the lamina submucosa and as time from injection of bacteria into the gut lumen until bacteria were observed in the lamina muscularis propria. Minimal transit times were expressed as mean +/- SD. Bacterial translocation into the submucosa and muscularis propria took 36 +/- 7 min and 81 +/- 9 min, respectively in control animals receiving saline. Aminoguanidine and L-NAME caused a marked delay of minimal transit time into the submucosa (63 +/- 5 min and 61 +/- 7 min, respectively; P < 0.05). Arginine significantly accelerated bacterial translocation into the muscularis propria (61 +/- 9 min, P < 0.05). GFP-uv E. coli were detected on frozen sections of small bowel, mesentery, liver, and spleen 2 h after GFP-uv E. coli administration in all animals. A marked upregulation of inducible NO synthase (NOS) in the obstructed bowel segment was demonstrated on immunohistochemistry. The assessment of a newly defined parameter, minimal bacterial transit time, may serve as an additional functional aspect of intestinal barrier function for pathophysiological and pharmacological studies. Aminoguanidine, L-NAME, and arginine were effective in influencing minimal transit time of E. coli during small bowel obstruction.     

Poly (ADP-ribose) synthetase mediates intestinal mucosal barrier dysfunction after mesenteric ischemia

Peroxynitrite-mediated DNA strand breaks trigger poly (ADP-ribose) synthetase (PARS) activation, resulting in intracellular energetic failure and organ dysfunction. We investigated the role of PARS activation on the inflammatory and functional response of the intestine to mesenteric ischemia-reperfusion injury. Anesthetized rats exposed to 15 min occlusion of the superior mesenteric artery showed an increased mucosal PARS activity (ex vivo incorporation of radiolabelled NAD+ in gut mucosal scrapings) as soon as 10 min after reperfusion. During the first 30 min of reperfusion, significant mucosal damage developed, as well as mucosal hyperpermeability to a 4000 MW fluorescent dextran (FD4). These alterations were significantly reduced by treatment with the NO synthase inhibitor L-NMA, which blocks the production of peroxynitrite, as well as with the PARS inhibitors 3-aminobenzamide and nicotinamide, whereas they were markedly enhanced by the glutathione depletor L-buthionine-(S,R)-sulfoximine. Also, PARS inhibition significantly reduced ileal neutrophil infiltration (myeloperoxidase activity) at 3 h reperfusion. In a second set of experiments, the effects of 15 or 30 min ischemia followed by 3 h reperfusion were evaluated in PARS knockout and wild-type mice. Significant protection against histological damage, neutrophil infiltration, and mucosal barrier failure (evaluated by the mucosal-to-serosal FD4 clearance of everted ileal sacs incubated ex vivo) was noted in PARS knockout mice, who also showed reduced alterations in remote organs, as shown by lesser lipid peroxidation (malondialdehyde formation) and neutrophil infiltration in the lung and liver. In conclusion, PARS plays a crucial role in mediating intestinal injury and dysfunction in the early and late phases of mesenteric reperfusion. Pharmacological inhibition of PARS may be a novel approach to protect tissues from reperfusion-related damage.     

肠源性内毒素移位后的体内分布

探讨肠源性内毒素移位后在腹膜炎大鼠各脏器中分布。方法以＾１２５Ｉ－ＬＰＳ对大鼠灌胃后,检测各脏器单位组织重量中内毒素含量。结果腹膜炎组各主要脏器单位重量中的内毒素含量增加,由至低为肾、肺、肝、胰、肠系膜淋巴结,心脏。结论急性感染腹膜炎可致肠源性内毒素移位增加。     

蛙皮素抑制失血-感染大鼠肠道细菌移位的实验研究

目的 :研究蛙皮素 (BBS)对失血感染模型大鼠肠黏膜屏障和肠道细菌移位的影响。方法 :从颈静脉插管放血制成单纯失血模型 ;从十二指肠插管灌注大肠杆菌液制成单纯感染模型 ;放血加十二指肠灌注大肠杆菌液制成失血感染模型。 80只大鼠随机分为假手术组、单纯失血组、单纯感染组、失血感染组和不同浓度的BBS干预组共 7组 ,BBS干预组分别用 5、2 0和 80 μg/kg剂量给失血感染大鼠皮下注射。观察大鼠肠系膜淋巴结 (ML N)和肝脏组织匀浆体外培养后的细菌量、细菌移位率以及门静脉内毒素水平。结果 :假手术组有16 .7%的组织培养为细菌阳性 ,单纯失血组和单纯感染组各有 5 0 .0 %大鼠组织细菌阳性 ,失血感染组组织细菌培养的阳性率达 95 .8% ,BBS各干预组阳性率则分别为 16 .7%、16 .7%和 72 .7% ,其中 5和 2 0μg/kg干预组与失血感染组相比均有显著性差异 (P均 <0 .0 1)。 5和 2 0μg/kg干预组肝及 ML N组织平均含菌量与失血感染组相比均有显著性差异 (P均 <0 .0 5 )。内毒素水平在 5和 2 0 μg/kg BBS干预组内毒素水平明显低于失血感染组 (P均 <0 .0 1)。结论 :一定剂量的 BBS有保护肠黏膜屏障抑制细菌移位的作用     

Orally inoculated Escherichia coli strains colonize the gut and increase bacterial translocation after stress in rats

Coliforms are the members of the indigenous gut flora that most often translocate to mesenteric lymph nodes. Very few strains of Escherichia coli found in cecal contents of rats are able to translocate. The present study investigated the role of the composition of the gut flora for the occurrence of bacterial translocation. Two strains of E. coli (KI-C1 and KI-C2), previously shown to translocate in rats subjected to stress, were given by oral inoculation to rats lacking these strains. A biochemical fingerprinting method was used to identify bacteria in cecal contents, on cecal epithelium, and in mesenteric lymph nodes. In a challenge study, the inoculated E. coli strains were shown to colonize the rats and persist for up to 75 days in cecum. Subsequently, one group was starved for 24 h and a second group was subjected to experimental hemorrhage and then starved for 24 h before sampling for bacteriological analyses from blood, cecum, and mesenteric lymph nodes. Two parallel groups of rats served as controls and were not inoculated but otherwise received the same treatment before sampling. In the inoculated group, starved for 24 h, seven out of 11 rats showed translocation, whereas in the noninoculated group one of 11 rats showed translocation (P < 0.05). In groups subjected to hemorrhage and then starved for 24 h, 15/22 rats in the inoculated and 5/20 rats in the noninoculated group showed translocation (P < 0.01). These findings show that orally inoculated KI-C1 and KI-C2 strains can colonize the gut and can substantially increase bacterial translocation in rats subjected to mild and severe stress. The composition of the gut flora seems to be an underestimated factor in the pathophysiology of bacterial translocation.     

The role of intravenous administration of dextran 70 in enteric bacterial translocation after partial hepatectomy in rats

The aim of this study was to assess the effect of intravenous dextran on bacterial translocation and intestinal vascular endothelial and epithelial barrier function after experimental partial hepatectomy. We determined systemic arterial pressure, enteric bacterial growth (proximal and distal small intestine and colon) and bacterial translocation (BT) to mesenteric lymph nodes (MLN), liver, lungs, spleen, kidneys and blood, as well as intestinal vascular endothelial and epithelial barrier permeability, after sham operation or partial hepatectomy (50% and 90%) with preoperative intravenous administration of saline, albumin or dextran 70. Subtotal hepatectomy induced a significant decrease in arterial pressure and an increase in the number of Escherichia coli in the distal small intestine. BT was not observed in sham-operated animals or in rats with 50% hepatectomy administered dextran. The number of positive cultures of enteric bacteria was significantly increased after hepatectomy, whereas dextran treatment decreased the number of animals with BT. Increased permeability of the intestinal vascular endothelial and epithelial barriers was noted in hepatectomized animals, while dextran prevented hepatectomy-induced vascular endothelial barrier injury. Enteric bacterial translocation occurred following partial hepatectomy in the rat, associated with bacterial overgrowth in the distal small intestine. Intravenous administration of dextran 70 prevented bacterial overgrowth and translocation, at least in part, by maintaining gut vascular endothelial barrier integrity.     

Spinal noradrenaline transporter inhibition by reboxetine and Xen2174 reduces tactile hypersensitivity after surgery in rats

Spinal noradrenaline (NA) released in response to noxious stimuli may play an important role in suppression of nociceptive transmission. Here, we investigated the efficacy of a competitive NA transporter inhibitor (reboxetine) and a noncompetitive NA transporter inhibitor peptide, Xen2174, isolated from the Pacific cone snail, to treat tactile hypersensitivity following paw incisional surgery. Male Sprague-Dawley rats were anesthetized, an incision of the plantar aspect of the hind paw was performed, and withdrawal threshold to von Frey filaments near the surgical site determined. Reboxetine (0.5-5 microg) and Xen2174 (0.3-100 microg) increased withdrawal threshold when injected 24h after paw incision, with a peak effect at 15-60 min, for Xen2174, an ED50 value of 0.64 microg. Administration of Xen2174 (3-30 microg) 15 min before incision also reduced hypersensitivity in a dose-dependent manner. Withdrawal threshold after the single 30 microg dose was greater than vehicle control even at 2, 3, and 5 days after incision. Doses 相似文献   

Amphibian peptides prevent endotoxemia and bacterial translocation in bile duct-ligated rats

OBJECTIVE: To investigate the efficacy of amphibian antimicrobial peptides in preventing bacterial translocation and neutralizing endotoxins in bile duct-ligated rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory in a university hospital. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: Adult male Wistar rats underwent sham operation or bile duct ligation (BDL). Eight groups were studied: sham operation with saline treatment, sham operation with 120 mg/kg tazobactam-piperacillin, sham operation with 2 mg/kg uperin 3.6, sham operation with 2 mg/kg magainin2, BDL with saline treatment, BDL with 120 mg/kg tazobactam-piperacillin, BDL with 2 mg/kg uperin 3.6, and BDL with 2 mg/kg magainin2. MEASUREMENTS AND MAIN RESULTS: Main outcome measures were: endotoxin and tumor necrosis factor-alpha concentrations in plasma and evidence of bacterial translocation in blood, peritoneum, liver, and mesenteric lymph nodes. Endotoxin and tumor necrosis factor-alpha plasma levels were significantly higher in BDL rats compared with sham-operated animals. All amphibian peptides achieved a significant reduction of plasma endotoxin and tumor necrosis factor-alpha concentration when compared with saline- and tazobactam-piperacillin-treated groups. On the other hand, both tazobactam-piperacillin and peptides significantly reduced bacterial growth compared with the control. Tazobactam-piperacillin and magainin2 exerted the maximal inhibition of bacterial growth. CONCLUSION: In conclusion, because of their multifunctional properties, amphibian peptides could be interesting compounds to inhibit bacterial translocation and endotoxin release in obstructive jaundice.     

组织胺抑制失血-感染大鼠肠道细菌移位的实验研究

目的 观察组织胺对失血感染模型大鼠肠道细菌移位的影响.方法 从十二指肠灌注大肠杆菌制成单纯感染模型,从颈静脉插管放血加十二指肠灌注大肠杆菌制成失血感染模型.大鼠随机分为假手术组、单纯感染组、失血感染组和1×10-6 mol/L浓度的组织胺对以上各组的干预组共6组.组织胺干预组分别用1×10-6 mol/L的组织胺对制成的模型大鼠进行肠内灌注.观察模型大鼠肠系膜淋巴结和肝脏匀浆体外培养后的细菌量,细菌移位率,小肠病理改变.结果 假手术组有10%的组织培养为细菌阳性,单纯感染组有50%大鼠组织细菌阳性,失血感染组组织细菌培养的阳性率高达95%.组织胺各干预组则分别为5%、20%、25%,HA干预组与失血感染组相比均有显著性差异(P＜0.01).HA干预组肝及MLN平均组织含菌量与失血感染组相比均有统计学意义(P＜0.05).1×10-6mol/L HA干预组肠黏膜病理损伤较失血-感染组也明显减轻(P＜0.01).结论 一定剂量的组织胺有保护肠黏膜屏障抑制细菌移位的作用.     

Renin-angiotensin system inhibition reduces glycine-induced glomerular hyperfiltration in conscious rats.

It has been reported that high protein intake or amino acid infusion-induced glomerular hyperfiltration are accompanied by an elevation of plasma renin activity and renal renin mRNA. We therefore investigated the effect of inhibition of the renin-angiotensin system by SK&F 108566, a novel, nonpeptide angiotensin II (AII) receptor antagonist, or by enalapril, an angiotensin converting enzyme inhibitor, on glycine-induced hyperfiltration. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by inulin and p-aminohippurate clearances in conscious chronically instrumented rats. Glycine infusion (3.7 mg/min i.v.; n = 8) significantly increased GFR by 27% (from 1.09 +/- 0.53 to 1.38 +/- 0.08 ml/min.100 g), ERPF by 22% (2.96 +/- 0.30 to 3.61 +/- 0.32 ml/min.100 g) and significantly decreased effective renal vascular resistance by 22% [from 25.4 +/- 2.9 to 20.8 +/- 2.5 mm Hg/(ml/min.100 g)]. SK&F 108566 (30 micrograms/kg.min) or enalapril (1 mg/kg), at doses which inhibited the pressor effects of AII or AI, respectively, but had no significant influence on base-line GFR and ERPF, significantly attenuated the glycine-induced glomerular hyperfiltration and hyperemia. In the presence of SK&F 108566 or enalapril, glycine resulted in only small, statistically insignificant changes in GFR (from 1.07 +/- 0.03 to 1.10 +/- 0.04 and from 1.19 +/- 0.03 to 1.21 +/- 0.08 ml/min.100 g, respectively), ERPF (from 3.27 +/- 0.21 to 3.53 +/- 0.26 and from 3.57 +/- 0.11 to 3.41 +/- 0.38 ml/min.100 g, respectively) and effective renal vascular resistance [from 21.2 +/- 1.9 to 19.2 +/- 1.6 and from 18.4 +/- 0.9 to 20.2 +/- 2.2 mm Hg/(ml/min.100 g], respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

组胺对失血感染模型大鼠肠道细菌易位的影响

目的观察组胺对失血感染模型大鼠肠道细菌易位的影响。方法从颈静脉插管放血制成单纯失血模型;经十二指肠插管灌注标准大肠杆菌液制成单纯感染模型;放血加十二指肠灌注大肠杆菌液制成失血感染模型。大鼠随机分为假手术组、单纯失血组、单纯感染组、失血感染组和不同浓度组胺治疗组共7个组。组胺治疗组分别用1×10     

Protective effect of poly(ADP-ribose) synthetase inhibition on multiple organ failure after zymosan-induced peritonitis in the rat.

BACKGROUND AND METHODS: In the present study, we tested the hypothesis that peroxynitrite and subsequent activation of the nuclear enzyme poly(ADP-ribose) synthetase (PARS) play a role in the pathogenesis of multiple organ failure induced by peritoneal injection of zymosan in the rat. Animals were randomly divided into six groups (ten rats for each group). The first group was treated with ip administration of saline solution (0.9% NaCl) and served as the sham group. The second group was treated with ip administration of zymosan (500 mg/kg suspended in saline solution). In the third and fourth groups, rats received ip administration of 3-aminobenzamide (10 mg/kg) 1 and 6 hrs after zymosan or saline administration, respectively. In the fifth and sixth groups, rats received ip administration of nicotinamide (50 mg/kg) 1 and 6 hrs after zymosan or saline administration, respectively. After zymosan or saline injection, animals were monitored for 72 hrs to evaluate systemic toxicity (conjunctivitis, ruffled fur, diarrhea, and lethargy), loss of body weight, and mortality. RESULTS: A severe inflammatory response, characterized by peritoneal exudation, high plasma and peritoneal levels of nitrate/nitrite (the breakdown products of nitric oxide), and leukocyte infiltration into peritoneal exudate, was induced by zymosan administration. This inflammatory process coincided with the damage of lung, small intestine, and liver as assessed by histologic examination and by an increase of myeloperoxidase activity, which is indicative of neutrophil infiltration. Zymosan-treated rats showed signs of systemic illness, significant loss of body weight, and high mortality rates. Peritoneal administration of zymosan in the rat also induced a significant increase in the plasma levels of peroxynitrite as measured by the oxidation of the fluorescent dihydrorhodamine 123. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine, a specific "footprint" of peroxynitrite, in the lung of zymosan-shocked rats. In vivo treatment with ip administration of 3-aminobenzamide (10 mg/kg, 1 and 6 hrs after zymosan injection) or nicotinamide (50 mg/kg, 1 and 6 hrs after zymosan injection) significantly decreased mortality, inhibited the development of peritonitis, and reduced peroxynitrite formation. In addition, PARS inhibitors were effective in preventing the development of organ failure because tissue injury and neutrophil infiltration, by myeloperoxidase evaluation, were reduced in the lung, small intestine, and liver. CONCLUSIONS: In conclusion, the major findings of our study are that peroxynitrite and the consequent PARS activation exert a role in the development of multiple organ failure and that PARS inhibition is an effective anti-inflammatory therapeutic tool.     

Poly(ADP-ribose) polymerase contributes to the development of myocardial infarction in diabetic rats and regulates the nuclear translocation of apoptosis-inducing factor

Activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP)-1 by oxidant-mediated DNA damage is an important pathway of cell dysfunction and tissue injury during myocardial infarction. Because diabetes mellitus can substantially alter cellular signal transduction pathways, we have now investigated whether the PARP pathway also contributes to myocardial ischemia/reperfusion (MI/R) injury in diabetes mellitus in rodents. Myocardial ischemia/reperfusion in control and streptozotocin-diabetic rats was induced by transient ligation of the left anterior descending coronary artery. PARP activation was inhibited by the isoindolinone derivative PARP inhibitor INO-1001. In diabetic rats, a more pronounced degree of myocardial contractile dysfunction developed, which also was associated with a larger infarct size, and significant mortality compared with nondiabetic rats. Inhibition of PARP provided a similar degree of myocardial protective effect in diabetic and nondiabetic animals and reduced infarct size and improved myocardial contractility. In diabetic rats, PARP inhibition reduced mortality during the reperfusion phase. There was marked activation of PARP in the ischemic/reperfused myocardium, which was blocked by INO-1001. In addition, there was a significant degree of mitochondrial-to-nuclear translocation of the cell death effector apoptosis-inducing factor (AIF) in myocardial infarction, which was blocked by pharmacological inhibition of PARP. The role of PARP in regulating AIF translocation in myocytes also was confirmed in an isolated perfused heart preparation. Overall, the current results demonstrate the importance of the PARP pathway in diabetic rats subjected to myocardial infarction and demonstrate the role of PARP in regulating AIF translocation in MI/R.     

丹参对大鼠烫伤后内毒素移位影响的实验研究

目的　探讨丹参对大鼠烫伤后内毒素移位的影响及其机制。方法　采用 30 %TBSA深Ⅱ度烫大鼠模型 ,检测伤前及伤后 3、6、12、2 4、4 8h大鼠血浆内毒素 (LPS)含量、肠黏膜血流量 (IMBF)、肠组织内一氧化氮 (NO)和内皮素 (ET)含量。结果　①伤后血浆LPS含量显著增高 (P <0 0 1) ,但治疗组显著低于烫伤组 (P <0 0 5 ,P <0 0 1) ;②伤后IMBF显著下降 (P <0 0 1) ,但治疗组下降幅度明显小于烫伤组 (P <0 0 5 ,P <0 0 1) ;③伤后肠组织内ET、NO含量均升高 ,尤以ET升高幅度较大 ,ET/NO比值上升 (P <0 0 5 ,P <0 0 1)。但治疗组与烫伤组相比较 ,ET含量降低、NO含量升高 ,ET/NO比值下降 (P <0 0 5 ,P <0 0 1)。结论　丹参能有效防治烫伤后内毒素移位 ,其作用机制可能与影响肠组织内ET、NO含量 ,调节ET/NO比值进而改善肠黏膜血液循环有关。     

肠淋巴途径在失血性休克大鼠肠源性细菌/内毒素移位发病学中的作用

目的观察失血性休克大鼠肠系膜淋巴液及门静脉血毒性物质的变化，同时观察结扎肠系膜淋巴管对重症失血性休克大鼠器官内毒素（ET）及肠系膜淋巴结和脾脏组织细菌培养的影响，探讨肠淋巴途径在休克大鼠肠源性细菌／内毒素移位（BET）发病学中的作用。方法雄性Wistar大鼠24只被随机分为休克组及对照组。复制重症失血性休克大鼠模型后，分别留取休克淋巴液、休克门静脉血、正常淋巴液、正常门静脉血，检测其中的ET、肿瘤坏死因子-α（TNF～α）、白细胞介素-6（IL-6）水平。另取30只大鼠被随机分为假手术组、休克组、结扎组。休克组与结扎组复制重症失血性休克大鼠模型。结扎组于休克复苏后行肠系膜淋巴管结扎术，分别于休克输液复苏3h和6h后，制备肺、肝、心、肾组织匀浆，检测其中ET含量；制备肠系膜淋巴结和脾组织匀浆，进行细菌培养。结果休克淋巴液中ET、TNF—α、IL-6的含量均显著高手休克血浆、正常血浆和正常淋巴液（P均〈0．01）；失血性休克大鼠输液复苏后3h和6h肺、肝、心、肾组织中ET含量均显著高于假手术组与结扎组（P〈0．05或P〈0．01）；休克组大鼠复苏后3h和6h肠系膜淋巴结及脾组织中均可见细菌生长，而结扎组大鼠相应组织中则无细菌生长。结论肠淋巴途径在失血性休克致大鼠肠道屏障功能下降、引起肠源性BET的发病学中具有首要作用。