Parks D A, Granger D N
Am J Physiol. 1983 Aug;245(2):G285-9. doi: 10.1152/ajpgi.1983.245.2.G285.
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.
先前研究的结果表明，氧衍生的自由基是肠道缺血1小时所导致的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肠段中氧自由基来源的假说；2）评估羟自由基在缺血诱导的血管损伤中的作用。通过猫回肠的淋巴蛋白流量数据，对以下情况的毛细血管渗透反射系数进行了估计：缺血、缺血加用别嘌呤醇（一种黄嘌呤氧化酶抑制剂）预处理、缺血加用二甲基亚砜（一种羟自由基清除剂）预处理。缺血所导致的血管通透性增加在很大程度上可通过别嘌呤醇或二甲基亚砜预处理来预防。这些发现支持了黄嘌呤氧化酶是缺血期间产生的氧自由基来源的假说。结果还表明，由超氧阴离子衍生而来的羟自由基是肠道缺血相关血管损伤的主要原因。
