Otamiri T, Franzén L, Lindmark D, Tagesson C
Clinical Research Center, Linköping University Hospital, Sweden.
Gut. 1987 Nov;28(11):1445-53. doi: 10.1136/gut.28.11.1445.
The influence of ischaemia and revascularisation on lipid peroxidation and phospholipid metabolism in the rat small intestinal mucosa was investigated. Two hours of total ischaemia followed by five minutes of revascularisation caused not only accumulation of malondialdehyde in the mucosa, but also increased activity of phospholipase A2, decreased activity of lysophospholipase, and increased ratio between lysophosphatidylcholine and phosphatidylcholine. Pretreatment with the phospholipase A2 inhibitor, quinacrine, prevented the increases in mucosal phospholipase A2 activity and lysophosphatidylcholine/phosphatidylcholine ratio after ischaemia and morphological examinations revealed that the mucosa was then also protected against ischaemic injury. These findings point to the possibility that activation of phospholipase A2 and accumulation of lysophosphoglycerides could be involved in mediating the mucosal injury caused by small intestinal ischaemia.
研究了缺血和再灌注对大鼠小肠黏膜脂质过氧化和磷脂代谢的影响。完全缺血两小时后再灌注五分钟,不仅导致黏膜中丙二醛蓄积,还使磷脂酶A2活性增加、溶血磷脂酶活性降低以及溶血磷脂酰胆碱与磷脂酰胆碱的比例升高。用磷脂酶A2抑制剂奎纳克林预处理可防止缺血后黏膜磷脂酶A2活性和溶血磷脂酰胆碱/磷脂酰胆碱比例升高,形态学检查显示黏膜此时也受到保护,免受缺血损伤。这些发现表明,磷脂酶A2的激活和溶血甘油酯的蓄积可能参与介导小肠缺血所致的黏膜损伤。