EFFECT OF ANTIOXIDANT THERAPY ON CYCLOOXYGENASE-DERIVED EICOSANOID RELEASE DURING INTESTINAL ISCHEMIA-REPERFUSION
EFFECT OF ANTIOXIDANT THERAPY ON CYCLOOXYGENASE-DERIVED EICOSANOID RELEASE DURING INTESTINAL ISCHEMIA-REPERFUSION
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DOI：
10.1159/000129146
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发表时间：
1991-05-01
影响因子：
1.6
通讯作者：
NAGY, S
中科院分区：
文献类型：
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作者：
BOROS, M;BAKO, L;NAGY, S
活性氧中间体与加氧酶衍生的类二十烷酸形成之间的关系已被报道。缺血1或2小时后，测定犬回肠段流出血中前列环素（PGI 2，以稳定代谢物6-酮-PGF 1-α测定）和血栓素A2（TxA 2，以TxB 2测定）的血浆水平。在再灌注过程中，两种类花生酸的合成都受到了显着刺激，但缺血间隔从60分钟延长至120分钟，随后并没有进一步增加。氧化剂的作用可能参与的过程中进行了研究，通过使用的材料，抑制黄嘌呤氧化酶产生的中间体。先前在相同的体内动物模型上的研究已经证明了抗氧化治疗在减少缺血后组胺释放方面的有效性。口服别嘌呤醇、过氧化氢酶、二甲亚砜、甘露醇或去铁胺治疗后，类花生酸合成量无显著变化。然而，脑内注射别嘌呤醇可显著升高缺血后6-keto-PGF 1-alpha/TxB 2比值。结果表明，这些抗氧化剂在抑制组胺释放的剂量是没有有效的影响缺血后类花生酸释放。腹腔注射别嘌呤醇可通过阻断黄嘌呤氧化酶以外的机制发挥潜在的有益作用。
Conflicting data have been reported on the relationship between reactive oxygen intermediates and the formation of oxygenase-derived eicosanoids. Plasma levels of prostacyclin (PGI2, measured as the stable metabolite 6-keto-PGF1-alpha) and thromboxane A2 (TxA2, measured as TxB2) in the effluent blood of a canine ileal segment were determined following 1 or 2 h of ischemia. The synthesis of both eicosanoids was significantly stimulated during reperfusion, but extension of the ischemic interval from 60 to 120 min was not followed by a further increase. The role of oxidants potentially involved in the process was investigated by using materials that inactivate the xanthine-oxidase-generated intermediates. Previous studies on the same in vivo animal model had demonstrated the effectiveness of antioxidant therapy in reducing the postischemic histamine release. There was no significant alteration in the amount of eicosanoids synthesized following oral allopurinol, catalase, dimethylsulfoxide, mannitol or desferrioxamine treatment. Intravenously administered allopurinol, however, significantly elevated the postischemic 6-keto-PGF1-alpha/TxB2 ratio. The results suggest that these antioxidants at doses inhibitory to histamine liberation are not effective in influencing the postischemic eicosanoid release. Intravenously administered allopurinol could exert a potentially beneficial effect through a mechanism other than the blockade of xanthine oxidase.