Hülsmann W C, Dubelaar M L
Department of Biochemistry I, Erasmus University Rotterdam, The Netherlands.
Cardiovasc Res. 1987 Sep;21(9):674-7. doi: 10.1093/cvr/21.9.674.
To determine the site of reperfusion damage after ischaemia the leakage of xanthine dehydrogenase and xanthine oxidase was assessed in vascular and interstitial effluents. Contractile function was reduced during hypoperfusion but improved after the addition of superoxide dismutase and vasoxin to the perfusion medium. Both interstitial fluid and coronary effluent showed dehydrogenase and oxidase activity after no flow ischaemia. Furthermore, the ratio of lactate dehydrogenase to creatine kinase in coronary effluents was reduced. These findings indicate that the myocardial interstitium may be a site of ischaemic membrane damage since this space contains hypoxanthine and xanthine oxidase. The protective effect of superoxide dismustase also indicates the possibility of damage due to oxygen derived radicals in the cardiac interstitium during low flow perfusion.
为了确定缺血后再灌注损伤的部位,对血管和组织间流出液中黄嘌呤脱氢酶和黄嘌呤氧化酶的渗漏情况进行了评估。在低灌注期间收缩功能降低,但在灌注介质中添加超氧化物歧化酶和血管毒素后功能得到改善。在无血流缺血后,组织间液和冠状动脉流出液均显示出脱氢酶和氧化酶活性。此外,冠状动脉流出液中乳酸脱氢酶与肌酸激酶的比率降低。这些发现表明,心肌间质可能是缺血性膜损伤的部位,因为该间隙含有次黄嘌呤和黄嘌呤氧化酶。超氧化物歧化酶的保护作用也表明在低流量灌注期间心脏间质中氧衍生自由基造成损伤的可能性。