Fibrinolytic activity in the abdominal cavity of rats with faecal peritonitis

Goor, Harry van; Graaf, J. S. de; Grond, J.; Sluiter, Wim J.; Meer, Jan van der; Bom, Vjj; Bleichrodt, Robert P.

doi:10.1002/bjs.1800810740

Cited by 69 publications

(43 citation statements)

References 21 publications

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“…injection of low dose LPS into healthy humans, tPA release into the circulation is transient (7,8). Previous studies also documented elevated tPA levels in peritoneal fluid of patients and rats with bacterial peritonitis (6,39,40). In our study, tPA levels remained undetectable in peritoneal lavage fluid, which was probably due to the high dilution factor since we performed the peritoneal lavages with 5 ml of saline.…”

Section: Discussionsupporting

confidence: 46%

Endogenous Tissue-Type Plasminogen Activator Is Protective duringEscherichia coli-Induced Abdominal Sepsis in Mice

Renckens

Roelofs

Florquin

et al. 2006

The Journal of Immunology

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Sepsis is associated with enhanced production of tissue-type plasminogen activator (tPA). We investigated the function of endogenous tPA in the immune responses to Escherichia coli-induced abdominal sepsis using tPA gene-deficient (tPA−/−) and normal wild-type (WT) mice. tPA−/− mice demonstrated an impaired defense against E. coli peritonitis as indicated by higher bacterial loads at the primary site of the infection, enhanced dissemination, and reduced survival. The protective function of tPA was independent of plasmin since plasminogen gene-deficient (Plg−/−) mice were indistinguishable from WT mice. Relative to WT mice, tPA−/− mice demonstrated similar neutrophil counts in the peritoneal cavity despite much higher bacterial loads and higher local concentrations of neutrophil attracting chemokines, suggesting a reduced migratory response. In line, tPA−/− mice demonstrated a reduced thioglycolate-induced neutrophil influx into the peritoneal cavity and i.p. injection of WT mice with a replication-defective adenoviral vector expressing tPA caused an enhanced cell migration to the peritoneal cavity during E. coli peritonitis. These findings identify a novel protective function of tPA in abdominal sepsis caused by E. coli that seems independent of its role in the generation of plasmin.

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Section: Discussionsupporting

confidence: 46%

Endogenous Tissue-Type Plasminogen Activator Is Protective duringEscherichia coli-Induced Abdominal Sepsis in Mice

Renckens

Roelofs

Florquin

et al. 2006

The Journal of Immunology

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“…27 In addition, intra-abdominal infection causes abdominal inflammation, peritoneal damage, and disrupts fibrinolysis resulting in abdominal adhesions. [28][29][30] This study demonstrates that covering colon anastomoses with BioGlue prevents anastomosis leakage; however, BioGlue does not have a significant effect on adhesion formation.…”

Section: Discussionmentioning

confidence: 72%

Effect of the Bioadhesive, BioGlue, on Impaired Colonic Anastomose Healing in Rats

Ekici

Akçay

Moray

2015

International Surgery

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Colonic anastomotic leakage is still a problem in general surgery practice. We sought to investigate the effect of a new tissue adhesive, BioGlue, on the healing of normal and impaired colonic anastomoses. Sixty-four rats were randomized into 4 groups. In all animals, a 1-cm segment of the left colon was resected, and an end-to-end sutured anastomosis was created. Animals were then divided into 2 groups: normal and impaired anastomosis. These 2 groups were further subdivided into 2 additional groups: animals that received BioGlue and those that did not. All rats received intraperitoneal injections of either 0.9% NaCl or 5-fluorouracil (5-FU). Anastomotic evaluation was done 7 days after surgery. Macroscopic healing, mechanical strength, and histopathologic healing parameters were evaluated. Leakage of the anastomosis was significantly higher in rats in the impaired group compared with those in the BioGlue groups (P ¼ 0.043). The adhesion formation score was significantly higher in rats in the impaired anastomosis group compared with the other groups. Bursting pressures were significantly lower in the impaired anastomosis group than in the other ones (P ¼ 0.001). Neoangiogenesis and fibroblast activity were different among the groups (P ¼ 0.001). Inflammatory cell infiltration and collagen deposition did not differ among the groups (P ¼ 0.07). Immediate postoperative intraperitoneal administration of 5-FU after colonic anastomosis inhibits intestinal wound healing. Covering colon anastomoses with BioGlue after suturing conferred beneficial effect on healing.

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“…[18,19] Intra-abdominal infections severely disrupt fibrinolysis, as evidenced by the high levels of plasminogen activator inhibitor in peritoneal tissue and fluid. [20] Peritoneal injury caused by bacteria results in accumulation of an inflammatory exudate that leads to fibrin deposition, resulting in fibrinous adhesions between adjacent organs. [21] In addition, invasion of fibroblasts at infection sites leads to deposition of collagen and subsequent formation of permanent fibrous adhesions.…”

Section: Discussionmentioning

confidence: 99%