Abstracts
1999 Digestive Disease Week

# 2171 DIRECT MEASUREMENT OF PHOSPHATIDYLCHOLINE HYDROPEROXIDE DISCLOSES THE MECHANISM OF RAT INTESTINAL ISCHEMIA-REPERFUSION INJURY.
Tsuyoshi Masuko, Iwao Sasaki, Yuji Funayama, Hiroo Naito, Kohei Fukushima, Chikashi Shibata, Tohoku Univ Sch of Medicine, Sendai Japan; Teruo Miyazawa, Kiyotaka Nakagawa, Tohoku Univ Sch of Agricul, Sendai Japan; Seiki Matsuno, Tohoku Univ Sch of Medicine, Sendai Japan

Aim: The role of lipid peroxide in ischemia-reperfusion injury has not been clarified, because the measurement of peroxidation of phosphatidylcholine (PC), major component of cell membrane, was impossible. We disclosed the different role of neutrophils and lipid peroxidation using the new measuring method of phosphatidylcholine hydroperoxide (PCOOH). Materials and Methods: Six male Sprague-Dawley rats (200 to 240 g) underwent 30 minutes of small intestinal ischemia followed by 30 minutes of reperfusion (group 1). Other 6 rats were given 50 mg/kg of allopurinol prior to the same procedure as in group 1 (group 2). Group 3 consisted of 6 rats applied 20 mg/kg of ONO-4057 (LTB4 antagonist) just before the same procedure as in group 1. Non-ischemic bowels from 6 rats were harvested as control group. Intestinal injury was scored into four grades histologically. Expression of ICAM-1 was observed immunohistochemically. Neutrophils infiltration was quantified using myeloperoxidase staining. PCOOH was measured by chemiluminescence detection-high performance liquid chromatography, which is a unique system to quantify peroxide of specific lipid molecule. Statistical difference was determined at a p-value less than 0.05 using Fisher's PLSD test. Results: Tissue damage and neutrophil infiltration increased in group 1, while it was significantly (p<0.05) suppressed in group 2 and 3. In group 1 and 3, ICAM-1 was strongly demonstrated not only in vascular endothelium but also in the matrix of lamina propria. The reactivity of ICAM-1 in group 2 was suppressed to the same level as in control group. Mucosal PCOOH level was significantly (p<0.05) increased in group 1 and 3 compared to group 2. Conclusion: The main source of radicals responsible for peroxidation of PC was thought to be xanthine oxidase but not neutrophils. PCOOH is suspected to be one of the promoting factors in ischemia-reperfusion injury. Neutrophils were thought to be the major effector cells in tissue damage.

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