Beller G A, Smith T W, Hood W B
Am J Cardiol. 1975 Dec;36(7):902-7. doi: 10.1016/0002-9149(75)90080-6.
The effects of coronary reperfusion on the uptake of digoxin by ischemic myocardium were studied in 17 open chest dogs undergoing anterior wall infarction produced by snaring confluent branches of the left coronary arterial system. Epicardial electrograms delineated ischemic, border and nonischemic zones. The hearts were reperfused by snare release after 1, 2 and 6 hours of occlusion. After 15 minutes of reperfusion, 1.0 mg of tritiated digoxin (3H-digoxin) was given intravenously, and 2 hours later the hearts were excised and endocardial and epicardial samples from each zone were analyzed for 3H-digoxin concentration. In another group of eight dogs regional myocardial blood flow was assessed utilizing 15 mu of radio-labeled microspheres administered during occlusion and reperfusion. In five dogs with 1 hour of coronary occlusion and subsequent reperfusion, 3H-digoxin uptake was comparable in endocardial and epicardial layers of all three zones. In six dogs undergoing reperfusion after 2 hours of occlusion, mean 3H-digoxin concentration was significantly (P less than 0.001) reduced from the mean nonischemic concentration, by 54 percent in endocardial and 35 percent in epicardial layers of the ischemic zone. Border zone endocardial and epicardial 3H-digoxin uptake was reduced by 21 percent and 16 percent, respectively (P less than 0.05). In six dogs undergoing reperfusion after 6 hours of occlusion, 3H-digoxin uptake in the ischemic zone was significantly (P less than 0.001) reduced by 85 percent in endocardial and 60 percent in epicardial layers from the concentration in the nonischemic zone. Border zone uptake was decreased by 54 percent in endocardial and 36 percent in epicardial regions (P less than 0.01). These alterations of in vivo digoxin binding could not be explained by impaired reflow of blood to ischemic myocardium. We conclude that coronary reperfusion after 2 to 6 hours of occlusion is associated with a marked reduction in myocardial digoxin uptake, which is more pronounced in subendocardial than in subepicardial regions of ischemic tissue.
在17只开胸犬身上进行了研究，这些犬通过圈套左冠状动脉系统的汇合分支造成前壁梗死，以观察冠状动脉再灌注对缺血心肌摄取地高辛的影响。心外膜电图描绘出缺血区、边缘区和非缺血区。在闭塞1、2和6小时后通过松开圈套进行心脏再灌注。再灌注15分钟后，静脉注射1.0毫克氚标记地高辛（3H-地高辛），2小时后取出心脏，分析每个区域的心内膜和心外膜样本中的3H-地高辛浓度。在另一组8只犬中，在闭塞和再灌注期间利用15微升放射性标记微球评估局部心肌血流量。在5只冠状动脉闭塞1小时并随后进行再灌注的犬中，所有三个区域的心内膜和心外膜层中3H-地高辛的摄取相当。在6只闭塞2小时后进行再灌注的犬中，缺血区心内膜层的平均3H-地高辛浓度较非缺血区平均浓度显著降低（P<0.001），降低了54%，心外膜层降低了35%。边缘区心内膜和心外膜的3H-地高辛摄取分别降低了21%和16%（P<0.05）。在6只闭塞6小时后进行再灌注的犬中，缺血区心内膜层的3H-地高辛摄取较非缺血区浓度显著降低（P<0.001），降低了85%，心外膜层降低了60%。边缘区心内膜摄取降低了54%，心外膜区域降低了36%（P<0.01）。体内地高辛结合的这些改变无法用缺血心肌血流再灌注受损来解释。我们得出结论，闭塞2至6小时后的冠状动脉再灌注与心肌地高辛摄取显著降低有关，这在缺血组织的心内膜下区域比心外膜下区域更明显。
