Galat J A, Robinson A V, Rhodes R S
Department of Surgery, Case Western Reserve University, Cleveland, Ohio 44106.
J Surg Res. 1990 Dec;49(6):488-92. doi: 10.1016/0022-4804(90)90173-y.
Oxygen free radicals (OFRs) generated during reperfusion are putative mediators of postischemic renal dysfunction. To address this issue, the renal response to ischemia and reperfusion was compared to the response to OFR generation without ischemia. Isolated rat kidneys were perfused at 37 degrees C and 90-100 mm Hg with an asanguinous modified Krebs' buffer. Kidneys were subjected to 30 min of ischemia followed by reperfusion or to OFRs generated by combining 25 mumole hypoxanthine with 1 unit xanthine oxidase. Both insults caused a 50% increase in vascular resistance. This was accompanied by a 30% reduction in perfusate flow rate and an 80% reduction in glomerular filtration and urine flow rates. The OFR scavengers, superoxide dismutase (SOD, 250 units/ml) and catalase (CAT, 500 units/ml), prevented these alterations after OFR generation but not after 30 min of ischemia and reperfusion. SOD and CAT also afforded no protection against the less severe dysfunction observed after 10 or 20 min of ischemia and reperfusion. OFRs do not appear to be prominent mediators of postischemic renal dysfunction; other factors, probably associated with ischemia must be primarily responsible.
再灌注过程中产生的氧自由基（OFRs）被认为是缺血后肾功能障碍的介质。为了解决这个问题，将肾脏对缺血和再灌注的反应与对无缺血情况下OFRs产生的反应进行了比较。将离体大鼠肾脏在37摄氏度和90 - 100毫米汞柱下用无血的改良克雷布斯缓冲液灌注。肾脏经历30分钟的缺血，随后再灌注，或者通过将25微摩尔次黄嘌呤与1单位黄嘌呤氧化酶结合产生OFRs。两种损伤均导致血管阻力增加50%。这伴随着灌注液流速降低30%，肾小球滤过率和尿流率降低80%。OFR清除剂超氧化物歧化酶（SOD，250单位/毫升）和过氧化氢酶（CAT，500单位/毫升）在OFR产生后可防止这些改变，但在30分钟缺血和再灌注后则不能。SOD和CAT对10或20分钟缺血和再灌注后观察到的较轻功能障碍也没有保护作用。OFRs似乎不是缺血后肾功能障碍的主要介质；其他因素，可能与缺血有关，必须是主要原因。
