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Background: The multiple organ dysfunction syndrome (multiple organ dysfunction syndrome, MODS) refers to severe trauma (including shock, severe pancreatitis), serious infections, and extensive burns, major surgery and pathological obstetrics primary disease occurs, systemic inflammatory response syndrome (, systemic inflammatory response syndrome SIRS) on the basis of, either simultaneously or sequential occurrence of two or more organ dysfunction resulting in failure of the clinical syndrome. The current MODS due to multiple organ failure (multiple organ failure, MOF) is still the major cause of death in patients with abdominal surgery. The present study: gastrointestinal the SIRS hub organs, the inflammatory mediators expansion, the power parts of MODS, MODS the target organ. MODS can cause damage to the gastrointestinal motor function, resulting in bacterial translocation, intestinal barrier dysfunction. Quality of Cajal of the gastrointestinal tract (interstitial cells of Cajal, ICC) to form a network-like structure is widely distributed in the gastrointestinal muscularis closely associated with the movement of the gastrointestinal tract. ICC is divided into two according to the function: myenteric ICC (ICC-MY), between the circular muscle and longitudinal muscle line into the network, the pacemaker cells; another deep myenteric plexus ICC (ICC- DMP), located both inside and outside the ring muscularis between excitatory and inhibitory intestinal motor nerve yuan domination. ICC and smooth muscle through gap junctions are closely linked, and together form the enteric plexus the intestinal nerve-ICC-smooth muscle network. The ICC is the enteric nervous system (enteric nerve system, ENS) intermediary smooth muscle cells (smooth muscle cells, SMC) to transmit signals to the gastrointestinal tract. As the basic functional unit of gastrointestinal motility, intestinal nerve-ICC-smooth muscle network is closely related to many diseases caused by gastrointestinal dysfunction. Objective: In this study, bacterial peritonitis induced the MODS rat model for the study, morphological changes observed MODS rat model of small intestine nerve-ICC-smooth muscle network, the mechanism of MODS induced gastrointestinal motility disorders. Methods: 60 healthy adult Wistar rats, male and female, weight 200g-250g, were randomly divided into a control group (20), the the MODS model group (40). The control group each animal to the intraperitoneal injection of 1.5ml saline. MODS model group each animal to the intraperitoneal injection 1.5ml E.coloi. With the suspension (serum type O127H6 in E. coli 8 × 108cfu/ml suspension containing 10% barium sulfate), to establish bacterial peritonitis caused MODS model . Modeling after 24 hours, take two groups of surviving rats in the upper section of the small intestine tissue. Production of ultrathin sections for transmission electron microscopy observations; Paraffin sections, using immunohistochemical methods, normal control group and the the MODS group specimens small intestine myometrial connexin 43 (connexin43, Cx43) expression. The results: 1. Specimens compared with the control group, MODS group rat gastrointestinal remarkable expansion. Serosal congestion and swelling, retinal bleeding spots. A large number of exudate in the abdominal cavity, a bloody ascites. Most of the intestine Chenganhongse congestion spots, dark red blood like retention of fluid in the intestinal lumen. Intestinal mucosal surface bleeding, necrosis; intestinal adhesions and obvious signs of peritonitis. Transmission electron microscopy observation ① ICC-DMP ultrastructure: the MODS group of ICC-DMP ultrastructure damage is obvious, nucleus shrinkage, perinuclear cytoplasmic damage and ICC processes, membrane bubbly. The the ultrastructure of the ② ICC network: Compared with the control group, the ICC-DMP and smooth muscle MODS group ICC network was damaged; ICC-DMP and smooth muscle cells, ICC-DMP mutual gap junctions between smooth muscle and smooth muscle and desmosomes connect significantly impaired. 3 immunohistochemistry compared with the control group, MODS group small intestine muscularis Cx43 did significantly reduce of Cx43 average optical density (mean density = IOD the SUM / area), weakened (P <0.01). Conclusion: ① bacterial peritonitis caused by extreme expansion of the the MODS group of rat gastrointestinal, gastrointestinal paralysis; ② The of MODS, ICC-DMP the Ultrastructural by injury; ③ MODS when, ICC network was damaged.
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