Otamiri T
Clinical Research Center, University of Linköping, Sweden.
Agents Actions. 1988 Dec;25(3-4):378-84. doi: 10.1007/BF01965046.
The influence of total ischaemia and revascularization on luminal phospholipid metabolism in the rat small intestine was investigated. Two hours of total ischaemia followed by five minutes of revascularization caused increases in phospholipase A2 activity, and lysophosphalidylcholine content in the gut lumen. The above treatment also resulted in mucosal damage expressed as an increase in N-acetyl-beta-glucosaminidase activity in the lumen. Pretreatment of animals with the phospholipase A2 inhibitor, quinacrine prevented the increases in luminal phospholipase A2 activity and mucosal damage following ischaemia and revascularization. Intraluminal injection of either phospholipase A2 purified from snake venom or Triton X-100 resulted in increased activity of N-acetyl-beta-glucosaminidase in the luminal content. Again, quinacrine pretreatment of animals prevented the increases in mucosal permeability and activity of N-acetyl-beta-glucosaminidase after intraluminal injection of purified phospholipase A2. On the other hand quinacrine pretreatment had no influence on the observed effects of Triton X-100 treatment. These findings suggest that an increase in luminal phospholipase A2 could be involved in mediating the mucosal injury caused by small intestinal ischaemia.
研究了完全缺血和再灌注对大鼠小肠管腔磷脂代谢的影响。完全缺血两小时后再灌注五分钟，导致肠腔内磷脂酶A2活性和溶血磷脂酰胆碱含量增加。上述处理还导致黏膜损伤，表现为肠腔内N-乙酰-β-葡萄糖苷酶活性增加。用磷脂酶A2抑制剂奎纳克林对动物进行预处理，可防止缺血和再灌注后肠腔内磷脂酶A2活性增加和黏膜损伤。向肠腔内注射从蛇毒中纯化的磷脂酶A2或曲拉通X-100，导致肠腔内容物中N-乙酰-β-葡萄糖苷酶活性增加。同样，对动物进行奎纳克林预处理可防止在向肠腔内注射纯化的磷脂酶A2后黏膜通透性增加和N-乙酰-β-葡萄糖苷酶活性增加。另一方面，奎纳克林预处理对曲拉通X-100处理所观察到的效应没有影响。这些发现表明，肠腔内磷脂酶A2的增加可能参与介导小肠缺血引起的黏膜损伤。
