[Abstract] [Full Text PDF] (in Japanese / 2972KB) [Members Only And Two Factor Auth.]

J.Jpn. Surg. Soc.. 94(9): 1017-1021, 1993


Original article

THE WORSENING OF TISSUE DAMAGE DUE TO THE TRANSIENT RELEASE DURING THE ISCHEMIA OF RAT SMALL INTESTINE
―THE RELATION WITH REACTIVE OXYGEN SPECIES AND LIPID PEROXIDATION―

The Second Department of Surgery, Department of Critical Care, Yokohama City University, School of Medicine, Yokohama, Japan
Emergency Medicine, Yokohama City University, School of Medicine, Yokohama, Japan

Yoshihiro Moriwaki, Hiroshi Katamura, Kunio Hashimoto, Yasushi Ichikawa, Mitsugi Sugiyama

Ischemia and reperfusion experiments were carried out using rat small intestine. Intestinal segment and supplying vessels was occluded and released after following procedure: In group I, 60 minute occlusion. In group II, 30 minute occlusion-10 minute release-20 minute occlusion. In group III, superoxide dismutase (SOD) and catalase (CAT) were given during the period of intermittent release in the same time schedule as in group II. Tissue damage was evaluated histopathologically and lipid peroxide (LPO) of involved segment and chemiluminescence (CL) of draining venous blood was investigated. It was concluded as follows: ① In these experiments, the tissue damage and the increment of LPO and CL were severer in group II than in group I. Then, the reactive oxygen species (ROS) derived from neutrophils was thought to play an important role in the tissue damage.② At the end of intermittent release, LPO and CL increased in group II, and these increments were surppressed by SOD and CAT treatment in group III. ③ After last release,the tissue damage in group II was diminished in group III. The severe tissue damage after intermittent occlusion is thought to be caused by reperfusion injury during the intermittent release.


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