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Role of Xanthine Oxidase in Reperfusion Injury In Ischemic Myocardium
허혈심근 재관류손상에 있어서 Xanthine Oxidase의 역할

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Authors
Lim, Young; Kim, Myung-suk
Issue Date
1988-06
Publisher
Seoul National University College of Medicine
Citation
Seoul J Med 1988;29(2):131-142
Keywords
Xanthine oxidaseOxygen free radicalReperfusion injuryMyocardial ischemia
Abstract
The present studies were conducted to confirm the hypothesis that xanthine oxidase-
linked cytotoxic oxygen free radicals play an important role in producing the reperfusion
injury of ischemic myocardium. The reperfusion injury was induced in isolated, Langendorff
preparations of rat hearts by 60 min of global ischemia with aortic clamping followed by 20
min of reperfusion with oxygenated Krebs- Henseleit solution. Upon reperfusion of ischemic
hearts, the release of creatine phosphokinase, lactic dehydrogenase and a lipid peroxidation
product, malondialdehyde into the coronary effluent was abruptly increased. The increase of
the enzymes and malondialdehyde was supprressed significantly in the presence of superoxide
dismutase or catalse during the reperfusion period. In the hearts removed from rats pretreated
with a specific xanthine oxidase inhibitor, allopurino1(20 mglkg, orally 24 hrs and 2 hrs before
study}, the increased release of the enzymes and malondialdehyde was also significantly depressed.
This effect of allopurinol was comparable to that of oxygen radical scavengers. When
ferricytochrome C was infused to the hearts starting with reperfusion, the SOD-inhibitable reduction
of ferricytochrome C increased during the first minute of reperfusion. Hydrogen peroxide
measured in the coronary effluents also increased markedly with the similar time course as
ferricytochrome C reduction. In the hearts treated with allopurinol, however, both the ferricytochrome
C reduction and HzOz were not increased significantly. Myocardial content of xanthine
oxidase was determined for D-form, O-form and D/O-form separately in the normal control
hearts and the ischemic ones. Total enzyme content was similar in both hearts. Compared
with the normal control, however, the ischemic hearts showed lower activities in D-form and
D/O-form, and higher activity in the oxygen radical producing O-form. The proportion of
O-form to the total enzyme was much higher in the ischemic heart than in the normal control
heart. After 60 min of ischemia, myocardial content of total adenine nucleotides were reduced
to 40% of the normal control value, while their catabolic products, hypoxanthine and xanthine
were accumulated significantly. These. results provide evidence that xanthine oxidase is involved
in the production of oxygen free radicals during the reperfusion of ischemic heart, and
plays a contributing role in the genesis of reperfusion injury.
ISSN
0583-6802
Language
English
URI
http://hdl.handle.net/10371/6373
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Medicine (의학과)The Seoul Journal of MedicineThe Seoul Journal of Medicine Vol. 29 No.2 (1988)
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