Dieulafoy lesion is an uncommon cause of gastrointestinal bleeding, reported to be only 2% of acute or chronic upper gastrointestinal bleeding episodes. Bleeding occurs from a small mucosal erosion involving an unusually large submucosal artery in an otherwise normal mucosa. It is associated with massive, life threatening hemorrhage and is difficult to diagnosis. In most cases the lesion is encountered in the proximal stomach, antrum, duodenum, colon and rectum. In particular, extragastric Dieulafoy lesion is an extremely rare source of intestinal bleeding. In Korea, no case of bleeding from a Dieulafoy lesion of the small intestine has been previously reported. We experienced one case of bleeding from a jejunal Dieulafoy lesion, which was confirmed by the pathologic examination of the resected specimen, and report here.
Adult ; Arteries/abnormalities* ; Case Report ; Female ; Gastric Mucosa/blood supply* ; Gastrointestinal Hemorrhage/etiology* ; Human ; Intestinal Mucosa/blood supply*

No abstract availble.
Adult ; Arteries/abnormalities ; Diagnosis, Differential ; Endoscopy, Gastrointestinal ; Gastrointestinal Hemorrhage/*etiology/pathology ; Humans ; Intestinal Mucosa/blood supply/pathology ; Jejunal Diseases/*etiology/pathology ; Jejunum/*blood supply/pathology ; Male

OBJECTIVETo investigate the influence of cervical sympathetic nerve block (SB) on blood flow volume and barrier function of intestinal mucosa after combined radiation and burn injury in rat.

METHODSSD rats were divided into three groups: control (n = 18), combined injury group (n = 100, rats with Co gamma ray body irradiation with a dose of 5 Gy plus 15% TBSA full-thickness burn injury), and combined injury with SB treatment (n = 100, with the same dose of gamma-ray irradiation and burn injury, treated with SB). Twenty rats were sacrificed on 0, 1, 5, 7 days after combined injuries for various observations. SB was conducted with injection of ropivhydrochloride into the neck bilaterally for the SB group, and same amount of normal saline was injected instead in the combined injury group. Blood flow volume, changes in villus height and crypt depth in jejunum, Na(+)-K+ ATPase activity, permeability of small intestine were measured at different time-points.

RESULTSThe blood flow volume in small intestinal mucosal on 1 post-injury days (PID) [(0.29 +/- 0.07) ml x min(-1) x g(-1)] were obviously decreased than that in normal controls [(1.26 +/- 0.23) ml x min(-1) x g(-1), P < 0.01 ], with serious destruction of pit cells, decrease in intestinal mucosal Na(+)-K+ ATPase activity, and increase in intestinal mucosal permeability. Compared with combined injury group, the blood flow volume was [(0.82 +/- 0.11) ml x min(-1) x g(-1) 1 day after combined injury, P < 0.01], and the Na(+)-K+ ATPase activity was obviously increased, and the permeability of small intestine was ameliorated.

CONCLUSIONSB can increase blood flow volume of rat small intestine after combined radiation and burn injury, promote the repair of intestinal epithelium and improve the barrier function of the intestinal wall.

Animals ; Autonomic Nerve Block ; Blood Volume ; physiology ; Burns ; physiopathology ; Intestinal Mucosa ; blood supply ; metabolism ; physiopathology ; Intestine, Small ; Radiation Injuries, Experimental ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Superior Cervical Ganglion

OBJECTIVETo observe the effect of Qihuang Decoction (QHD) on epithelial cell apoptosis of ischemia-reperfusion (I/R) injured intestinal mucosa in rat.

METHODSThe I/R injured intestinal mucosa rat model was established by clamping superior mesenteric artery (SMA) for 45 min and reperfusing for 60 min. The pathomorphological Changes and epithelial cell apoptosis in the injured intestinal mucosa were observed and compared among groups: the sham-operated group (A), the model group (B), the glutamine treated group (C) and the QHD treated group (D).

RESULTSpathomorphological examination showed that in group A, the intestinal villus was intact; in group B, the intestinal subepithelial space were dilated, and showed evident cleavage between the epithelial top and the lamina propria with bare capillaries, bleeding and ulceration; in group C and D, the above-mentioned pathomorphological changes were alleviated to some extents, appeared only in part of the villa, and the alleviation was more significant in group D than in group C. Chiu's scoring showed that the lowest score (zero) presented in group A and the highest presented in group B; scores in group C and D was significantly lower than that in group B (P < 0.05), but showed insignificant difference between the two groups (P > 0.05). Epithelial cell apoptosis detection showed that the least apoptosis rate presented in group A, and the highest in the group B; while in the group C, it lied between group A and B (all P < 0.05), and showed no statistical significance to group D (P > 0.05), though appeared a lowering trend.

CONCLUSIONQHD could reduce the I/R injured intestinal epithelial mucosa, and its protective mechanism may be related to the inhibition on apoptosis of intestinal mucosal epithelial cells.

Animals ; Apoptosis ; drug effects ; Astragalus Plant ; Drugs, Chinese Herbal ; pharmacology ; Epithelial Cells ; drug effects ; Intestinal Mucosa ; blood supply ; drug effects ; pathology ; Male ; Rats ; Rats, Wistar ; Reperfusion Injury ; pathology

OBJECTIVETo study the effect of berberine on the release of nitric oxide (NO) by rat intestinal mucous microvascular endothelial cells (RIMECs) cultured in vitro for exploring the pharmacological mechanism of berberine in treating intestinal disease.

METHODSCultured RIMECs in vitro were identified adopting immunofluorescent stain with factor VIII-related antigen. NO level in the supernatant of normal cell culture or cell culture treated with different concentrations of berberine was detected with colorimetry at the 3rd, 6th, 9th and 12th h and compared.

RESULTSCompared with that in the normal control group, NO level increased more obviously in the berberine treated groups, and the best effect was shown in the 5 microg/mL berberine treated group.

CONCLUSIONOne of the important pharmacological mechanisms of berberine might be through promoting the endogenous NO release to induce endothelium-dependent dilatation of microvascular in intestinal mucosa, thus to improve the local microcirculation of intestine.

Animals ; Berberine ; pharmacology ; Cells, Cultured ; Colorimetry ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Intestinal Mucosa ; blood supply ; cytology ; Nitric Oxide ; biosynthesis ; Rats ; Time Factors

AIMTo investigate the protective effects of glucagon-like peptide 2(GLP-2) on intestinal ischemia/reperfusion (I/R) injury in mice.

METHODSIntestinal ischemia/reperfusion model in mice were set up and 32 mice of Kunming species were divided randomly into 4 groups (n=8): Sham group, I/R group, I/R + GLP-2 group and I/R + glutamine group. The morphologic changes of intestinal mucosa were observed under LM. The villus height and crypt depth of intestine, the activity of diamine oxidase (DAO) in intestine and bacterial translocation rates of mesenteric lymph nodes (MLN) were detected.

RESULTSCompared with sham operation group, the intestinal villi were sloughed in I/R group with decreased villus height and crypt depth (P < 0.01), the DAO activities were decreased (P < 0.01), and MLN bacterial translocation rates were increased (P < 0.05). While GLP-2 administration improved the villus damage, increased DAO activity (P < 0.01), and decreased MLN bacterial translocation rates (P < 0.05), compared with I/R group.

CONCLUSIONGLP-2 have protective effects on intestinal morphology and barrier function after ischemia/reperfusion injury in mice.

Animals ; Disease Models, Animal ; Glucagon-Like Peptide 2 ; pharmacology ; Intestinal Mucosa ; drug effects ; pathology ; physiopathology ; Intestine, Small ; blood supply ; Male ; Mice ; Mice, Inbred Strains ; Reperfusion Injury ; pathology ; physiopathology

Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition. AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gut-origin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP's severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP's process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemic reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.
Acute Disease ; Animals ; Humans ; Intestinal Mucosa ; blood supply ; injuries ; metabolism ; Malnutrition ; pathology ; Microcirculation ; metabolism ; Pancreatitis ; complications ; metabolism ; pathology ; physiopathology ; Reperfusion Injury ; pathology

OBJECTIVETo investigate the expression of R-spondin1 (RSpo1) in the intestinal epithelium of mice with intestinal ischemia-reperfusion injury and explore its significance.

METHODSFifty normal male Kunming mice were randomized into sham-operated group (n=10) and intestinal ischemia-reperfusion injury group (n=40), and in the latter group, the mice were subjected to 20-min intestinal mesenteric artery occlusion followed by reperfusion for 6, 12, 24, or 48 h. Enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to detect intestinal RSpo1 expression of the mice.

RESULTSThe results of RT-PCR and ELISA showed that RSpo1 expression was significantly decreased in mice at 6 h of reperfusion following the intestinal ischemia (P<0.05), and increased gradually with prolonged repersuion time, reaching the peak level at 24 h (P<0.05). The expression underwent rapid decrease afterwards to a significantly lower level than that in the control group at 48 h (P<0.05).

CONCLUSIONIntestinal ischemia-reperfusion injury may inhibit expression of RSpo1 in the early stage, and enhance its expression in the middle stage. RSpo1 can promote proliferation and differentiation of intestinal epithelial stem cells and plays an important role in the repair intestinal mucosal damage.

Animals ; Cell Proliferation ; Intestinal Mucosa ; cytology ; metabolism ; Intestines ; blood supply ; metabolism ; Male ; Mice ; Random Allocation ; Reperfusion Injury ; metabolism ; Stem Cells ; cytology ; Thrombospondins ; genetics ; metabolism

OBJECTIVE: To investigate the influence of treatment with total hepatic vascular exclusion and reperfusion on the intestinal barrier in rats. METHODS: The total hepatic vascular exclusion and reperfusion model was built after the block of hepatic portal, suprahepatic and infraheptic vena cava for 20 minutes. Sixty Sprague-Dawley rats were divided randomly into 2 groups: sham operation group (Group A, n=30) and total hepatic vascular exclusion and reperfusion treatment group (Group B, n=30). Each group was subdivided randomly into 3 subgroups (n=10) according to different experiment time points as follows: at the end of the total hepatic vascular exclusion (T0), 4 reperfusion after total hepatic vascular exclusion (T1) and the 48 h survival. Portal vein blood gas was analysed at T0. At T0 and T1 the following items were detected: the level of portal vein blood D-lactate, tumor necrosis factor-alpha (TNF-alpha), the MDA concentration and pathologic morphology change of intestinal mucosa. RESULTS: Compared with Group A, the PCO2 at T0 in Group B increased while pH, P02, and HCO3- decreased significantly (P < 0.05). The level of portal blood D-lactate, TNF-alpha and intestinal mucosa MDA at T0 and T1 was significantly higher (P < 0.05, or P < 0.01). The histologic damage in the intestinal mucosa was observed in Group B, and the rat survival in Group B was lower than that in Group A (P < 0.05). CONCLUSION The treatment with total hepatic vascular exclusion and reperfusion can damage the intestinal barrier in rats.
Animals ; Bacterial Translocation ; Female ; Intestinal Mucosa ; microbiology ; pathology ; Ischemia ; pathology ; physiopathology ; Liver ; blood supply ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology ; physiopathology

OBJECTIVETo observe the effects of Pogostemon cablin (Blanco) Benth. (PCB), a Chinese aromatic herbal medicine, on serum levels of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), and membrane fluidity of intestinal epithelial cells (IMC) in rats undergoing lower limbs ischemic reperfusion (I/R), for exploring its action in protecting intestinal barrier and the possible mechanisms, and to seek a new way, viewing from Chinese medicine, for providing the experimental bases of gastrointestinal protection against trauma or surgical operation.

METHODSEighty adult Wistar rats were induced into lower limb I/R model and randomized equally into the model group, the three PCB water extract groups treated respectively with high- (4 g x kg(-1) x d(-10), middle- (3 g x kg(-1) x d(-1)), and low-dose (2 g x kg(-1) x d(-1)) of PCB water extract, and three PCB volatile oil groups treated respectively with high- (4 g x kg(-1) x d(-1)), middle- (3 g x kg(-1) x d(-1)), low-dose (2 g x kg(-1) d(-1) of PCB volatile oil. Besides, 10 healthy rats was allocated in a normal control group. PCB preparation was given via gastric infusion for 5 successive days just before modeling. The serum levels of NO and TNF-alpha were monitored, and the membranous fluidity of IMC at I/R region was determined by fluorescence polarization technique.

RESULTSCompared with the control group, both serum NO and TNF-alpha levels in model rats were significantly higher (P < 0.01), and the fluorescence polarization value (P) of IMC obviously increased at the same time (P < 0.05). As compared with the model group, the serum level of NO and TNF-alpha significantly reduced in all the PCB treated groups (P < 0.01 or P < 0.05). As for the membrane fluidity, significant difference was shown between the model group with low-dose of PCB water extract and middle-dose of PCB volatile oil (P < 0.05).

CONCLUSIONPCB could effectively protect the intestinal barrier function by way of maintaining the membrane fluidity of IMC through regulating the level of NO and TNF-alpha in serum.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Epithelial Cells ; drug effects ; Extremities ; blood supply ; Intestinal Mucosa ; cytology ; Membrane Fluidity ; drug effects ; Nitric Oxide ; blood ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; Tumor Necrosis Factor-alpha ; blood