Schoenberg M H, Fredholm B B, Haglund U, Jung H, Sellin D, Younes M, Schildberg F W
Acta Physiol Scand. 1985 Aug;124(4):581-9. doi: 10.1111/j.1748-1716.1985.tb00051.x.
Characteristic mucosal lesions develop in the small intestine during ischaemia and hypotension. This tissue damage can be further aggravated in the immediate reperfusion phase, presumably secondary to the generation of oxygen free radicals which have been proposed to be generated in this situation through the hypoxanthine-xanthine oxidase system. This was further investigated in the cat small intestine using a standardized regional intestinal hypotension model in which the effects of allopurinol (a xanthine oxidase inhibitor) were compared to those of an exogenous supply of inosine. The grade of mucosal damage, the nucleotide levels, the concentrations of hypoxanthine, total and oxidized glutathione, and of conjugated dienes were measured in the intestinal tissue. The results indicate that oxygen radicals generated by xanthine oxidase are very important, but not the only significant factor in the small intestinal reperfusion damage.
在缺血和低血压期间，小肠会出现特征性的黏膜病变。这种组织损伤在即刻再灌注阶段可能会进一步加重，推测是由于氧自由基的产生，有人提出在这种情况下氧自由基是通过次黄嘌呤-黄嘌呤氧化酶系统产生的。在猫小肠中使用标准化的区域性肠低血压模型对此进行了进一步研究，其中将别嘌呤醇（一种黄嘌呤氧化酶抑制剂）的作用与外源性供应肌苷的作用进行了比较。在肠组织中测量了黏膜损伤程度、核苷酸水平、次黄嘌呤浓度、总谷胱甘肽和氧化型谷胱甘肽以及共轭二烯的浓度。结果表明，黄嘌呤氧化酶产生的氧自由基非常重要，但不是小肠再灌注损伤中唯一的重要因素。
