Bacteria translocation (BT) induced enterogenous infection in multiple organs dysfunction syndrome (MODS) is closely related with the stress pyemia and MODS. For prevention of BT, western medicine stresses to improve the blood and oxygen supply of intestinal tract, mucosa protection, and application of microorganism preparation, while traditional Chinese medicine could also win good effect by using such drugs as rhubarb, red sage root, and compound decoctions.
Animals ; Bacterial Translocation ; drug effects ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Intestinal Mucosa ; physiopathology ; Multiple Organ Failure ; microbiology ; Phytotherapy

OBJECTIVE: To investigate the protective effects of shen-mai injection on intestinal barrier function in the early stage of 30% 3° scald, and to provide experimental basis for the prevention and control of enterogenic infection. METHODS: A total of 60 Wistar rats were randomly divided into 6 groups: normal control group (without treatment), model control group (with 30% total body surface area (TBSA) fully thickness burn on the back), hexadecadrol (5 mg/kg) group, Shenmai injection (5, 10, 15 mg/kg) groups, with 10 rats in each group. After burned by scald apparatus, rats in each group were treated with drugs immediately by intraperitoneal injection once a day. At 72 hours after burned, the levels of plasma endotoxin, diamine oxidase (DAO), tumor necrosis factor-alpha (TNF-α), interleukins-6(IL-6) in all rats were detected and the mesenteric lymph nodes, liver and spleen were homogenized to culture for bacteria. The change of secretory immunoglobulin A (sIgA) in intestinal mucosa was measured. RESULTS: Compared with normal control group, bacterial translocation quantity in mesenteric lymph nodes(MLN), liver, and spleen, and the plasma levels of DAO, endotoxin, TNF-α, IL-6 and the level of sIgA in intestinal mucosa in model control group were increased significantly (P＜0.01); compared with model control group, bacterial translocation quantity in MLN, liver, and spleen, and the plasma levels of DAO, endotoxin, TNF-α, IL-6 and the level of sIgA in intestinal mucosa in hexadecadrol (5 mg/kg) group and shen-mai injection (5, 10, 15 mg/kg) groups were decreased significantly (P＜0.05 or P＜0.01). CONCLUSION Shen-mai injection can alleviate intestinal mucosa injury caused by severe scald, and the effects are similar with those of dexamethasone, and the effect is better in the high-dose group.
Animals ; Bacterial Translocation ; drug effects ; Burns ; complications ; Drug Combinations ; Drugs, Chinese Herbal ; pharmacology ; Intestinal Mucosa ; drug effects ; pathology ; Random Allocation ; Rats ; Rats, Wistar

BACKGROUND/AIMS: NSAIDs induce gut damage throughout the entire gastrointestinal tract and bacterial translocation. The aim of this study was to examine if administration of glutamine was able to prevent the NSAID-induced gut damages and bacterial translocation in the animal models. METHODS: Rats were utilized into 5 groups; control group, diclofenac group, and diclofenac with glutamine 0.8, 1.6, and 3.2 g/kg/day group. The animals with glutamine were fed with L-glutamine for 4 days before diclofenac administration. Gut injury was induced by administration of a single dose of diclofenac (80 mg/kg orally). Intestinal permeability (24 hour urinary excretion of phenolsulfonphthalein), enteric aerobic bacterial counts, serum biochemical profiles and bacterial translocation to mesenteric lymph nodes, liver and spleen were measured. RESULTS: Diclofenac caused the increase in intestinal permeability, enteric bacterial count, enteric protein and albumin loss and bacterial translocation. Administration of glutamine reduced the increase in intestinal permeability, protein losing enteropathy, enteric bacterial overgrowth and bacterial translocation induced by diclofenac. CONCLUSIONS: Glutamine may have beneficial effects on NSAID-induced gut damage and bacterial translocation.
Animals ; Anti-Inflammatory Agents, Non-Steroidal/*pharmacology/toxicity ; Bacterial Translocation/*drug effects ; Diclofenac/*pharmacology/toxicity ; English Abstract ; Glutamine/*pharmacology ; Intestines/drug effects/*microbiology ; Male ; Rats

OBJECTIVETo investigate the effects of ulinastatin on gut mucosal apoptosis and bacterium translocation in a rat model of sepsis.

METHODSFifty rats were randomly assigned into 4 groups, namely the control (n=5, no operation or drugs), ulinastatin pretreatment (n=15, treated with 25,000 U/kg ulinastatin 2 h before operation), ulinastatin treatment (n=15, treated with 25,000 U/kg ulinastatin 2 h after operation) and sepsis model (n=15, without drug treatment) groups. The rats in the later 3 groups were subjected to cecal ligation and puncture (CLP). At 3, 6 and 12 h after CLP, the rats were sacrificed and the ileum was removed to examine the pathology and apoptosis of the mucosa. The DNA of Bacillus coli in the whole blood was detected using PCR.

RESULTSSepsis caused of epithelial cell loss in the ileal villi, ulceration and blebbing of the lamina propria. Ulinastatin treatment administered before and after the operation both significantly alleviated these morphological anomalies. The sepsis rats showed significantly increased intestinal mucosal apoptotic index as compared with the other 3 groups (P<0.05). Ulinastatin pretreatment, in comparison ulinastatin treatment 12 h after CLP, significantly increased the intestinal mucosal apoptotic index (P<0.05). Bacillus coli DNA was positive in sepsis and postoperative ulinastatin treatment groups but negative in the control and pretreated groups.

CONCLUSIONIncreased intestinal musocal apoptosis and gut bacterial translocation occur in rats following sepsis, and ulinastatin can effectively decrease intestinal mucosal apoptosis and inhibit bacterial translocation.

Animals ; Apoptosis ; drug effects ; Bacterial Translocation ; drug effects ; Female ; Glycoproteins ; pharmacology ; therapeutic use ; Ileum ; drug effects ; microbiology ; pathology ; Intestinal Mucosa ; drug effects ; microbiology ; pathology ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sepsis ; drug therapy ; Trypsin Inhibitors ; pharmacology ; therapeutic use

BACKGROUNDChemotherapy causes breakdown of the intestinal barrier, which may lead to bacterial translocation. Paclitaxel, an anti-tubulin agent, has many side effects; however, its effect on the intestinal barrier is unknown. Previous studies show that granulocyte colony-stimulating factor (G-CSF) plays an important role in modulating intestinal barrier function, but these studies are not conclusive. Here, we investigated the effects of paclitaxel on the intestinal barrier, and whether G-CSF could prevent paclitaxel-induced bacterial translocation.

METHODSTwenty-four male Sprague-Dawley rats were divided into three groups: control group, paclitaxel group and paclitaxel + G-CSF group. Intestinal permeability was measured by the urinary excretion rates of lactulose and mannitol administered by gavage. The mesenteric lymph nodes, spleen and liver were aseptically harvested for bacterial culture.Endotoxin levels and white blood cell (WBC) counts were measured and bacterial quantification performed using relative real-time PCR. Jejunum samples were also obtained for histological observation. Intestinal apoptosis was evaluated using a fragmented DNA assay and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate(dUTP)-biotin nick end-labeling staining. One-way analysis of variance and Fisher's exact test were used to compare differences between groups.

RESULTSPaclitaxel induced apoptosis in 12.5% of jejunum villus cells, which was reduced to 3.8% by G-CSF treatment.Apoptosis in the control group was 0.6%. Paclitaxel treatment also resulted in villus atrophy, increased intestinal permeability and a reduction in the WBC count. G-CSF treatment resulted in increased villus height and returned WBC counts to normal levels. No bacterial translocation was detected in the control group, whereas 6/8, 8/8, and 8/8 rats in the paclitaxel group were culture-positive in the liver, spleen and mesenteric lymph nodes, respectively. Bacterial translocation was partially inhibited by G-CSF.

CONCLUSIONSPaclitaxel disrupts the intestinal barrier, resulting in bacterial translocation. G-CSF treatment protects the intestinal barrier, prevents bacterial translocation, and attenuates paclitaxel-induced intestinal side-effects.

Animals ; Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Bacterial Translocation ; drug effects ; Endotoxins ; blood ; Granulocyte Colony-Stimulating Factor ; pharmacology ; Intestinal Absorption ; drug effects ; Intestines ; drug effects ; metabolism ; pathology ; Leukocyte Count ; Male ; Paclitaxel ; pharmacology ; Permeability ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the effects of traditional Chinese herbal medicine Sijunzi decoction on amelioration of postburn intestinal injury in scalded rats.

METHODSOne hundred and eighty Wistar rats were randomly divided into 3 groups, i.e. scald and treatment (T), scald control (S) and normal control (C) groups. The rats in T group were gavaged with the decoction consisting of tangshen, tuckahoe, large head atractylodes rhizome, glycyrrhizic and rhubarb in a dose of 2 ml twice daily, while the rats in C group were just gavaged with the same amount of distilled water. The rats were sacrificed according to the scheduled postburn observation timepoints. The contents of TNF, NO, MDA and ATPase activity in rat plasma and the intestinal mucosa and the S-IgA content in the intestinal mucus were determined respectively. The changes in histopathology of intestinal mucosa were observed. The samples from internal organ tissue and blood were obtained for bacterial culture.

RESULTSThe contents of TNF, NO and MDA in the intestinal mucosa tissue and the rat plasma in scalded rats were lowered significantly by Sijunzi decoction. Furthermore, S-IgA secretion from intestinal mucous cells was maintained by Sijunzi decoction. T cell count was recovered and intestinal mucous barrier injury were lessened, and the bacterial positive rate in the internal organs was decreased.

CONCLUSIONTraditional Chinese herbal medicine Sijunzi decoction might be helpful in alleviation of postburn intestinal injury and in the prevention of intestinal bacterial translocation.

Animals ; Bacterial Translocation ; drug effects ; Burns ; blood ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Intestinal Mucosa ; metabolism ; pathology ; Intestines ; microbiology ; Male ; Rats ; Rats, Wistar

OBJECTIVESTo further investigate the effects of cisapride on intestinal bacterial overgrowth (IBO), bacterial and endotoxin translocation, intestinal transit and permeability in cirrhotic rats.

METHODS25 normal control rats, 25 cirrhotic rats, 20 cirrhotic rats received saline, and 20 cirrhotic rats treated with cisapride were included in the study. All animals were assessed with many variables including bacterial and endotoxin translocation, IBO, intestinal transit and permeability.

RESULTSBacterial translocation was found in 48%(12/25) cirrhotic rats and none of control rats. Among the 20 rats with IBO, there were 11 rats with bacterial translocation (BT) while only one rats occurred BT out of the 5 rats without IBO. Cirrhotic rats with IBO had a significantly higher rate of endotoxin translocation, higher intestinal permeability and longer intestinal transit than those without IBO. BT of a specific organism was always associated with IBO of that organism. Compared with the placebo group, cisapride-treated rats had lower rates of bacterial and endotoxin translocation and IBO, which had close relationship with shorter intestinal transit and lower permeability.

CONCLUSIONEndotoxin and bacterial translocation in cirrhotic rats may be the result of IBO and higher permeability. IBO may be the result of longer transit. Cisapride which can accelerate intestinal transit and improve intestinal permeability is helpful in preventing and treating intestinal bacterial and endotoxin translocation.

Animals ; Bacterial Translocation ; drug effects ; Biological Transport ; Cisapride ; pharmacology ; Endotoxins ; metabolism ; Liver Cirrhosis, Experimental ; microbiology ; Male ; Permeability ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effects of lactulose on intestinal bacterial overgrowth (IBO), bacterial translocation (BT), intestinal transit and permeability in cirrhotic rats.

METHODSBT in all animals was assessed by bacterial culture of mesenteric lymph node (MLN), liver and spleen, and IBO was assessed by a jejunal bacterial count of the specific organism. Intestinal permeability was determined by the 24-hour urinary (99m)Tc-diethylenetriamine pentaacetatic acid ((99m)Tc-DTPA) excretion, and intestinal transit was determined by measuring the distribution of (51)Cr in the intestine.

RESULTSBT and IBO were found in 48% and 80% of the cirrhotic rats, respectively, while not in the control rats. Cirrhotic rats with IBO had significantly higher levels of intestinal endotoxin higher rates of bacterial translocation, shorter intestinal transit time and higher intestinal permeability than those without IBO. It was also found that BT were closely associated with IBO and injury of the intestinal barrier. Compared with the placebo group, lactulose-treated rats had lower rates of BT and IBO, which were closely associated with increased intestinal transit and improved intestinal permeability by lactulose.

CONCLUSIONSOur study indicate that endotoxin and bacterial translocation in cirrhotic rats may attribute to IBO and increased intestinal permeability. Lactulose that accelerates intestinal transit and improves intestinal permeability might be helpful in preventing intestinal bacterial and endotoxin translocation.

Animals ; Bacterial Translocation ; drug effects ; Endotoxins ; analysis ; Gastrointestinal Agents ; pharmacology ; Intestines ; metabolism ; microbiology ; Lactulose ; pharmacology ; Liver Cirrhosis, Experimental ; metabolism ; microbiology ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effect of ulinastatin on intestinal mucosal barrier function of rats with obstructive jaundice.

METHODSSeventy-two male SD rats were randomly divided into sham operation, obstructive jaundice, and ulinastatin treatment groups (groups A, B, and C, respectively). In groups B and C, the common bile duct was ligated to induce obstructive jaundice. The rats in group C were given intraperitoneal injection of ulinastatin at the daily dose of 40,000 IU/kg after the operation, while those in groups A and group B received equal amount of normal saline. At 3, 5, 7 and 10 days after the operation, the liver function and plasma endotoxin level were evaluated and measured, and bacterial culture of the mesenteric lymph nodes, liver and spleen was performed. The terminal ileum mucosa was observed under light microscope, and the intestinal villi and mucosal thinckness was examined with image analysis system.

RESULTSThe indices relative to the liver function and plasma endotoxin level were higher at different time points of observation in group B than in group A (P<0.01), and were lower in group C than in group B (P<0.01). Plasma endotoxin level was similar between groups A and C 3 days after the operation (P>0.05). The rate of bacterial translocation was higher in group B than in group A and C (P<0.01, P<0.05), but comparable between groups A and C (P>0.05). Intestinal mucosal injury was observed in group B 3 days after operation, and aggravated with the passage of time. The injury was milder in group C. The intestinal villus length and mucosal thickness were greater in groups A and C than in group B (P<0.01 or P<0.05), but comparable between the former two groups 3 days after operation (P>0.05).

CONCLUSIONIn early stage of obstructive jaundice, the intestinal mucosal barrier may sustain injuries which aggravate with time; ulinastatin has significant effect in protecting the mucosal barrier function especially against early pathological changes.

Animals ; Bacterial Translocation ; drug effects ; Endotoxins ; blood ; Glycoproteins ; pharmacology ; Intestinal Mucosa ; drug effects ; microbiology ; pathology ; physiopathology ; Jaundice, Obstructive ; blood ; microbiology ; pathology ; physiopathology ; Liver ; drug effects ; physiopathology ; Male ; Rats ; Rats, Sprague-Dawley ; Time Factors

BACKGROUNDDamage to the gut barrier often occurs during critical illnesses. In such cases, it is very important to alleviate impairment of the intestinal barrier and protect intestinal barrier function. This study investigated the protective effect of growth hormone on intestinal barrier function in rats under stress.

METHODSThis study consisted of prospective, randomized, and controlled animal experiments. Twenty-five Sprague-Dawley rats served as total parenteral nutrition (TPN) models and were divided into three groups: TPN group, sepsis (Sep) group, and growth hormone (GH) group. Another 8 rats served as normal controls. Each group received different stress stimuli. Rats were fed for 7 days, and samples were taken for examination 24 hours after gavaging with dual saccharides.

RESULTSThe architecture of the small intestinal mucosa in the Sep group showed the most severe damage among all groups. Nitric oxide levels in blood plasma and immunoglobulin A levels in the intestinal mucosa of the GH group were significantly lower than in the Sep group (P < 0.02). There were no significant changes in CD3 counts and in the CD4/CD8 ratio between the four groups. Dual sugar tests and bacteriological examinations revealed that intestinal permeability and rate of bacterial translocation in the GH group were lower than in the Sep group (P < 0.01, respectively).

CONCLUSIONProphylactic treatment with growth hormone can alleviate damage to intestinal barrier function caused by trauma and endotoxemia in rats under stress.

Animals ; Bacterial Translocation ; drug effects ; Growth Hormone ; therapeutic use ; Intestinal Mucosa ; drug effects ; physiology ; Parenteral Nutrition, Total ; adverse effects ; Prospective Studies ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological ; physiopathology