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

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

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 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

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

OBJECTIVE: To observe the effect of chloroquine on the apoptosis of intestinal mucosa epithelial cell and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats. METHODS: The rat total hepatic ischemia-reperfusion model was built by blocking the hepatic portal, suprahepatic and infrahepatic vena cava for 20 minutes. Ninety Sprague-Dawley rats were assigned randomly into the sham operation group (Group A, n = 30), total hepatic ischemia-reperfusion treatment group (Group B, n = 30), and chloroquine administrated group (Group C, n = 30). Each group was subdivided randomly into 3 subgroups (n = 10) according to different experiment time phases as follows: after 20 minutes of total hepatic vascular exclusion (T0), 4 hours after reperfusion (T1), and the 48 hours of survival. Group A and Group B were intravenously injected with normal saline 1 mL/kg while Group C received chloroquine 10 mg/kg which dissolved in 1 mL/kg normal saline intravenously. The levels of portal blood D-lactate, TNF-alpha, endotoxin, and the intestinal mucosa MDA concentration were measured at T0 and T1; the portal blood, mesenteric lymph node, and spleen tissues were cultured for bacteria; and the apoptotic index of intestinal mucosa epithelial cells at T0 and T1 and the survival rate after 48 hour reperfusion were obtained. RESULTS: Compared with Group A, the levels of portal blood D-lactate, TNF-alpha, endotoxin and the intestinal mucosa MDA in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). These indexes of Group C were lower than those of Group B (P < 0.05). The portal vein blood, mesenteric lymph node and spleen tissues existed the bacterium translocation both in Group B and Group C, and the positive rate in Group C was lower than that in Group B (P < 0.05). Apoptotic index of the intestinal mucosa epithelial cell increased significantly in Group B (P < 0.01) and Group C (P < 0.05), but the apoptotic index in Group C was lower than that in Group B (P < 0.05); the 48 hour survival rate of the rats in Group C was higher than that in group B (P < 0.05). CONCLUSION Chloroquine may decrease the intestinal mucosa epithelial cell apoptosis and the enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion and increase the survival rate of the rats.
Animals ; Bacterial Translocation ; drug effects ; Chloroquine ; pharmacology ; Epithelial Cells ; pathology ; Escherichia coli ; physiology ; Female ; Intestinal Mucosa ; pathology ; Intestine, Small ; microbiology ; pathology ; Liver ; blood supply ; Male ; Phospholipases A ; antagonists & inhibitors ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; microbiology ; pathology

The present study aimed to investigate the change of cytochrome c in postconditioning-attenuated ischemia-reperfusion (I/R)-induced mucosal apoptosis in rat intestine compared with ischemic preconditioning (IPC). Using rat model of intestine I/R injury, male Sprague-Dawley rats weighing 220-250 g were divided into 4 groups which were Sham operation group, I/R group, IPC group and ischemic postconditioning (IPOST) group. In these groups, I/R procedure was performed by the occlusion of the superior mesenteric artery (SMA) for 45 min followed by reperfusion for 1 h. In Sham group, there was no intervention. In IPC group, SMA was occluded for 5 min and reperfused for 5 min, for two cycles, before the prolonged occlusion. In IPOST group, three cycles of 30-s reperfusion and 30-s reocclusion were preceded at the start of reperfusion. After the reperfusion, the small intestines were sampled for experimental detection. Intestinal mucosal mitochondrial membrane potential was detected by confocal laser scanning microscopy. Expressions of cytochrome c and caspase-3 proteins were detected using Western-blot method. The apoptosis of intestinal mucosal cells was determined with agarose gel electrophoresis and deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling (TUNEL) technique. Compared with I/R group, the mitochondrial membrane potentials and the expressions of cytochrome c protein were significantly increased, while the expressions of caspase-3 and the apoptotic rates were decreased in IPOST and IPC groups (P<0.05). There were no significant differences between IPOST and IPC groups (P>0.05). These data provide substantial evidence that IPOST attenuates I/R-induced mucosal apoptosis by reducing the release of cytochrome c from mitochondria in the rat small intestine.
Animals ; Apoptosis ; physiology ; Cytochromes c ; metabolism ; Intestinal Mucosa ; metabolism ; pathology ; Intestines ; blood supply ; Ischemic Postconditioning ; methods ; Male ; Membrane Potential, Mitochondrial ; Mitochondria ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control

Animals ; Colon ; blood supply ; pathology ; Colonic Diseases ; drug therapy ; etiology ; physiopathology ; Hemodynamics ; Hepatic Veins ; pathology ; physiopathology ; Hypertension, Portal ; complications ; physiopathology ; Intestinal Mucosa ; blood supply ; drug effects ; pathology ; Liver Cirrhosis, Experimental ; complications ; Losartan ; administration & dosage ; therapeutic use ; Male ; Microscopy ; Portal Pressure ; drug effects ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo study the effect of Huoxiang Zhengqi soft capsule on protecting intestinal barrier.

METHODLower limb ischemic reperfusion model was induced in Wistar rats. The Chinese medicine groups were administered orally with Huoxiang Zhengqi soft capsule before inoculation respectively. The small intestinal histopathology and ultrastructural of rats were observed with optical microscope and electronic microscope respectively. Mucus was observed under AB-PAS staining, mast cells were studied under toluidine blue staining, and serum NO was determined.

RESULTAfter Lower limb ischemic reperfusion, the intestinal barrier function was severely damaged. Huoxiang Zhengqi soft capsule could significantly reduce the levels of the serum NO (P < 0.01).

CONCLUSIONHuoxiang Zhengqi soft capsule has apparent protective effect on the intestinal barrier function in lower limb ischemic reperfusion rats.

Animals ; Capsules ; Drug Combinations ; Drugs, Chinese Herbal ; administration & dosage ; isolation & purification ; pharmacology ; Female ; Hindlimb ; blood supply ; Ileum ; pathology ; Intestinal Mucosa ; pathology ; ultrastructure ; Ischemia ; complications ; Male ; Mast Cells ; drug effects ; Mucus ; drug effects ; Plants, Medicinal ; chemistry ; Protective Agents ; pharmacology ; Rats ; Rats, Wistar ; Reperfusion Injury ; pathology