International journal of urology : official journal of the Japanese Urological Association · 2026
Intraperitoneal Urine Exposure Does Not Elicit Peritoneal Inflammation or Gastrointestinal Dysmotility: A Histopathological and Functional Study in Rats.
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Yukimoto Minika, Kawasaki Maki, Maeda Akihiro, Nagase Kei, Kusano Shuhei, Nishiyama Megumi, Kakinoki Hiroaki, Tobu Shohei, Tanaka Yoshimasa, Ihara Eikichi, Aoki Shigehisa, Noguchi Mitsuru
Аннотация
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.
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.