CONTRIBUTION OF NO-REFLOW PHENOMENON TO HEPATIC-INJURY AFTER ISCHEMIA-REPERFUSION - EVIDENCE FOR A ROLE FOR SUPEROXIDE ANION

被引:186
作者
KOO, A
KOMATSU, H
TAO, GM
INOUE, M
GUTH, PH
KAPLOWITZ, N
机构
[1] KUMAMOTO UNIV,SCH MED,DEPT BIOCHEM,KUMAMOTO 860,JAPAN
[2] VET ADM MED CTR BRENTWOOD,LOS ANGELES,CA 90073
[3] UNIV CALIF LOS ANGELES,SCH MED,CTR ULCER RES & EDUC,LOS ANGELES,CA 90024
关键词
D O I
10.1002/hep.1840150325
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Controversy exists as to the role of oxygen-derived free radicals in tissue injury and the no-reflow phenomenon in reperfusion injury after ischemia. In this study using an experimental rat model, left hepatic lobar ischemia followed by reperfusion resulted in an increase of serum glutamic pyruvic transaminase at 30 min with concomitant histological evidence of hepatocellular necrosis at 24 hr. In the in vivo liver microcirculation, reperfusion after ischemia resulted in an initial transient return of blood flow, but stasis of blood flow later developed in the liver sinusoids. Thus a no-reflow phenomenon in the microcirculation was demonstrated. Intravenous administration of a long-acting form of superoxide dismutase (half-life 6 hr, dose 4 or 8 mg/kg) significantly decreased the hepatocellular necrosis and reduced the microcirculatory stasis in the liver sinusoids. These studies established the important contribution of the no-reflow phenomenon in ischemia-reperfusion injury to the liver and the participation of superoxide anions in mediating the no-reflow phenomenon.
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页码:507 / 514
页数:8
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