Small intestinal submucosa for reinforcement of colonic anastomosis.

BACKGROUND: Different materials have been evaluated for anastomotic reinforcement to prevent gastrointestinal anastomotic leakage. In this experimental study, small intestinal submucosa (SIS) was tested as a sealing for stapled colonic anastomosis in a porcine model. The aims of this study were to determine the macroscopic and microscopic outcomes and to evaluate the safety and feasibility of applying SIS for anastomotic sealing. MATERIALS AND METHODS: Circular stapled anastomoses were performed in 18 pigs. Standard anastomosis in the control group (n = 8) was compared to an SIS-sealed anastomosis in the study group (n = 10). After 30 days, anastomotic segments were examined for macroscopic and microscopic regeneration and their resistance to mechanical stress. Furthermore, animal survival and clinical course were evaluated. RESULTS: None of the animals developed anastomotic leakage, intraabdominal abscess, or peritonitis. Shrinkage of SIS was evident in nine of ten animals. Encapsulation and displacement of the SIS patches were seen in two animals. Quantity of anastomotic granulation tissue and rate of complete mucosal coverage of anastomotic line were increased in SIS-sealed anastomoses without reaching significance. Moreover, no significant differences were found in the rate of survival of the animals, anastomotic stricture formation, intraabdominal adhesions, anastomotic bursting pressure, and microscopic healing parameters of the anastomosis between stapled colonic standard anastomosis and anastomosis protected by SIS. CONCLUSION: The results of this study indicate a safe use of SIS for anastomotic reinforcement in a porcine model. Adverse effects like strictures, increased adhesions, and anastomotic abscesses were absent. Promoting effects on colonic wound healing by SIS were microscopically evident. The results argue for a careful clinical evaluation in humans.

The pig as an experimental model for colonic healing study of leakage and ischemia in colonic anastomosis.

BACKGROUND: The object of this experimental study was to develop a model of anastomotic failure due to primary leakage and ischemia in porcine large bowel anastomosis. METHODS: End-to-end anastomosis was constructed at descending colon in 12 pigs. The pigs were randomly divided into three groups. In Group A, the anastomosis was applied with a leak of 18 mm. In Group B, in addition to primary leakage, an artificial ischemia of the proximal anastomotic bowel segment was created by ligation of supplying vessels over 5 cm. In Group C, an artificial ischemia was created in the same manner at the proximal and distal anastomotic segment and the anastomosis was applied with an intentional leakage as in Groups A and B. The animals were sacrificed immediately in case of clinical signs of anastomotic dehiscence, sepsis, peritonitis, or ileus. The animals were sacrificed on day 28. The peritoneal cavity was examined for peritonitis, anastomotic wound dehiscence, and pericolic abscess formation. RESULTS: Distinct fibrinous coverings and adhesions at the anastomotic area were found in all animals. In cases of primary leakage without ischemia, only one of the four animals developed abscess at anastomotic side with clinical sepsis. In cases of primary leakage with ischemia of the proximal anastomotic bowel segment, one of the four animals presented generalized peritonitis with sepsis. In Group C, there were no signs of leakage or peritonitis, although three of the four animals developed colonic ileus due to obturation of the colonic lumen by a clot of necrotic bowel wall. CONCLUSION: Large anastomotic dehiscence and local ischemia of the bowel wall are not reliable factors for the development of intra-abdominal abscess, peritonitis, or sepsis in the pig model.

Small intestinal submucosa as a bioscaffold for tissue regeneration in defects of the colonic wall.

BACKGROUND: Small intestinal submucosa (SIS) has proved considerable regenerative capacity for repair of bowel wall defects at different locations. This study assesses the effectiveness of SIS in the repair of defects at a gastrointestinal location with strong bacterial contamination. METHODS: Fourteen domestic pigs had a 4.5 x 1.5 cm full-thickness defect created on the wall of the descending colon. Repair was done by suturing an SIS patch to the defect. Grafts were harvested after 30, 60, and 90 days. Outcomes were evaluated on the basis of animal survival, clinical course, and macroscopic, histological, and immunohistochemical assessment. RESULTS: All animals survived the scheduled observation period. No patch failure and no postoperative leakage occurred. No luminal narrowing occurred at SIS-patched colon. Morphometric examination revealed contraction of the patched area of 77% after 30 days and more than 90% after 60 and 90 days. By 60 and 90 days, all animals showed mucosal regeneration at the margins of the graft. By 90 days, regeneration of smooth muscle cells was present at the original site of the muscularis mucosae. None of the reconstructed areas showed complete mucosal coverage or regeneration of a structured muscular layer. CONCLUSION: SIS can be used effectively for patch repair of colonic defects in a porcine model. Distinctive contraction of the reconstructed area and limited architectural regeneration of the bowel wall suggest limitation of morphologic regenerative capacities in large-bowel regeneration.

Endotoxin preconditioning in pancreatic ischemia/reperfusion injury.

OBJECTIVES: Prospective organ donors are exposed to various stress types. The effect of endotoxin pretreatment (ETX) on pancreatic ischemia/reperfusion injury (IRI) is unclear. We investigated, using a rat model of pancreatic IRI of an in situ isolated pancreatic tail segment, the effect of ETX on postischemic microcirculation and organ damage. METHODS: Twenty-four hours before pancreatic dissection, either intraperitoneal application of ETX (1 mg/kg in 0.9% NaCl) or saline only (control) was performed. Two-hour normothermic ischemia of the pancreatic tail was induced by clamping the splenic vessels and was followed by a reperfusion period of 2 hours. Microcirculatory parameters were measured by intravital epifluorescence microscopy [functional capillary density (FCD), adherent leukocytes (ALs), and histology]. The presented data represent the mean +/- SEM/SD as appropriate. RESULTS: ETX pretreatment caused a significantly greater decrease in FCD (497 +/- 6 cm/cm2 baseline versus 326 +/- 15 cm/cm2 2 hours of reperfusion) compared with controls (498 +/- 8 versus 258 +/- 15 cm/cm2) 2 hours after reperfusion (P < 0.01). Two hours after reperfusion, ALs were significantly decreased in ETX animals compared with controls (ETX: 141 +/- 37 versus 273 +/- 36 cells/mm2, P < 0.05). Histologic damage was less in ETX (6.4 score points +/- 0.32 versus 8.8 +/- 0.33 control, P < 0.05). CONCLUSION: ETX preconditioning decreases microcirculatory deterioration caused by IRI by means of less loss of nutritive tissue perfusion, decrease in ALs, and less histologic damage. This indicates a protective effect of ETX preconditioning in pancreatic IRI.