Itoh M, Guth P H
Gastroenterology. 1985 May;88(5 Pt 1):1162-7. doi: 10.1016/s0016-5085(85)80075-5.
This study was designed to determine whether oxygen-derived free radicals play a role in the pathogenesis of gastric lesions produced by hypotensive ischemia in the rat. To achieve this goal, allopurinol, an inhibitor of xanthine oxidase (the enzyme responsible for the formation of superoxide radicals); superoxide dismutase, a scavenger of superoxide radicals (O2-); and dimethyl sulfoxide, a scavenger of hydroxyl radicals (OH) were used. In the anesthetized rat, HCl (0.1 N) was instilled into the pylorus-ligated stomach, and the rat was bled to reduce the blood pressure to less than 30 mmHg. The blood pressure was maintained at less than 30 mmHg for 20 min and then the shed blood was retransfused. Twenty minutes after the retransfusion the rat was killed, the stomach was removed, and the area of gastric mucosal lesions was measured. Both allopurinol and superoxide dismutase, but not dimethyl sulfoxide, significantly protected against hemorrhagic shock-induced gastric lesions. These findings suggest that oxygen-derived free radicals, particularly O2-, play an important role in the formation of gastric lesions produced by ischemia plus HCl.
本研究旨在确定氧衍生的自由基是否在大鼠低血压缺血所致胃损伤的发病机制中起作用。为实现这一目标,使用了黄嘌呤氧化酶(负责超氧阴离子自由基形成的酶)抑制剂别嘌呤醇、超氧阴离子自由基(O2-)清除剂超氧化物歧化酶以及羟自由基(OH)清除剂二甲基亚砜。在麻醉的大鼠中,将0.1N盐酸注入幽门结扎的胃内,然后放血使血压降至30mmHg以下。将血压维持在30mmHg以下20分钟,然后回输所放的血。回输20分钟后处死大鼠,取出胃,测量胃黏膜损伤面积。别嘌呤醇和超氧化物歧化酶均能显著保护大鼠免受失血性休克诱导的胃损伤,而二甲基亚砜则不能。这些发现表明,氧衍生的自由基,尤其是O2-,在缺血加盐酸所致胃损伤的形成中起重要作用。