Erlansson M, Bergqvist D, Marklund S L, Persson N H, Svensjö E
Department of Pharmacology, AB Draco, Lund, Sweden.
Free Radic Biol Med. 1990;9(1):59-65. doi: 10.1016/0891-5849(90)90050-s.
The purpose was to elucidate the involvement of superoxide radical (O2-.) in the postischemic increase in the vascular permeability in the hamster cheek pouch. Cheek pouches of anesthetized hamsters were everted, prepared for intravital microscopy, and superfused with a bicarbonate buffered saline solution. Local ischemia for 30 min was obtained using a cuff placed around the proximal part of the cheek pouch. The vascular permeability in the postcapillary venules was quantified as leakage of intravenously injected fluorescein labeled dextran (FITC-dextran, Mw 150,000), using intravital microscopy and fluorimetry. There was a significant and reversible permeability increase after the reperfusion started. In the first series of experiments, combined intravenous infusion and topical application of human recombinant extracellular superoxide dismutase C (EC-SOD C) reduced the postischemic permeability response by 80%. Bovine CuZn-SOD given in exactly the same way reduced the response by 60%. In the second series of experiments, inactivated EC-SOD C was given to the control animals and active EC-SOD C was given to the treated animals. The topical treatment was excluded. Only active EC-SOD C reduced significantly the postischemic permeability increase when present during the ischemic period. Treatment with mannitol (i.v.) did not alter the postischemic response. Since active EC-SOD C and CuZn-SOD but not inactivated EC-SOD C effectively inhibited the response, we suggest that the superoxide anion is involved in the mediation of the postischemic permeability increase in the hamster.
目的是阐明超氧阴离子自由基（O2-·）在仓鼠颊囊缺血后血管通透性增加中的作用。将麻醉的仓鼠颊囊外翻，准备进行活体显微镜检查，并用碳酸氢盐缓冲盐溶液进行灌注。使用围绕颊囊近端放置的袖带造成局部缺血30分钟。利用活体显微镜检查和荧光测定法，将毛细血管后微静脉中的血管通透性定量为静脉注射的荧光素标记葡聚糖（FITC-葡聚糖，分子量150,000）的渗漏量。再灌注开始后，通透性有显著且可逆的增加。在第一组实验中，联合静脉输注和局部应用人重组细胞外超氧化物歧化酶C（EC-SOD C）可使缺血后通透性反应降低80%。以完全相同的方式给予牛CuZn-SOD可使反应降低60%。在第二组实验中，将灭活的EC-SOD C给予对照动物，将活性EC-SOD C给予处理组动物。排除局部治疗。仅当在缺血期存在活性EC-SOD C时，可显著降低缺血后通透性增加。用甘露醇（静脉注射）治疗未改变缺血后反应。由于活性EC-SOD C和CuZn-SOD而非灭活的EC-SOD C有效抑制了该反应，我们认为超氧阴离子参与了仓鼠缺血后通透性增加的介导过程。
