Otamiri T, Sjödahl R, Tagesson C
Acta Chir Scand. 1987 Jan;153(1):51-6.
We have developed a simple experimental model for studying reversible intestinal ischemia. The model is based on tenting the mesenteric vessels (artery and vein) to a tied loop of the small bowel in rat and, after a certain time, lowering them down again. Total and partial ischemia (created by tenting 2 and 1 cm, respectively) were demonstrated by laser Doppler flowmetry, as was the revascularization obtained after bringing the vessels down again. Alterations in mucosal permeability after ischemia were determined by depositing fluorescent dextran 3000 in the tied loop and measuring its concentration in the portal blood, and mucosal damage due to ischemia was assessed by measuring the activity of N-acetyl-beta-glucosaminidase, a lysosomal enzyme, in the gut lumen. There was a significant increase in the intestinal permeability to dextran 3000 after total ischemia for 10 min or more, and the permeability was directly related to the duration of the ischemia. After the intestine had been subjected to total ischemia for 30 min or more, the activity of N-acetyl-beta-glucosaminidase in the luminal contents was significantly increased. The permeability after partial ischemia for 30 min was less than that after total ischemia for 30 min. After total ischemia for 10 min followed by revascularization for 30 or 60 min, the permeability did not differ from that in animals not subjected to ischemia. It is concluded that this simple model may be used to study reversible small intestinal ischemia and factors that influence mucosal permeability.
我们开发了一种用于研究可逆性肠缺血的简单实验模型。该模型基于将肠系膜血管（动脉和静脉）固定到大鼠小肠的一个系扎环上，经过一定时间后再将它们松开。通过激光多普勒血流仪证实了完全和部分缺血（分别通过固定2厘米和1厘米造成），以及血管再次松开后获得的再灌注。缺血后黏膜通透性的改变通过在系扎环中注入荧光右旋糖酐3000并测量其在门静脉血中的浓度来确定，缺血导致的黏膜损伤通过测量肠腔内溶酶体酶N-乙酰-β-氨基葡萄糖苷酶的活性来评估。完全缺血10分钟或更长时间后，肠道对右旋糖酐3000的通透性显著增加，且通透性与缺血持续时间直接相关。肠道完全缺血30分钟或更长时间后，肠腔内容物中N-乙酰-β-氨基葡萄糖苷酶的活性显著增加。部分缺血30分钟后的通透性低于完全缺血30分钟后的通透性。完全缺血10分钟后再灌注30或60分钟，其通透性与未经历缺血的动物无差异。结论是，这个简单的模型可用于研究可逆性小肠缺血以及影响黏膜通透性的因素。
