Sakio H, Okuda C
Second Department of Anesthesiology, Dokkyo University School of Medicine, Tochigi.
Masui. 1990 Dec;39(12):1646-51.
Our previous studies demonstrated that the bilateral hindlimb ischemia/reperfusion stimulates thromboxane A2 (TXA2) production. The present study tests the role of xanthine oxidase-derived oxygen free radicals in mediating this event. In twelve anesthetized dogs, the abdominal aorta and the inferior vena cava were clamped for 150 min, declamped and reperfused for 30 min. Two groups were studied: untreated control group and pretreated group with xanthine oxidase inhibitor, allopurinol 100 mg.kg-1 orally 24 hr before clamping plus 25 mg.kg-1 intravenously 15 min before clamping. In the control group, plasma TXB2 levels increased markedly after reperfusion. On the other hand, prior treatment with allopurinol attenuated the increase in plasma TXB2 levels at 30 min after reperfusion. This model revealed partial ischemia, because the femoral arterial blood flow was approximately 15% of baseline during clamping. However, the present study suggests that ischemia/reperfusion stimulates TXA2 production, which may be partly affected by hypoxanthine-xanthine oxidase-derived oxygen free radicals and may be an important mechanism responsible for reperfusion injury.
我们之前的研究表明，双侧后肢缺血/再灌注会刺激血栓素A2（TXA2）的产生。本研究旨在测试黄嘌呤氧化酶衍生的氧自由基在介导这一过程中的作用。在12只麻醉犬中，夹闭腹主动脉和下腔静脉150分钟，然后松开并再灌注30分钟。研究分为两组：未治疗的对照组和用黄嘌呤氧化酶抑制剂别嘌呤醇预处理的组，别嘌呤醇剂量为100mg·kg-1，在夹闭前24小时口服，夹闭前15分钟静脉注射25mg·kg-1。在对照组中，再灌注后血浆TXB2水平显著升高。另一方面，用别嘌呤醇预先处理可减轻再灌注后30分钟时血浆TXB2水平的升高。该模型显示为部分缺血，因为夹闭期间股动脉血流量约为基线的15%。然而，本研究表明，缺血/再灌注会刺激TXA2的产生，这可能部分受次黄嘌呤-黄嘌呤氧化酶衍生的氧自由基影响，并且可能是再灌注损伤的重要机制。
