| Project/Area Number |
11671274
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Showa University |
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Principal Investigator |
TSUNODA Akira Showa University, School of medicine lecturer, 医学部, 講師 (10183485)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBUSAWA Miki Showa University, School of medicine assistant professor, 医学部, 助教授 (90138496)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Lactobacillus / Faecal peritonitis / Survival |
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| Research Abstract |
Methods. Cecal ligation and tip resection (CLTR)-induced fecal peritonitis was developed as a novel mouse model of abdominal sepsis, and the effects of LC9018 pretreatment on the survival after CLTR, the peritoneal exudate cells (PECs) before or after CLTR, and the bacterial growth in the peritoneal cavity after CLTR were investigated. Results. Mortality after CLTR varied directly with the length of the opened bowel. To obtain a sublethal experimental group, the length of the opened bowel was fixed at 4mm, where the mortality was 87%, for further experiments. CLTR surgery followed by the excision of the opened bowel and saline peritoneal irrigation (CLTRI) at specific time intervals revealed that all mice survived if intervention was performed after 3h, whereas removal of the septic focus after 12h did not prevent death. Survival of mice after CLTR was augumented in mice that had been pretreated i.p. with LC9018 24h previously. Viable bacterial growth in the peritoneal cavity was markedly inhibited in LC9018-pretreated mice. Peritoneal exudate cells accumulation observed 24h after i.p. injection of LC9018 was significantly enhanced, suggesting that augumentation of the resistance of mice to CLTR was caused by especially the induction of polymorphonuclear cells.
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