Existence and participation of xanthine oxidase in reperfusion injury of ischemic rabbit myocardium.
Existence and participation of xanthine oxidase in reperfusion injury of ischemic rabbit myocardium.
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黄嘌呤氧化酶的存在及其在兔缺血心肌再灌注损伤中的参与
DOI：
10.1152/ajpheart.1991.260.3.h805
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Repine,JE
中科院分区：
文献类型：
--
作者：
Terada,LS;Rubinstein,JD;Lesnefsky,EJ;Horwitz,LD;Leff,JA;Repine,JE
使用一个高度特异性的测定，最大限度地减少酶失活在体外，我们发现，兔心肌组织中含有低水平的黄嘌呤氧化酶（XO）和黄嘌呤脱氢酶（XD）的活性，有效地抑制预处理的心脏别嘌呤醇。与此同时，别嘌呤醇治疗也改善了心室发展压力，收缩压峰值和冠状动脉流量在离体心脏进行30分钟的常温全脑缺血和30分钟的再灌注。尽管别嘌呤醇治疗可保护功能，但别嘌呤醇未改变肌酸激酶（CK）释放。别嘌呤醇抑制心肌XO不增加心肌ATP或磷酸肌酸。此外，别嘌呤醇在体外不清除超氧阴离子和过氧化氢。结果支持的可能性，相对较低的XO活性，类似于人类心肌中报道的水平，可能有助于心脏缺血再灌注损伤。
Using a highly specific assay that minimizes enzyme inactivation in vitro, we found that rabbit myocardial tissue contained low levels of xanthine oxidase (XO) and xanthine dehydrogenase (XD) activity that were effectively inhibited by pretreatment of hearts with allopurinol. In parallel, allopurinol treatment also improved ventricular developed pressure, peak systolic pressure, and coronary flow in isolated hearts subjected to 30 min of normothermic global ischemia and 30 min of reperfusion. Although function was protected by allopurinol treatment, creatine kinase (CK) release was not altered by allopurinol. Inhibition of myocardial XO with allopurinol did not increase myocardial ATP or phosphocreatine. In addition, allopurinol did not scavenge superoxide anion or hydrogen peroxide in vitro. The results support the possibility that relatively low amounts of XO activity, similar to levels reported in human myocardium, may contribute to cardiac ischemia-reperfusion injury.