O-2 FREE-RADICALS - CAUSE OF ISCHEMIA-REPERFUSION INJURY TO CARDIAC NA+-K+-ATPASE
O-2 FREE-RADICALS - CAUSE OF ISCHEMIA-REPERFUSION INJURY TO CARDIAC NA+-K+-ATPASE
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DOI：
10.1152/ajpheart.1987.252.2.h252
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发表时间：
1987-02-01
影响因子：
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通讯作者：
AKERA, T
中科院分区：
文献类型：
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作者：
KIM, MS;AKERA, T
在离体豚鼠心脏中，使用外源性O2自由基清除剂和黄嘌呤氧化酶抑制剂，研究了O2自由基在缺血心脏再灌注过程中减少肌层Na+-K+- atp酶的作用。缺血和再灌注降低了心室肌匀浆中Na+-K+- atp酶的活性和特定[3H]瓦阿因与酶的结合，也显著降低了心室肌片对瓦阿因敏感的86Rb+摄取估计的钠泵活性。o2自由基清除剂，如超氧化物歧化酶、过氧化氢酶、二甲亚砜、组氨酸或维生素E，或黄嘌呤氧化酶抑制剂别嘌呤醇，在不同程度上阻止了缺血和再灌注的这些影响。这些药物提供的保护程度与减少心肌组织脂质过氧化的程度相似，估计是丙二醛产生的结果。这些结果强烈提示O2自由基在缺血心脏再灌注时对肌层Na+-K+- atp酶的损伤中起重要作用。
The role of O2 free radicals in the reduction of sarcolemmal Na+-K+-ATPase, which occurs during reperfusion of ischemic heart, was examined in isolated guinea pig heart using exogenous scavengers of O2 radicals and an inhibitor of xanthine oxidase. Ischemia and reperfusion reduced Na+-K+-ATPase activity and specific [3H]ouabain binding to the enzyme in ventricular muscle homogenates and also markedly lowered sodium pump activity estimated from ouabain-sensitive 86Rb+ uptake by ventricular muscle slices. These effects of ischemia and reperfusion were prevented to various degrees by O2-radical scavengers, such as superoxide dismutase, catalase, and dimethylsulfoxide, histidine, or vitamin E or by te xanthine oxidase inhibitor, allopurinol. The degree of protection afforded by these agents paralleled that of reduction in enhanced lipid peroxidation of myocardial tissue as estimated form malondialdehyde production. These results strongly suggest that O2 radicals play a crucial role in the injury to sarcolemmal Na+-K+-ATPase during reperfusion of ischemic heart.