1997 Fiscal Year Final Research Report Summary
Study of intestinal ischemic disease in newborn patients
| Project/Area Number |
08457473
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
小児外科
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| Research Institution | Osaka University |
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Principal Investigator |
OKADA Akira Osaka University Medical School, Professor, 医学部, 教授 (40028569)
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| Co-Investigator(Kenkyū-buntansha) |
WASA Masafumi Osaka University Medical School, Assistant Professor, 医学部, 助手 (10240467)
KUBOTA Akio Kinki University Medical School, Lecturer, 医学部, 講師
KAMATA Schinkichi Osaka University Medical School, Associate Professor, 医学部, 助教授 (40161202)
TAKAGI Yoji Osaka University Medical School, Professor, 医学部, 教授 (40154760)
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| Project Period (FY) |
1996 – 1997
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| Keywords | iNOSmRNA / Sepsis / L-NAME / NO / NOS-IIImRNA / Mucosal damage |
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| Research Abstract |
We measured tissue expression of mRNA encoding iNOS by Northern blot analysis and reverse transcription PCR.The iNOS mRNA was detectable at 1 h, peaked at 4 h after endotoxin injection in esophagus, duodenum, jejunum, ileum arid colon. Pre-treatment with dexamethasone attenuated the rise of iNOS mRNA.Both dexamethasone and NOS inhibitor, L-NAME, ameliorated the endotoxin-induced increase in intestinal mucosal permeability. Our results indicate that there is tissue-specific expression of iNOS mRNA in the digestive tract. The maniprations that decrease NO production may have therapeutic potential in preserving intestinal mucosal integrity in sepsis.
We characterized the tissue distribution of mRNA for endothelial nitric oxide synthase (NOS-III) and to examine its response to endotoxin challenge in vivo. The expression of NOS-III mRNA and protein in mucosa was demonstrated throughout the gastrointestinal tract. NOS-Ill mRNA expression in the gastrointestinal mucosa was down-regulated in rats treated with endotoxin. The decreased NOS-III mRNA, in parallel to induction of inducible NOS mRNA, may contribute to the impaired endothelium-dependent relaxation and damaged mucosal integrity during sepsis.
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