Cueva J P, Hsueh W
Department of Pathology, Children's Memorial Hospital, Northwestern University Medical School, Chicago, IL 60614.
Gut. 1988 Sep;29(9):1207-12. doi: 10.1136/gut.29.9.1207.
The mechanism of tissue and cell injury in ischaemic bowel necrosis is unclear. The present study investigated the role of oxygen derived free radicals in the development of bowel necrosis using injections of platelet activating factor (PAF) into the mesenteric vasculature. Animals were pretreated with allopurinol or superoxide dismutase together with catalase, before administration of PAF. Superoxide dismutase/catalase markedly improved the PAF-induced lesions, indicating that most of the intestinal damage after PAF injection is because of the release of oxygen radicals. The major source of oxygen radicals is xanthine oxidase, as allopurinol ameliorated small bowel lesions. Pretreatment with allopurinol produced a significant (p less than 0.01) preventive effect on PAF induced hypotension. In contrast, superoxide dismutase/catalase did not alter PAF induced hypotension. Superoxide dismutase/catalase pretreatment improved PAF induced haemoconcentration and leucopenia, while allopurinol showed no effect.
缺血性肠坏死中组织和细胞损伤的机制尚不清楚。本研究通过向肠系膜血管注射血小板活化因子（PAF），探讨氧自由基在肠坏死发生发展中的作用。在给予PAF之前，用别嘌呤醇或超氧化物歧化酶加过氧化氢酶对动物进行预处理。超氧化物歧化酶/过氧化氢酶显著改善了PAF诱导的损伤，表明注射PAF后大部分肠道损伤是由于氧自由基的释放。氧自由基的主要来源是黄嘌呤氧化酶，因为别嘌呤醇改善了小肠损伤。别嘌呤醇预处理对PAF诱导的低血压产生了显著（p小于0.01）的预防作用。相比之下，超氧化物歧化酶/过氧化氢酶并未改变PAF诱导的低血压。超氧化物歧化酶/过氧化氢酶预处理改善了PAF诱导的血液浓缩和白细胞减少，而别嘌呤醇则无此作用。
