Hatori N, Sjöquist P O, Marklund S L, Rydén L
Department of Cardiology, Karolinska Hospital, Stockholm, Sweden.
Free Radic Biol Med. 1992 Sep;13(3):221-30. doi: 10.1016/0891-5849(92)90018-c.
The efficacy of human extracellular-superoxide dismutase type C (EC-SOD C) to limit infarct size after ischemia and reperfusion was explored and compared to that of EC-SOD C combined with catalase (CAT) and to that of CAT alone. EC-SOD C binds to heparan sulphate proteoglycan on the cell surfaces. Thirty-two pigs were subjected to 45 min of myocardial ischemia followed by 4 h of reperfusion. Control pigs (group A; n = 8) received 300 mL of saline into the great cardiac vein during a 30-min period started 5 min prior to reperfusion; pigs in group B (EC-SOD C; n = 8) got 16.6 mg of EC-SOD C; pigs in group C (EC-SOD C + CAT; n = 8) got 16.6 mg of EC-SOD C together with 150 mg of CAT. Pigs in group D (CAT; n = 8) received 150 mg of CAT. In groups B, C, and D, the drug was dissolved in saline and infused into the great cardiac. Infarct size expressed as percent of area at risk was smaller in groups B (14.5 +/- 16.7%) and C (40.8 +/- 13.3%) than in groups A (78.8 +/- 8.6%) and D (67.2 +/- 18.6%; p less than .05). Creatine kinase (CK) activity in ischemic myocardium was higher in groups B (1740 +/- 548 U/g) and C (1729 +/- 358 U/g) than in groups A (1184 +/- 237 U/g) and D (1251 +/- 434 U/g; p less than .05). There was an inverse relation (r = -.83) between infarct size and CK content. The EC-SOD C infusions resulted in only minimal increases in plasma SOD activities. In conclusion, the presence of SOD on the cell surfaces is of importance in the prevention of reperfusion injury rather than circulating SOD.
探讨了人C型细胞外超氧化物歧化酶（EC-SOD C）限制缺血再灌注后梗死面积的疗效，并将其与EC-SOD C联合过氧化氢酶（CAT）以及单独使用CAT的疗效进行比较。EC-SOD C与细胞表面的硫酸乙酰肝素蛋白聚糖结合。32头猪经历45分钟的心肌缺血，随后进行4小时的再灌注。对照组猪（A组；n = 8）在再灌注前5分钟开始的30分钟内，经大冠状静脉注入300 mL生理盐水；B组猪（EC-SOD C；n = 8）给予16.6 mg的EC-SOD C；C组猪（EC-SOD C + CAT；n = 8）给予16.6 mg的EC-SOD C和150 mg的CAT。D组猪（CAT；n = 8）给予150 mg的CAT。在B、C和D组中，药物溶解于生理盐水中并注入大冠状静脉。以危险区域面积百分比表示的梗死面积，B组（14.5±16.7%）和C组（40.8±13.3%）小于A组（78.8±8.6%）和D组（67.2±18.6%；p <.05）。缺血心肌中的肌酸激酶（CK）活性，B组（1740±548 U/g）和C组（1729±358 U/g）高于A组（1184±237 U/g）和D组（1251±434 U/g；p <.05）。梗死面积与CK含量之间存在负相关（r = -.83）。注入EC-SOD C仅使血浆SOD活性略有增加。总之，细胞表面存在SOD对预防再灌注损伤很重要，而非循环中的SOD。
