Perry M A, Wadhwa S, Parks D A, Pickard W, Granger D N
Gastroenterology. 1986 Feb;90(2):362-7. doi: 10.1016/0016-5085(86)90933-9.
Ischemia in a stomach that contains acid may produce severe gastric mucosal injury. The extent to which oxygen-derived free radicals are involved in the pathogenesis of this injury was investigated in the present study. Local gastric ischemia was achieved by reducing celiac artery pressure to 30 mmHg for 1 h. Ischemic injury was assessed by recording the loss of 125I-albumin and 51Cr-red cells across the gastric mucosa. Cats were treated with a xanthine oxidase inhibitor (allopurinol), a superoxide radical scavenging enzyme (superoxide dismutase), and a scavenger of hydroxyl radicals (dimethyl sulfoxide). The damage associated with ischemia only occurred during reperfusion of the stomach and was worst in the antrum. The level of xanthine oxidase in the antrum was twice that of the corpus. Treatment with allopurinol, superoxide dismutase, and dimethyl sulfoxide reduced 51Cr-red cell loss to 15%, 25%, and 21% of control (untreated) animals, respectively. The data indicate that oxygen-derived free radicals play a role in ischemic injury to the stomach and that the hydroxyl radical, a secondary radical produced from the superoxide anion, appears to be the major oxygen radical contributing to ischemic damage.
含有胃酸的胃部发生局部缺血时，可能会导致严重的胃黏膜损伤。本研究旨在探究氧自由基在这种损伤发病机制中的作用程度。通过将腹腔动脉压力降至30 mmHg并持续1小时来实现局部胃缺血。通过记录125I-白蛋白和51Cr-红细胞透过胃黏膜的损失情况来评估缺血性损伤。给猫使用黄嘌呤氧化酶抑制剂（别嘌呤醇）、超氧化物自由基清除酶（超氧化物歧化酶）和羟自由基清除剂（二甲基亚砜）进行治疗。与缺血相关的损伤仅在胃再灌注期间出现，且在胃窦部最为严重。胃窦部黄嘌呤氧化酶水平是胃体部的两倍。使用别嘌呤醇、超氧化物歧化酶和二甲基亚砜治疗后，51Cr-红细胞损失分别降至未治疗（对照）动物的15%、25%和21%。数据表明，氧自由基在胃缺血性损伤中起作用，并且羟自由基作为由超氧阴离子产生的次级自由基，似乎是导致缺血性损伤的主要氧自由基。
