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[The effect of xanthine oxidase inhibitor on hindlimb ischemia-induced thromboxane A2 release].

Abstract
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.
AuthorsH Sakio, C Okuda
JournalMasui. The Japanese journal of anesthesiology (Masui) Vol. 39 Issue 12 Pg. 1646-51 (Dec 1990) ISSN: 0021-4892 [Print] JAPAN
PMID2098592 (Publication Type: English Abstract, Journal Article)
Chemical References
  • Thromboxane A2
  • Allopurinol
  • Xanthine Oxidase
Topics
  • Allopurinol (pharmacology)
  • Animals
  • Dogs
  • Hindlimb (blood supply)
  • Ischemia (blood)
  • Reperfusion
  • Thromboxane A2 (blood)
  • Xanthine Oxidase (antagonists & inhibitors)

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