Contribution of No‐reflow phenomenon to hepatic injury after ischemia‐reperfusion: Evidence for a role for superoxide anion

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 t...

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Published in:Hepatology (Baltimore, Md.) Md.), 1992-03, Vol.15 (3), p.507-514
Main Authors: Koo, Anthony, Komatsu, Hirokazu, Tao, Gongming, Inoue, Masayashu, Guth, Paul H., Kaplowitz, Neil
Format: Article
Language:English
Subjects:
Animals
Anions - metabolism
Biological and medical sciences
Gastroenterology. Liver. Pancreas. Abdomen
Ischemia - pathology
Ischemia - physiopathology
Liver - pathology
Liver Circulation
Male
Medical sciences
Necrosis
Rats
Rats, Inbred Strains
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Superoxide Dismutase - pharmacology
Superoxides - metabolism
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Summary: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 longacting 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.
ISSN:0270-9139
1527-3350
DOI:10.1002/hep.1840150325