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Intraperitoneal Urine Exposure Does Not Elicit Peritoneal Inflammation or Gastrointestinal Dysmotility: A
Minika Yukimoto1, Maki Kawasaki1, Akihiro Maeda1
1Department of Urology, Faculty of Medicine, Saga University, Saga, Japan.
Insights
Intra-abdominal urine exposure in rats did not cause peritonitis or gastrointestinal dysmotility. Sterile urine alone is unlikely to trigger postoperative ileus after urologic surgery.
Area of Science:
- Urology
- Gastroenterology
- Surgical Pathology
Background:
- Intra-abdominal urine leakage can occur during pediatric urologic procedures.
- Postoperative symptoms resembling ileus (gastrointestinal dysmotility) are sometimes observed.
- The effects of urine on the peritoneum and GI tract are not fully understood.
Purpose of the Study:
- To investigate if sterile urine exposure causes peritonitis or gastrointestinal dysmotility.
- Utilized a rat model to simulate intra-abdominal urine leakage.
Main Methods:
- Four groups of rats were used: sham, intraperitoneal autologous urine, mechanical peritonitis, and chemical peritonitis.
- Histological analysis of peritoneal and small intestinal tissues was performed.
- Gastrointestinal motility was assessed using FITC-dextran and geometric center calculations.
Main Results:
- No significant peritoneal inflammation or inflammatory cell infiltration was found in the urine exposure group.
- Gastrointestinal motility remained normal in rats exposed to urine.
- Peritonitis groups showed delayed intestinal transit and reduced geometric center values.
Conclusions:
- Intra-abdominal sterile urine exposure did not induce peritoneal inflammation or significant gastrointestinal dysmotility in rats.
- Sterile urine is unlikely to independently cause postoperative peritoneal inflammation or ileus.
Objective:
Intra-abdominal urine leakage can occur during pediatric urologic surgeries such as laparoscopic pyeloplasty. While some patients exhibit postoperative symptoms resembling ileus, the pathophysiological effects of urine exposure on the peritoneum remain unclear. This study aimed to determine whether intraabdominal exposure to sterile urine induces peritonitis or gastrointestinal (GI) dysmotility using a rat model.
Methods:
Four groups were established using 9-week-old female Sprague-Dawley rats: the sham group, the intraperitoneal autologous urine exposure group, the mechanical peritonitis group, and the chemical peritonitis group. One week later, peritoneal and small intestinal tissues were harvested for histological evaluation. Immunohistochemical analysis was performed to assess inflammatory cell infiltration. GI motility was evaluated using orally administered FITC-dextran, and the fluorescence signal distribution was analyzed to calculate the geometric center.
Results:
In the sham and autologous urine exposure groups, no significant thickening of the peritoneum or infiltration of inflammatory cells was observed, in contrast to the chemical peritonitis group, which exhibited marked histopathological changes. GI motility was preserved in the urine exposure group, as evidenced by a normal FITC distribution and normal geometric center values. In contrast, the peritonitis groups showed delayed intestinal transit and significantly reduced geometric center values.
Conclusion:
Intraabdominal exposure to sterile urine did not induce histological peritoneal inflammation or significant impairment of gastrointestinal motility in this rat model. These findings suggest that sterile urine alone is unlikely to serve as an independent trigger of postoperative peritoneal inflammation or ileus under controlled experimental conditions.
