SUPEROXIDE-DISMUTASE REDUCES REPERFUSION ARRHYTHMIAS BUT FAILS TO SALVAGE REGIONAL FUNCTION OR MYOCARDIUM AT RISK IN CONSCIOUS DOGS
SUPEROXIDE-DISMUTASE REDUCES REPERFUSION ARRHYTHMIAS BUT FAILS TO SALVAGE REGIONAL FUNCTION OR MYOCARDIUM AT RISK IN CONSCIOUS DOGS
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DOI：
10.1161/01.cir.79.1.143
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发表时间：
1989-01-01
期刊：
影响因子：
37.8
通讯作者：
VATNER, SF
中科院分区：
文献类型：
--
作者：
NEJIMA, J;KNIGHT, DR;VATNER, SF
为了确定冠状动脉再灌注前给予氧自由基清除剂是否可以限制再灌注心律失常，增加缺血心肌局部功能的恢复，并减少90分钟冠状动脉闭塞和再灌注后1周时的组织坏死，在冠状动脉再灌注前和后1小时对清醒的狗进行超氧化物歧化酶（SOD）和过氧化氢酶治疗。另一组则用重组 SOD (rSOD) 治疗，因为市售的 SOD 和过氧化氢酶含有内毒素。在左心室压力计、左心室后壁超声壁厚计、左心房导管、左冠状动脉回旋支上的动脉导管、多普勒血流传感器和液压封堵器植入后3-4周，对清醒的狗进行研究。观察到的唯一有益效果是，与冠状动脉再灌注后的对照组相比，rSOD 治疗组每分钟心律失常的次数显着降低 (p < 0.05)。当以危险区域的百分比或缺血区侧支血流的函数表示时，治疗既不会增加缺血区壁增厚的恢复量，也不会减少梗塞面积。例如，梗塞面积占危险区域的百分比为 32.6 .+-。 5.8%, 37.4.+-. 6.4%, 28.3.+-.对照组、SOD 和过氧化氢酶处理组以及 rSOD 处理组分别为 5.1%。因此，尽管氧自由基清除剂的治疗导致再灌注心律失常的数量暂时减少，但与对照组相比，这种对清醒狗的治疗未能改善局部心肌功能障碍或减少坏死量。缺乏持续的有益作用可能表明在慢性制剂中需要使用自由基清除剂进行更长时间的治疗。
To determine if oxygen free radical scavengers administered before coronary artery reperfusion can limit reperfusion arrhythmias, increase the return of regional function in ischemic myocardium, and reduce tissue necrosis at 1 week after 90-minute coronary artery occlusion and reperfusion, conscious dogs were treated with superoxide dismutase (SOD) and catalase before and for 1 hour after coronary artery reperfusion. Another group was treated with recombinant SOD (rSOD) because the commercially available SOD and catalase contained endotoxin. The conscious dogs were studied 3-4 weeks after implanting left ventricular pressure gauges, ultrasonic wall thickness gauges in the posterior left ventricular wall, left atrial catheters, and arterial catheters, Doppler flow transducers, and hydraulic occluders on the left circumflex coronary artery. The only beneficial effect observed was that the number of arrhythmic beats per minute in the rSOD-treated group was significantly lower (p < 0.05) when compared with a control group after coronary artery reperfusion. Treatment neither increased the amount of recovery of wall thickening in the ischemic zone nor reduced infarct size when expressed either as a percentage of the area at risk or as a function of collateral blood flow in the ischemic zone. For example, infarct size as a percentage of the area at risk was 32.6 .+-. 5.8%, 37.4 .+-. 6.4%, 28.3 .+-. 5.1% in the control, SOD and catalase-, and rSOD-treated groups, respectively. Thus, although treatment with oxygen free radical scavengers invoked a transient reduction in the number of reperfusion arrhythmias, this treatment in conscious dogs failed to improve regional myocardial dysfunction or reduce the amount of necrosis when compared with a control group. The lack of a sustained salutary effect may indicate that longer periods of treatment with free radical scavengers are required in chronic preparations.