| Co-Investigator(Kenkyū-buntansha) |
FUKUCHINA Kohei Research Associate.Tohoku Univ.School of Medicine, 医学部, 助手 (20271900)
NAITO Hiro First Dep.Surg.Tohoku Univ.Hspital Lecturer, 医学部附属病院, 講師 (90180223)
MIYAZAWA Teruo Associate Prof.Tohoku Univ.School of Agriculture, 農学部, 助教授 (20157639)
SASAKI Iwao Associate Prof.Fivst Dep.Surg.Tohoku Univ., 医学部, 助教授 (60125557)
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| Research Abstract |
1.The aim of this study is to evaluate intestinal mucosal lipid peroxidation induced by ischemiareperfusion in comparison with phosphatidylcholine hydroperoxide (PCOOH ; the peoxide of the major composition of phospholipid in rats intestinal mucosa) quantification and thiobarbituric acid reacting substance (TBARS) measurement. S-D male rats were used. The model in which superior mesenteric artery (SMA) was occuluded for 30 minutes followed by 0,30,60,120,180 or 360 minutes of reperfusion. Mucosal TBARS and PCOOH were measured. Chemiluminescence high performance liquid chromatography (CL-HPLC) method, with high sensitivity and specificity for lipid peroxides, was used to detect mucosal PCOOH.Histological assessment of the mucosal injury and neutrophil recruitment were performed. Mucosal TBARS level showed no significant difference by ischemia alone or ischemia reperfusion in comparison with sham operated control. Mucosal PCOOH level increased by 30 minutes reperfusion and decreased gradually according to time course. Disruption of epithelial cells in almost full length of villi were observed in the model of 30 minutes to 120 minutes reperfusion. The number of mucosal neutrophils increased in the model of 30,120,180 minutes of reperfusion and thereafter decreased to the same level of sham operated model by 360 minutes. In conclusion, the evedence for lipid peroxidation can be detected by measuring mucosal PCOOH level and PCOOH is sensitive parameter to evaluate lipid peroxidation.
2.To investigate a role of lipid peroxidation in the pathogenesis of hypoxia induced acute gastric mucosal lesion (AGML), the contents of PCOOH in the gastric mucosa during hypoxic air inhalation were measured by the CL-HPLC methods. The restraint under the hypoxic condition produced AGML and increased the level of PCOOH in the gastric mucosa. These results suggested that lipid peoxidation play an important role in the pathogenesis of AGML induced by hypoxia.
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