期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：1992
卷号：13
期号：1
页码：31-43
DOI：10.3164/jcbn.13.31
出版社：The Society for Free Radical Research Japan
摘要：Studies were made in dogs on ischemic injury of the liver induced by clamping the portal triad and inferior vena cava and on the influences of urinary trypsin inhibitor (Ulinastatin) on the ischemic changes. The increases in aspartate aminotransferase and alanine aminotransferase activities in the peripheral blood serum induced by ischemia and reperfusion were lowered by perfusion treatment of ischemic liver with ulinastatin for 60min or its injection into the general circulation 5min before reperfusion. The increase in lipid peroxides, measured by the TBA-method, in the post-ischemic liver was also decreased by administration of ulinastatin. α-Tocopherol in the liver decreased during ischemia-reperfusion, and its decrease was completely prevented by ulinastatin treatment. However, infiltration of neutrophils into post-ischemic liver tissue was not inhibited by ulinastatin. The effect of in vitro addition of ulinastatin on the formation of superoxide anion radicals by the xanthine-xanthine oxidase system and NADPH oxidase in polymorphonuclear leukocytes (PMNs) was also investigated. Ulinastatin did not affect xanthine oxidase activity or O2- formation. It also did not scavenge O2-. On the contrary, it inhibited O2- formation by PMNs induced by N-formylmethionylleucylphenylalanine, concanavalin A plus cytocalasin B, or phorbol 12-myristate 13-acetate. The mechanisms of the protective effect of ulinastatin on ischemic liver injury are discussed from the view point of its antioxidant properties.
