Ischemia-induced vascular changes: role of xanthine oxidase and hydroxyl radicals.
Ischemia-induced vascular changes: role of xanthine oxidase and hydroxyl radicals.
复制标题
缺血引起的血管变化：黄嘌呤氧化酶和羟自由基的作用。
DOI：
10.1152/ajpgi.1983.245.2.g285
复制
发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Granger,DN
中科院分区：
文献类型：
--
作者：
Parks,DA;Granger,DN
先前的研究结果表明，氧自由基是造成肠道缺血1小时后血管通透性增加的原因。本研究的目的是 1) 检验黄嘌呤氧化酶是缺血性肠中氧自由基来源的假设，2) 评估羟基自由基在缺血引起的血管损伤中的作用。根据以下条件下猫回肠中的淋巴蛋白通量数据估算毛细血管渗透反射系数：缺血、缺血加别嘌呤醇（一种黄嘌呤氧化酶抑制剂）预处理，以及缺血加二甲亚砜（羟自由基清除剂）预处理。用别嘌呤醇或二甲亚砜进行预处理很大程度上可以防止缺血引起的血管通透性增加。这些发现支持黄嘌呤氧化酶是缺血期间产生的氧自由基的来源的假设。结果还表明，源自超氧阴离子的羟基自由基是与肠道缺血相关的血管损伤的主要原因。
The results of previous studies indicate that oxygen-derived free radicals are responsible for the increased vascular permeability produced by 1 h of intestinal ischemia. The aims of this study were 1) to test the hypothesis that the enzyme xanthine oxidase is the source of oxygen radicals in the ischemic bowel and 2) to assess the role of the hydroxyl radical in the ischemia-induced vascular injury. The capillary osmotic reflection coefficient was estimated from lymphatic protein flux data in the cat ileum for the following conditions: ischemia, ischemia plus pretreatment with allopurinol (a xanthine oxidase inhibitor), and ischemia plus pretreatment with dimethyl sulfoxide (a hydroxyl radical scavenger). The increased vascular permeability produced by ischemia was largely prevented by pretreatment with either allopurinol or dimethyl sulfoxide. These findings support the hypothesis that xanthine oxidase is the source of oxygen radicals produced during ischemia. The results also indicate that hydroxyl radicals, derived from the superoxide anion, are primarily responsible for the vascular injury associated with intestinal ischemia.