Ischemia/reperfusion alters uric acid and ascorbic acid levels in liver

被引:25
作者
Layton, ME
Wood, JG
Yan, ZY
Forster, J
机构
[1] UNIV KANSAS, MED CTR, DEPT PHARMACOL TOXICOL & THERAPEUT, KANSAS CITY, KS 66160 USA
[2] UNIV KANSAS, MED CTR, DEPT SURG, KANSAS CITY, KS 66160 USA
关键词
D O I
10.1006/jsre.1996.0297
中图分类号
R61 [外科手术学];
学科分类号
摘要
Tissue damage in ischemia/reperfusion injury may be mediated by oxidative stress caused by reactive oxidant species. Since such reactive species are difficult to measure directly, changes in antioxidant concentrations are often used as an indication of oxidative stress, In this study, microdialysis membranes were inserted into the livers of anesthetized rats to determine the effects of ischemia/reperfusion on the extracellular concentrations of two antioxidants, uric acid and ascorbic acid, Total hepatic ischemia was induced for 30 min by clamping the portal triad and was followed by 60 min of reperfusion, Uric acid and ascorbic acid concentrations were measured in microdialysis perfusates by high-performance liquid chromatography with electrochemical detection. Initial uric acid and ascorbic acid concentrations were high after insertion of membranes into the liver and decreased rapidly within 90 min (P < 0.001; ANOVA with repeated measures), Uric acid concentrations increased over 300% after ischemia and by 600% during the first 30 min of reperfusion (n = 8; P < 0.05). Ascorbic acid concentrations were 60% higher than controls after ischemia and 90% higher during the first 30 min of reperfusion (n = 8; P < 0.05), Alterations in concentrations of these redox-active molecules may be associated with oxidative stress in liver extracellular fluid during ischemia/reperfusion. (C) 1996 Academic Press, Inc.
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页码:1 / 5
页数:5
相关论文
共 38 条
[11]   ALLOPURINOL INHIBITS URIC-ACID ACCUMULATION IN THE RAT-BRAIN FOLLOWING FOCAL CEREBRAL-ISCHEMIA [J].
KANEMITSU, H ;
TAMURA, A ;
KIRINO, T ;
OKA, H ;
SANO, K ;
IWAMOTO, T ;
YOSHIURA, M ;
IRIYAMA, K .
BRAIN RESEARCH, 1989, 499 (02) :367-370
[12]   CHANGES OF URIC-ACID LEVEL IN RAT-BRAIN AFTER FOCAL ISCHEMIA [J].
KANEMITSU, H ;
TAMURA, A ;
SANO, K ;
IWAMOTO, T ;
YOSHIURA, M ;
IRIYAMA, K .
JOURNAL OF NEUROCHEMISTRY, 1986, 46 (03) :851-853
[13]   XANTHINE AND URIC-ACID LEVELS IN RAT-BRAIN FOLLOWING FOCAL ISCHEMIA [J].
KANEMITSU, H ;
TAMURA, A ;
KIRINO, T ;
KARASAWA, S ;
SANO, K ;
IWAMOTO, T ;
YOSHIURA, M ;
IRIYAMA, K .
JOURNAL OF NEUROCHEMISTRY, 1988, 51 (06) :1882-1885
[14]   EVIDENCE THAT FK506 ALLEVIATES ISCHEMIA-REPERFUSION INJURY TO THE RAT-LIVER - IN-VIVO DEMONSTRATION FOR SUPPRESSION OF TNF-ALPHA PRODUCTION IN RESPONSE TO ENDOTOXEMIA [J].
KAWANO, K ;
ILKIM, Y ;
KAI, T ;
ISHII, T ;
TATSUMA, T ;
MORIMOTO, A ;
TAMURA, Y ;
KOBAYASHI, M .
EUROPEAN SURGICAL RESEARCH, 1994, 26 (02) :108-115
[15]   INVESTIGATION OF THE RENAL INJURY CAUSED BY LIVER ISCHEMIA-REPERFUSION IN RATS [J].
KUDO, Y ;
EGASHIRA, T ;
TAKAYAMA, F ;
YAMANAKA, Y ;
SHIMADA, T .
ARCHIVES OF TOXICOLOGY, 1993, 67 (07) :502-509
[16]   EXTRACELLULAR ANTIOXIDANTS AND AMINO-ACIDS IN THE CORTEX OF THE RAT - MONITORING BY MICRODIALYSIS OF EARLY ISCHEMIC CHANGES [J].
LANDOLT, H ;
LUTZ, TW ;
LANGEMANN, H ;
STAUBLE, D ;
MENDELOWITSCH, A ;
GRATZL, O ;
HONEGGER, CG .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1992, 12 (01) :96-102
[17]  
MARTENSSON J, 1991, P NATL ACAD SCI USA, V88, P6898
[18]  
MCCORD JM, 1968, J BIOL CHEM, V243, P5753
[19]   STUDIES OF ASCORBATE-DEPENDENT, IRON-CATALYZED LIPID-PEROXIDATION [J].
MILLER, DM ;
AUST, SD .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1989, 271 (01) :113-119
[20]   GLUTATHIONE DEFICIENCY DECREASES TISSUE ASCORBATE LEVELS IN NEWBORN RATS - ASCORBATE SPARES GLUTATHIONE AND PROTECTS [J].
MRTENSSON, J ;
MEISTER, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (11) :4656-4660